' By Sofia Quaglia Flip open any neuroscience textbook and the depiction of a neuron will be roughly the same: a blobby, amoebalike cell body shooting out a long, thick strand. That strand is the axon, which conducts electrical signals to terminals where the cell communicates with other neurons. Axons have long been depicted as smooth and cylindrical, but a new study of mouse neurons challenges that view. Instead, it suggests their natural shape is more like a string of pearls. Even more provocatively, the authors propose those pearly bumps serve as control knobs, influencing how quickly and precisely the cell fires its signals. The study, published today in Nature Neuroscience, should “100%” change how we’ve been thinking about neurons and their signals, says senior author Shigeki Watanabe, a molecular neuroscientist at John Hopkins University. Some outsiders agree. The findings are “highly significant and I think have been overlooked for quite some time,” says evolutionary biologist Pawel Burkhardt of the University of Bergen, who recently spotted similar pearl structures in neurons from tiny marine invertebrates known as comb jellies. Yet several experts in the field contest the findings. Some cite potential confounding effects of the preparation and freezing method used to preserve cells before imaging. And some doubt the work totally upends what’s known about the true shape of the axon. “I think it’s true that [the axon is] not a perfect tube, but it’s not also just this kind of accordion that they show,” says neuroscientist Christophe Leterrier from Aix-Marseille University, who calls the study “a controversial addition to the literature.” Since the mid-1960s, microscopists have seen that axons can scrunch up to form beads when they are diseased or under other stress. Leterrier has called these temporary beads “stress balls for the brain” and found evidence that they prevent cellular damage from spreading. Other studies suggest even normal axons bulge temporarily when cargo traveling to and from the cell nucleus forms a traffic jam, like the elephant bulging inside the body of a boa in the children’s book The Little Prince.

Keyword: Brain imaging
Link ID: 29586 - Posted: 12.04.2024

By Annie Liontas In 2016, Marchell Taylor lay in his windowless, six-by-eight cell in the Denver County Jail. Only 36 days after being released after serving time for drug and robbery convictions, he robbed a Papa John’s and assaulted an employee. Because of his record, Mr. Taylor faced 300 years of imprisonment. He asked himself: Why am I back here? Answering his question may require looking back to 1978, when he was 9 years old and his family’s car slammed into a wall. He woke up to blood on his face. The brain injury he sustained went untreated. Shortly after that, his behavior changed, and he became, in his words, “snappy and violent.” By age 10, he was regularly turning to marijuana and alcohol. At 13, he was breaking into houses. At 14, he robbed a 7-Eleven. In 1993 he was picked up for aggravated robbery and ended up in a maximum security facility. For the next two decades, Mr. Taylor was in and out of institutions like this. That is until the Brain Injury Alliance of Colorado diagnosed him with a brain injury in 2016 while he was awaiting trial. After administering a screening, psychologists at the Men’s Mental Health Transition Unit — a pioneering mental health program in the Denver County Jail — gave Mr. Taylor access to therapies for mental health, including cognitive behavioral therapy and eye movement desensitization and reprocessing therapy, which helps process traumatic memories and experiences. These treatments taught him about his brain, and he says it has made all the difference. It is tempting to dismiss brain injury at an early age as the cause of years of criminal behavior. It’s certainly true in Mr. Taylor’s case that there were other contributing factors, including ongoing substance abuse, a lack of money and weak social and psychological support. But after spending years researching brain injuries in an effort to understand my own recovery from several and as a friend of Mr. Taylor’s, I’m reckoning with the fact that experts are only now beginning to recognize the connection between brain injury and incarceration. While such trauma may not offer a tidy explanation for histories like his, growing insight into this connection offers an opportunity to change the grim legacy of incarceration and mental illness in this country by treating an underlying factor that can fuel recidivism. © 2024 The New York Times Company

