By Miryam Naddaf Researchers have identified 13 proteins in the blood that predict how quickly or slowly a person’s brain ages compared with the rest of their body. Their study1, published in Nature Aging on 9 December, used a machine-learning model to estimate ‘brain ages’ from scans of more than 10,000 people. The authors then analysed thousands of scans alongside blood samples and found eight proteins that were associated with fast brain ageing, and five linked to slower brain ageing. “Previous studies mainly focused on the association between the proteins and the chronological age, that means the real age of the individual,” says study co-author Wei-Shi Liu, a neurologist at Fudan University in Shanghai, China. However, studying biomarkers linked to a person’s brain age could help scientists to identify molecules to target in future treatments for age-related brain diseases. “These proteins are all promising therapeutic targets for brain disorders, but it may take a long time to validate them,” says Liu. Using machine learning to analyse brain-imaging data from 10,949 people, Liu and his colleagues created a model to calculate a person’s brain age, on the basis of features such as the brain’s volume, surface area and distribution of white matter. They wanted to identify proteins that are associated with a large brain age gap — the difference between brain age and chronological age. To do this, the researchers analysed levels of 2,922 proteins in blood samples from 4,696 people, more than half of whom were female, and compared them with the same people’s brain ages derived from the scans. They identified 13 proteins that seemed to be connected with large brain age gaps, some of which are known to be involved in movement, cognition and mental health.

Keyword: Development of the Brain
Link ID: 29597 - Posted: 12.11.2024

By Grace Huckins Genes on the X and Y chromosomes—and especially those on the Y—appear to be associated with autism likelihood, according to a study focused on people who have missing or extra sex chromosomes. The findings add to the ongoing debate about whether autism’s sex bias reflects a male vulnerability, a female protective effect or other factors. “The Y chromosome is often left out of genetic discovery studies. We really have not interrogated it in [autism] studies very much,” says Matthew Oetjens, assistant professor of human genetics at Geisinger Medical Center’s Autism and Developmental Medicine Institute, who led the new work. There is a clear sex difference in autism prevalence: Men are about four times as likely as women to have a diagnosis. But uncovering the reasons for that discrepancy has proved challenging and contentious. Multiple biological factors may play a role, in addition to social factors—such as the difficult-to-measure gulfs between how boys and girls are taught to behave. Add on the possibility of diagnostic bias and the question starts to look less like a scientific problem and more like a politically toxic Gordian knot. But there are some threads that researchers can pull to disentangle these effects, as the new study illustrates. People with sex chromosome aneuploidies—or unusual combinations of sex chromosomes, such as XXY in those with Klinefelter syndrome or a single X in Turner syndrome—provide a unique opportunity to examine how adding or taking away chromosomes can affect biology and behavior. Previous studies noted high rates of autism in people with sex chromosome aneuploidies, but those analyses were subject to ascertainment bias; perhaps those people found out about their aneuploidies only after seeking support for their neurodevelopmental conditions. © 2024 Simons Foundation

Keyword: Autism; Sexual Behavior
Link ID: 29596 - Posted: 12.11.2024

By Derek Thompson At 3 a.m. I’m jolted awake. The room is dark and still. I grab my phone and scan sports scores and Twitter. Still awake. A faceless physician whispers in my mind: To overcome middle-of-the-night insomnia, experts say you ought to get out of bed … I get out of bed. I pour a glass of water and drink it. I go back to bed. Still awake. Perhaps you know the feeling. Like millions of Americans and hundreds of millions of people around the world, I suffer from so-called mid-sleep awakenings that can keep me up for hours. One day, I was researching my nocturnal issues when I discovered a cottage industry of writers and sleep hackers who claim that sleep is a nightmare because of the industrial revolution, of all things. Essays in The Guardian, CNN, The New York Times, and The New York Times Magazine recommended an old fix for restlessness called “segmented sleep.” In premodern Europe, and perhaps centuries earlier, people routinely went to sleep around nightfall and woke up around midnight—only to go back to sleep a few hours later, until morning. They slept sort of like I do, but they were Zen about it. Then, the hackers claim, modernity came along and ruined everything by pressuring everybody to sleep in one big chunk. The romanticization of preindustrial sleep fascinated me. It also snapped into a popular template of contemporary internet analysis: If you experience a moment’s unpleasantness, first blame modern capitalism. So I reached out to Roger Ekirch, the historian whose work broke open the field of segmented sleep more than 20 years ago. In the 1980s, Ekirch was researching a book about nighttime before the industrial revolution. One day in London, wading through public records, he stumbled on references to “first sleep” and “second sleep” in a crime report from the 1600s. He had never seen the phrases before. When he broadened his search, he found mentions of first sleep in Italian (primo sonno), French (premier sommeil), and even Latin (primo somno); he found documentation in Africa, the Middle East, South Asia, and Latin America. © 2024 The Atlantic Monthly Group.