Keyword: Aggression; Brain Injury/Concussion
Link ID: 29585 - Posted: 12.04.2024

By Giorgia Guglielmi For years, scientists have thought of hunger regulation as a tug-of-war between two types of neurons in the hypothalamus: those that express the AGRP gene and increase hunger, and those that express the POMC gene and act as a brake. Now a new study challenges this long-standing model, revealing a third player in the hunger-satiety network—a neuron type that expresses the BNC2 gene and suppresses hunger faster than those that express POMC. These BNC2 neurons are activated by leptin—a hormone that helps suppress appetite and boost metabolism. Their discovery “reshapes our understanding of feeding behavior,” says lead investigator Han Tan, “and how leptin regulates body weight.” Tan is a research associate in Jeffrey Friedman’s lab at Rockefeller University. “We’ve known for a long time there must be [other] neurons in the brain that are sensing leptin and decreasing appetite, but we didn’t know who they were until now,” says John Campbell, assistant professor of biology at the University of Virginia, who wasn’t involved in the study. The results jibe with two other recent reports of leptin-sensitive neurons in the arcuate nucleus—a region in the hypothalamus that processes signals related to hunger and satiety. The neurons generate feelings of fullness, an independent team reported in Science in June, and they dampen appetite by inhibiting AGRP-expressing “hunger neurons,” according to a preprint Campbell and his colleagues posted on bioRxiv in July. The studies all point to a unique group of neurons that inhibit hunger, says Martin Myers, professor of internal medicine and molecular and integrative physiology at the University of Michigan, who was not involved in the work. “The three groups essentially found [these neurons] simultaneously.” © 2024 Simons Foundation

Keyword: Obesity
Link ID: 29584 - Posted: 12.04.2024

By Lisa Sanders, M.D. The 62-year-old woman shifted in her seat. The flight to Honolulu was full, the mood a little giddy. The unbroken ocean and sky filled the window. She and her daughter were four hours into the trip from Los Angeles to the wedding of a close family friend; it was going to be a great week. Then, she caught herself scratching lightly at a place on her forearm, just below the crease of her elbow. She lifted her arm to look at the spot. Nothing there. Immediately she was filled with dread. She reached over her head to touch the call button. She needed ice, lots of ice, and she needed it right away. The mild itch had already exploded into spasms of an intense sensation — it seemed wrong to call it an itch; surely there was a better word for it. The fierce intensity of the feeling shocked her. It was a feeling that insisted she scratch. Except scratching never helped. And she had the scars to prove it. She had suffered episodes of itching like this a few times in the past couple of years, though never quite as bad as it was on this flight. Her doctor back home had no idea what caused the crazy itch or what more she might do about it. These attacks came out of nowhere but immediately brought life to a standstill as she tried to ease the unbearable sensation. A bout could last for hours and almost always ended with her arm a bloody mess. When her daughter first saw her mother raking her nails over the invisible injury and the distress she felt fighting this unwinnable battle, she had offered her a Valium. And it helped. The itch was still there but the intensity somehow lessened. On the flight, the woman retrieved the pills she now carried with her all the time. The little bags of ice brought by the flight attendant melted slowly, numbing the hand that pressed them against her arm and easing the itch. She knew from experience that as soon as the ice was removed, the itch would roar back. The attendant brought an ice bucket. But within the hour, she needed more ice. More Valium. She was drenched with the condensation. Her clothes were dotted with blood. She didn’t care. She just had to get through it. © 2024 The New York Times Company

Keyword: Pain & Touch
Link ID: 29583 - Posted: 12.04.2024

By Christina Caron The holidays offer an excuse to gather with loved ones, let loose and indulge: Plates loaded with comfort foods. Unapologetic napping. All the pie. And, for some, plenty of alcohol. But heavy drinking is not limited to the holiday season. Nor is it mainly the pastime of college students. Overall binge drinking rates are now equivalent among young adults and those in midlife. That’s because young people, especially young men, are bingeing less — while middle-aged adults are throwing back more alcohol in a single session than they previously did. We’ve long been warned about the risks of binge drinking, usually defined as having four or five drinks in a two-hour span. And now researchers are increasingly focused on a more dangerous pattern of alcohol use that they call high-intensity drinking: consuming eight or more drinks in a row for women and 10 or more drinks in a row for men. High-intensity drinking is even riskier than binge drinking, and it’s on the rise among certain segments of the population. How does high-intensity drinking differ from binge drinking? The definition of binge drinking stems from the work of Henry Wechsler, a social psychologist at Harvard University who in 1993 tracked alcohol use among college students across the country. He found that young women who reported consuming at least four drinks in a night and men who consumed at least five experienced the most drinking-related problems. But other researchers noticed that some of the worst consequences associated with binge drinking, such as blackouts and alcohol poisoning, tended to happen when people had much more than four or five drinks. Over the years, experts have referred to heavier levels of binge drinking in different ways, including “extreme drinking” and the far less catchy “extreme ritualistic alcohol consumption.” In recent years they settled on “high-intensity drinking.” © 2024 The New York Times Company

Keyword: Drug Abuse
Link ID: 29582 - Posted: 11.30.2024

By Iris Berent Seeing the striking magenta of bougainvillea. Tasting a rich morning latte. Feeling the sharp pain of a needle prick going into your arm. These subjective experiences are the stuff of the mind. What is “doing the experiencing,” the 3-pound chunk of meat in our head, is a tangible object that works on electrochemical signals—physics, essentially. How do the two—our mental experiences and physical brains—interact? The puzzle of consciousness seems to be giving science a run for its money. The problem, to be clear, isn’t merely to pinpoint “where it all happens” in the brain (although this, too, is far from trivial). The real mystery is how to bridge the gap between the mental, first-person stuff of consciousness and the physical lump of matter inside the cranium. Some think the gap is unbreachable. The philosopher David Chalmers, for instance, has argued that consciousness is something special and distinct from the physical world. If so, it may never be possible to explain consciousness in terms of physical brain processes. No matter how deeply scientists understand the brain, for Chalmers, this would never explain how our neurons produce consciousness. Why should a hunk of flesh, teeming with chemical signals and electrical charges, experience a point of view? There seems to be no conceivable reason why meaty matter would have this light of subjectivity “on the inside.” Consciousness, then, is a “hard problem”—as Chalmers has labeled it—indeed. The possibility that consciousness itself isn’t anything physical raises burning questions about whether, for example, an AI can fall in love with its programmer. And since consciousness is a natural phenomenon, much like gravity or genes, these questions carry huge implications. Science explains the natural world by physical principles only. So if it turns out that one natural phenomenon transcends the laws of physics, then it is not only the science of consciousness that is in trouble—our entire understanding of the natural world would require serious revision. © 2024 NautilusNext Inc.,

Keyword: Consciousness
Link ID: 29581 - Posted: 11.30.2024

By Margot Sanger-Katz The Biden administration, in one of its last major policy directives, proposed on Tuesday that Medicare and Medicaid cover obesity medications, a costly and probably popular move that the Trump administration would need to endorse to become official. The proposal would extend access of the drugs to millions of Americans who aren’t covered now. The new obesity drugs, including Wegovy from Novo Nordisk and Zepbound from Eli Lilly, have been shown to improve health in numerous ways, but legislation passed 20 years ago prevents Medicare from covering drugs for “weight loss.” The new proposal sidesteps that restriction, specifying that the drugs would be covered to treat the disease of obesity and prevent its related conditions. “We don’t want to see people having to wait until they have these additional diseases before they get treatment,” said Chiquita Brooks-LaSure, the administrator of the Centers for Medicare and Medicaid Services, or C.M.S., noting the growing medical consensus that obesity is a chronic health condition. The classification would also mean that every state Medicaid program would be required to cover the drugs. Currently, only a handful do. C.M.S. estimates that around 3.4 million more patients in Medicare would become eligible for obesity drugs, and around four million patients in Medicaid would gain coverage, costing the programs billions of dollars. Medicare mostly covers Americans 65 and older; Medicaid mostly covers poor and disabled Americans. The proposal is part of an annual policy update for all Medicare drug plans and private Medicare Advantage plans starting in 2026. In a conference call with reporters Tuesday, Daniel Tsai, the top Medicaid official, said Medicaid coverage could start sooner than 2026. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29580 - Posted: 11.30.2024

Andrew Gregory Health editor Failing to stick to a regular time for going to bed and waking up increases the risk of stroke, heart attack and heart failure by 26%, even for those who get a full night’s sleep, the most comprehensive study of its kind suggests. Previous studies have focused on the links between sleep duration and health outcomes, with people advised to get between seven and nine hours shut-eye a night. That advice still stands. But researchers are increasingly focusing on sleep patterns, and in particular the impact of irregular sleep – defined as variations in the time a person goes to sleep and wakes up. The new study found irregular sleep – going to bed and waking up at different times each day – was “strongly associated” with a higher risk of major adverse cardiovascular events. Even getting eight hours of sleep was insufficient to offset the harmful effects of consistently varying bed and wake-up times, experts said. The research, published in the Journal of Epidemiology and Community Health, involved 72,269 people aged 40 to 79 from the UK Biobank study. It did not establish precisely how close you have to get to the same bed and wake-up time – only that the further away you are, the higher the risk of harm. The lead author, Jean-Philippe Chaput, of the University of Ottawa, said: “We should aim to wake up and go to sleep within 30 minutes of the same time each night and each morning, including weekends. Within an hour of the same time is good but less good than 30 minutes, and even better is to have zero variation. “Beyond an hour’s difference each night and each morning means irregular sleep. That can have negative health impacts. The closer you are to zero variation the better. “No one is perfect across a whole year, and if you don’t have a regular sleep pattern for one or two days a week, it’s not going to kill you. But if you repeatedly have irregular sleep, five or six days a week, then it becomes chronic, and that is a problem.” Chaput said waking up at the same time each day was more important than going to bed at the same time. “Waking up at different times each morning really messes with your internal clock, and that can have adverse health consequences,” he said. © 2024 Guardian News & Media Limited

Keyword: Sleep
Link ID: 29578 - Posted: 11.27.2024

By Teddy Rosenbluth Cassava Sciences, a small biotechnology company based in Austin, Texas, announced it would stop the advanced clinical trial for an experimental Alzheimer’s drug, ending a long-contested bid for regulatory approval. The company announced on Monday that the drug, simufilam, did not significantly reduce cognitive decline in people with mild to moderate Alzheimer’s disease in the trial, which enrolled more than 1,900 patients. “The results are disappointing for patients and their families who are living with this disease and physicians who have been looking for novel treatment options,” the company’s chief executive, Richard J. Barry, said in a statement. These results were unsurprising to many dementia researchers, who had questioned why the trial had been allowed to proceed in the first place, since much of the drug’s underlying science had been called into question. Studies that once seemed to support the drug have been retracted from scientific journals. A consultant researcher who helped conduct some of the drug’s foundational studies was charged with fraud by a federal grand jury for allegedly falsifying data to obtain research grants. In September, the company settled with the Securities and Exchange Commission over allegations that Cassava had made misleading statements about the results of earlier clinical trial data. However, the company neither admitted nor denied wrongdoing. © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29577 - Posted: 11.27.2024

By Andrea Tamayo Kidney cells can make memories too. At least, in a metaphorical sense. Neurons have historically been the cell most associated with memory. But far outside the brain, kidney cells can also store information and recognize patterns in a similar way to neurons, researchers report November 7 in Nature Communications. “We’re not saying that this kind of memory helps you learn trigonometry or remember how to ride a bike or stores your childhood memories,” says Nikolay Kukushkin, a neuroscientist at New York University. “This research adds to the idea of memory; it doesn’t challenge the existing conceptions of memory in the brain.” In experiments, the kidney cells showed signs of what’s called a “massed-space effect.” This well-known feature of how memory works in the brain facilitates storing information in small chunks over time, rather than a big chunk at once. Outside the brain, cells of all types need to keep track of stuff. One way they do that is through a protein central to memory processing, called CREB. It, and other molecular components of memory, are found in neurons and nonneuronal cells. While the cells have similar parts, the researchers weren’t sure if the parts worked the same way. In neurons, when a chemical signal passes through, the cell starts producing CREB. The protein then turns on more genes that further change the cell, kick-starting the molecular memory machine (SN: 2/3/04). Kukushkin and colleagues set out to determine whether CREB in nonneuronal cells responds to incoming signals the same way. © Society for Science & the Public 2000–2024.

Keyword: Learning & Memory
Link ID: 29576 - Posted: 11.27.2024

Heather Margonari The opioid crisis remains a significant public health challenge in the United States. In 2022, over 2.5 million American adults had an opioid use disorder, and opioids accounted for nearly 76% of overdose deaths. Some patients are fearful of using opioids after surgery due to concerns about dependence and potential side effects, even when appropriately prescribed by a doctor to manage pain. Surgery is often the first time patients receive an opioid prescription, and their widespread use raises concerns about patients becoming long-term users. Leftover pills from a patient’s prescriptions may also be misused. Researchers like us are working to develop a personalized and comprehensive surgical experience that doesn’t use opioids. Our approach to opioid-free surgery addresses both physical and emotional well-being through effective anesthesia and complementary pain-management techniques. What is opioid-free anesthesia? Clinicians have used morphine and other opioids to manage pain for thousands of years. These drugs remain integral to anesthesia. Help us raise up the voices of experts. Most surgical procedures use a strategy called balanced anesthesia, which combines drugs that induce sleep and relax muscles with opioids to control pain. However, using opioids in anesthesia can lead to unwanted side effects, such as serious cardiac and respiratory problems, nausea and vomiting, and digestive issues. Concerns over these adverse effects and the opioid crisis have fueled the development of opioid-free anesthesia. This approach uses non-opioid drugs to relieve pain before, during and after surgery while minimizing the risk of side effects and dependency. Studies have shown that opioid-free anesthesia can provide similar levels of pain relief to traditional methods using opioids. Copyright © 2010–2024, The Conversation US, Inc.

Keyword: Pain & Touch
Link ID: 29575 - Posted: 11.27.2024

By Diana Kwon Since a schizophrenia drug, the first in decades with an innovative mechanism of action, gained US regulatory approval in September, some researchers have proclaimed a new era for psychiatric medicine. About half a dozen similar drugs — for schizophrenia, Alzheimer’s disease and other conditions involving the brain — are in various stages of development, most in early-stage clinical trials. But the success of these medicines is not a given. Last week, a trial of a highly anticipated schizophrenia drug reported disappointing results. For decades, schizophrenia drugs worked in essentially the same way. They blunted the activity of dopamine, a chemical involved in the disorder’s hallmark symptoms, such as hallucinations and delusions. The new kid on the block is KarXT, sold as Cobenfy. It targets muscarinic receptors and leads to antipsychotic and cognitive benefits. “I don’t think I’ve ever seen this much buzz and excitement over a new approach in psychiatry in my career,” says Jeffrey Conn, a pharmacologist at Vanderbilt University in Nashville, Tennessee, who was one of the company’s scientific co-founders. KarXT’s success in winning US regulatory approval has revived interest in muscarinic drugs. “Drug discovery is coming back to psychiatry,” says Arthur Christopoulos, a molecular pharmacologist at Monash University in Melbourne, Australia, who was involved in the development of KarXT. But developing new medicines is a hard, long road. On 11 November, Abbvie, a pharmaceutical company in North Chicago, Illinois, announced that its muscarinic drug for schizophrenia, called emraclidine, had failed to outperform a placebo. What this means for other muscarinic drugs in development remains to be seen, Christopoulos says. “It is still early days.” © 2024 Springer Nature Limited

Keyword: Schizophrenia
Link ID: 29574 - Posted: 11.23.2024

By Sofia Quaglia It’s amazing what chimpanzees will do for a snack. In Congolese rainforests, the apes have been known to poke a hole into the ground with a stout stick, then grab a long stem and strip it through their teeth, making a brush-like end. Into the hole that lure goes, helping the chimps fish out a meal of termites. How did the chimps figure out this sophisticated foraging technique and others? “It’s difficult to imagine that it can just have appeared out of the blue,” said Andrew Whiten, a cultural evolution expert from the University of St. Andrews in Scotland who has studied tool use and foraging in chimpanzees. Now Dr. Whiten’s team has set out to demonstrate that advanced uses of tools are an example of humanlike cultural transmission that has accumulated over time. Where bands of apes in Central and East Africa exhibit such complex behaviors, they say, there are also signs of genes flowing between groups. They describe this as evidence that such foraging techniques have been passed from generation to generation, and innovated over time across different interconnected communities. In a study published on Thursday in the journal Science, Dr. Whiten and colleagues go as far as arguing that chimpanzees have a “tiny degree of cumulative culture,” a capability long thought unique to humans. From mammals to birds to reptiles and even insects, many animals exhibit some evidence of culture, when individuals can socially learn something from a nearby individual and then start doing it. But culture becomes cumulative over time when individuals learn from others, each building on the technique so much that a single animal wouldn’t have been able to learn all of it on its own. For instance, some researchers interpret using rocks as a hammer and anvil to open a nut as something chimpanzees would not do spontaneously without learning it socially. Humans excel at this, with individual doctors practicing medicine each day, but medicine is no one single person’s endeavor. Instead, it is an accumulation of knowledge over time. Most chimpanzee populations do not use a complex set of tools, in a specific sequence, to extract food. © 2024 The New York Times Company

Keyword: Evolution; Learning & Memory
Link ID: 29573 - Posted: 11.23.2024

By Janna Levin It’s fair to say that enjoyment of a podcast would be severely limited without the human capacity to create and understand speech. That capacity has often been cited as a defining characteristic of our species, and one that sets us apart in the long history of life on Earth. Yet we know that other species communicate in complex ways. Studies of the neurological foundations of language suggest that birdsong, or communication among bats or elephants, originates with brain structures similar to our own. So why do some species vocalize while others don’t? In this episode, Erich Jarvis, who studies behavior and neurogenetics at the Rockefeller University, chats with Janna Levin about the surprising connections between human speech, birdsong and dance. JANNA LEVIN: All animals exhibit some form of communication, from the primitive hiss of a lizard to the complex gestures natural to chimps, or the songs shared by whales. But human language does seem exceptional, a vast and discrete cognitive leap. Yet recent research is finding surprising neurological connections between our expressive speech and the types of communication innate to other animals, giving us new ideas about the biological and developmental origins of language. Erich is a professor at the Rockefeller University and a Howard Hughes Medical Institute investigator. At Rockefeller, he directs the Field Research Center of Ethology and Ecology. He also directs the Neurogenetics Lab of Language and codirects the Vertebrate Genome Lab, where he studies song-learning birds and other species to gain insight into the mechanism’s underlying language and vocal learning. ERICH JARVIS: So, the first part: Language is built-in genetically in us humans. We’re born with the capacity to learn how to produce and how to understand language, and pass it on culturally from one generation to the next. The actual detail is learned, but the actual plan in the brain is there. Second part of your question: Is it, you know, special or unique to humans? It is specialized in humans, but certainly many components of what gives rise to language is not unique to humans. There’s a spectrum of abilities out there in other species that we share some aspects of with other species. © 2024 Simons Foundation

Keyword: Language; Evolution
Link ID: 29572 - Posted: 11.23.2024

By Claudia López Lloreda For decades, researchers have considered the brain “immune privileged”—protected from the vagaries of the body’s immune system. But building evidence suggests that the brain may be more immunologically active than previously thought, well beyond its own limited immune response. The choroid plexus in particular—the network of blood vessels and cerebrospinal-fluid (CSF)-producing epithelial cells that line the organ’s ventricles—actively recruits immune cells from both the periphery and the CSF, according to a new study in mice. The epithelial layer of the choroid plexus shields the rest of the brain from toxic substances, pathogens and other molecules that circulate in the blood. Dysfunction and neuroinflammation in the choroid plexus is associated with aging and many neurological conditions, such as amyotrophic lateral sclerosis and Alzheimer’s disease. Even in the absence of inflammation, the choroid plexus harbors immune cells, some of which reside in the space between the vessels and the epithelial layer, and some on the epithelial surface. During an immune response, it also contains recruited cells, such as macrophages and other leukocytes, and pro-inflammatory signals, previous research has shown. But those findings offered only a snapshot of the cells’ locations, says Maria Lehtinen, professor of pathology at Harvard Medical School, who led the new work. “Just because [the cell] is in the tissue doesn’t mean it’s necessarily crossing or has gone in the direction that you anticipate that it would be going in.” How the choroid plexus gatekeeps immune cells remains a big question in the field, says Michal Schwartz, a neuroimmunologist at the Weizmann Institute of Science, who was not involved with the new work. © 2024 Simons Foundation

Keyword: Neuroimmunology
Link ID: 29571 - Posted: 11.23.2024

By Roni Caryn Rabin The number of deaths caused by alcohol-related diseases more than doubled among Americans between 1999 and 2020, according to new research. Alcohol was involved in nearly 50,000 deaths among adults ages 25 to 85 in 2020, up from just under 20,000 in 1999. The increases were in all age groups. The biggest spike was observed among adults ages 25 to 34, whose fatality rate increased nearly fourfold between 1999 and 2020. Women are still far less likely than men to die of an illness caused by alcohol, but they also experienced a steep surge, with rates rising 2.5-fold over 20 years. The new study, published in The American Journal of Medicine, drew on data from the Centers for Disease Control and Prevention. Deaths related to alcohol included those caused by certain forms of heart disease, liver disease, nerve damage, muscle damage, pancreatitis and alcohol poisoning, as well as related mental and behavioral disorders. The study did not include other deaths influenced by alcohol, such as accidents. “The totality of the evidence indicates that people who consume moderate to large amounts of alcohol have a markedly increased incidence of premature deaths and disability,” said Dr. Charles Hennekens, a professor of medicine at Charles E. Schmidt College of Medicine at Florida Atlantic University and one of the study’s authors. The increase at the onset of the pandemic appears to have persisted. Adults reported more heavy drinking and binge drinking in 2022, another recent study found. Some 48,870 alcohol-related deaths were reported in 2020, up from 19,356 in 1999, the new study found. The mortality rate rose to 21.6 deaths per 100,000 in 2020, an increase from 10.7 deaths per 100,000 in 1999. © 2024 The New York Times Company

Keyword: Drug Abuse
Link ID: 29570 - Posted: 11.23.2024

By Tomas Weber Trinian Taylor, a 52-year-old car dealer, pushed his cart through the aisles of a supermarket as I pretended not to follow him. It was a bright August day in Northern California, and I had come to the store to meet Emily Auerbach, a relationship manager at Mattson, a food-innovation firm that creates products for the country’s largest food and beverage companies: McDonald’s and White Castle, PepsiCo and Hostess. Auerbach was trying to understand the shopping behavior of Ozempic users, and Taylor was one of her case studies. She instructed me to stay as close as I could without influencing his route around the store. In her experience of shop-alongs, too much space, or taking photos, would be a red flag for the supermarket higher-ups, who might figure out we were not here to shop. “They’d be like, ‘You need to exit,’” she said. Auerbach watched in silence as Taylor, who was earning $150 in exchange for being tailed, propelled his cart through snack aisles scattered with products from Mattson’s clients. He took us straight past the Doritos and the Hostess HoHos, without a side glance at the Oreos or the Cheetos. We rushed past the Pop-Tarts and the Hershey’s Kisses, the Lucky Charms and the Lay’s — they all barely registered. Clumsily, close on his heels, Auerbach and I stumbled right into what has become, under the influence of the revolutionary new diet drug, Taylor’s happy place: the produce section. He inspected the goods. “I’m on all of these,” he told us. “I eat a lot of pineapple. A lot of pineapple, cucumber, ginger. Oh, a lot of ginger.” Taylor, who lives in Hayward, Calif., used to nurse a sugar addiction, he said, but he can no longer stomach Hostess treats. A few days earlier, his daughter fed him some candy. “I just couldn’t,” he said. “It was so sweet it choked me.” His midnight snack used to be cereal, but now he stirs at night with strange urges. Salads. Chicken. He has sworn off canned sodas and fruit juices and infuses his water with lemon and cucumber. He dropped a heavy bag of lemons into the cart and sauntered over to the leafy vegetables. “I love Swiss chard,” he said. “I eat a lot of kale.” For decades, Big Food has been marketing products to people who can’t stop eating, and now, suddenly, they can. The active ingredient in Ozempic, as in Wegovy, Zepbound and several other similar new drugs, mimics a natural hormone, called glucagon-like peptide-1 (GLP-1), that slows digestion and signals fullness to the brain. Around seven million Americans now take a GLP-1 drug, and Morgan Stanley estimates that by 2035 the number of U.S. users could expand to 24 million. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29569 - Posted: 11.20.2024

Ian Sample Science editor Losing weight can be a frustrating game: after months of successful slimming, the kilos may soon pile on again, leaving people back where they started. No one factor drives the yo-yo effect, but new research points to fatty tissue as a leading culprit. Fat “remembers” past obesity and resists attempts to lose weight, scientists found. Researchers identified the biological memory after examining fat tissue from people with obesity before and after they lost weight after bariatric surgery. The tissues were further compared with fat from healthy individuals who had never been obese. The analysis showed that fat cells were affected by obesity in a way that altered how they responded to food, potentially for years. In tests, the cells grew faster than others by absorbing nutrients more swiftly. Prof Ferdinand von Meyenn, a senior author on the study at the Federal Institute of Technology in Zurich, said: “Our study indicates that one reason maintaining body weight after initial weight loss is difficult is that the fat cells remember their prior obese state and likely aim to return to this state. “The memory seems to prepare cells to respond quicker, and maybe also in unhealthy ways, to sugars or fatty acids.” Further work on mouse cells traced the biological memory to chemical modifications on DNA or the proteins DNA is wrapped around. These epigenetic changes alter gene activity and metabolism. Writing in Nature, the scientists describe how formerly obese mice gained weight faster than others when put on a high-fat diet, suggesting a shift in metabolism that made it easier for them to gain weight. The memory of obesity in fat cells was not solely to blame, however. The scientists suspect a similar memory exists in brain cells that affects how much food animals consume and how much energy they expend. © 2024 Guardian News & Media Limited

Keyword: Obesity
Link ID: 29568 - Posted: 11.20.2024

By Joanne Silberner To describe the destructive effects of intense health anxiety to his young doctors in training at Columbia University Irving Medical Center in New York City, psychiatrist Brian Fallon likes to quote 19th-century English psychiatrist Henry Maudsley: “The sorrow which has no vent in tears may make other organs weep.” That weeping from other parts of the body may come in the form of a headache that, in the mind of its sufferer, is flagging a brain tumor. It may be a rapid heartbeat a person wrongly interprets as a brewing heart attack. The fast beats may be driven by overwhelming, incapacitating anxiety. Hal Rosenbluth, a businessman in the Philadelphia area, says he used to seek medical care for the slightest symptom. In his recent book Hypochondria, he describes chest pains, breathing difficulties and vertigo that came on after he switched from a daily diabetes drug to a weekly one. He ended up going to the hospital by ambulance for blood tests, multiple electrocardiograms, a chest x-ray, a cardiac catheterization and an endoscopy, all of which were normal. Rosenbluth’s worries about glucose levels had led him to push for the new diabetes drug, and its side effects were responsible for many of his cardiac symptoms. His own extreme anxiety had induced doctors to order the extra care. Hypochondria can, in extreme cases, leave people unable to hold down a job or make it impossible for them to leave the house, cook meals, or care for themselves and their families. Recent medical research has shown that hypochondria is as much a real illness as depression and post-traumatic stress disorder. This work, scientists hope, will convince doctors who believed the disorder was some kind of character flaw that their patients are truly ill—and in danger. A study published just last year showed that people with hypochondria have higher death rates than similar but nonafflicted people, and the leading nonnatural cause of death was suicide. It was relatively rare, but the heightened risk was clear.

Keyword: Stress; Attention
Link ID: 29567 - Posted: 11.20.2024

By Laura Sanders Growing up, Roberto S. Luciani had hints that his brain worked differently than most people. He didn’t relate when people complained about a movie character looking different than what they’d pictured from the book, for instance. But it wasn’t until he was a teenager that things finally clicked. His mother had just woken up and was telling him about a dream she had. “Movielike,” is how she described it. “Up until then, I assumed that cartoon depictions of imagination were exaggerated,” Luciani says, “I asked her what she meant and quickly realized my visual imagery was not functioning like hers.” That’s because Luciani has a condition called aphantasia — an inability to picture objects, people and scenes in his mind. When he was growing up, the term didn’t even exist. But now, Luciani, a cognitive scientist at the University of Glasgow in Scotland, and other scientists are getting a clearer picture of how some brains work, including those with a blind mind’s eye. In a recent study, Luciani and colleagues explored the connections between the senses, in this case, hearing and seeing. In most of our brains, these two senses collaborate. Auditory information influences activity in brain areas that handle vision. But in people with aphantasia, this connection isn’t as strong, researchers report November 4 in Current Biology. While in a brain scanner, blindfolded people listened to three sound scenes: A forest full of birds, a crowd of people, and a street bustling with traffic. In 10 people without aphantasia, these auditory scenes create reliable neural hallmarks in parts of the visual cortex. But in 23 people with aphantasia, these hallmarks were weaker. © Society for Science & the Public 2000–2024.

Keyword: Attention
Link ID: 29566 - Posted: 11.20.2024