Keyword: Sleep
Link ID: 29595 - Posted: 12.11.2024

By Joshua Cohen Earlier this fall, the Centers for Disease Control and Prevention reported data showing that adult obesity rates — long trending upwards — had fallen modestly over the past few years, from 41.9 to 40.3 percent. The decline sparked discussion on social media and in major news outlets about whether the U.S. has passed so-called “peak obesity” — and whether the growing use of certain weight-loss drugs might account for the shift. An opinion piece in the Financial Times suggested that the public health world might look back on the current moment in much the same way that it now reflects on 1963, when cigarette sales hit their high point and then dropped dramatically over the following decades. The article’s author, John Burn-Murdoch, speculated that the dip is “highly likely” to be caused by the use of glucagon-like peptide-1 receptor agonists, or GLP-1s, for weight loss. It’s easy to see why one might make that connection. Although GLP-1s have been used for nearly two decades in the treatment of type 2 diabetes, their use for obesity only took off more recently. In 2014, the Food and Drug Administration approved a GLP-1 agonist named Saxenda specifically for this purpose. Then in the late 2010s, a GLP-1 drug named Ozempic, made from the active ingredient semaglutide, began to be used off-label. The FDA also authorized Wegovy, another semaglutide-based GLP-1 medication, explicitly for weight loss in 2021. Still, it is premature to declare that GLP-1s have caused overall declining obesity rates in the U.S. There are a number of ways to interpret the CDC data, and not all of them suggest that obesity rates have actually fallen. Further, recent evidence indicates that GLP-1s might not be as effective for weight loss as initially thought. And there are reasons to question the comparison to cigarette sales. Taken together, all of this suggests that we may need to wait to understand how this new class of drugs affects weight loss at the population level.

Keyword: Obesity
Link ID: 29594 - Posted: 12.11.2024

7 Things Everyone Should Know About Antidepressants By Christina Caron Even if you’ve never taken an antidepressant, you’re probably familiar with the criticism and controversy that surrounds these drugs. It’s not uncommon to hear things like: “Those pills are just a placebo.” “You’ll definitely gain weight.” “Once you start, you’ll become dependent on them.” Is any of this true? Some of these statements have “a kernel of truth,” said Dr. Gerard Sanacora, a professor of psychiatry at the Yale School of Medicine. And it’s important to set the record straight because the expectations people have about their treatment — whether good or bad — “really do play a large role in how the treatment actually unfolds,” he added. Dr. Sanacora and other experts addressed some common questions and misconceptions about antidepressants. Will antidepressants change who I am? When an antidepressant starts to work, you may feel like a different person in some ways, said Naomi Torres-Mackie, a clinical psychologist in New York City. “Picture this giant, dark cloud weighing you down — as that lifts, the world is going to look different,” she said, adding: “But as you get used to it, you may see that it actually allows you to have more joy in your life.” On the other hand, up to half of people who take antidepressants may experience some degree of emotional blunting or numbed emotions, and research suggests that the blunting is more likely to happen with a higher medication dosage. When antidepressants are working correctly, patients should still feel a range of emotions, even if the sadness they used to feel every day is gone, said Dr. Laine Young-Walker, chair of the department of psychiatry at the University of Missouri School of Medicine. © 2024 The New York Times Compan

Keyword: Depression
Link ID: 29593 - Posted: 12.11.2024

By Max Kozlov Joylessness triggered by stress creates a distinct brain signature, according to research in mice1. The study also reveals one brain pattern that seems to confer resilience to stress — and another that makes stressed animals less likely to feel pleasure, a core symptom of depression. These findings, published today in Nature, offer clues as to how the brain gives rise to anhedonia, a resistance to enjoyment and pleasure. The results also provide a new avenue for treating the condition — if the findings are validated in humans. “Their approach in this study is spot on,” says Conor Liston, a neuroscientist at Weill Cornell Medicine in New York City, who was not involved in the work. The experiments fill “a big gap”, he says. “Anhedonia is something we don’t understand very well.” More than 70% of people with severe depression experience anhedonia, which is also common in those with schizophrenia, Parkinson’s disease and other neurological and psychiatric conditions. The symptom is notoriously difficult to treat, even in those taking medication, Liston says. “Anhedonia is something that patients care about the most, and feel like it’s least addressed by current treatments,” he says. To understand how the brain gives rise to anhedonia, Mazen Kheirbek, a systems neuroscientist at the University of California, San Francisco, and his colleagues studied mice that had been placed under stress by exposure to larger, more aggressive mice. Typically, mice have a sweet tooth and prefer sugar water over plain water if given the option. But some stressed mice instead preferred plain water — which Kheirbek and his colleagues interpreted as a rodent version of anhedonia. Other mice subjected to the same stress preferred the sugar water. The authors labelled these animals ‘resilient’. © 2024 Springer Nature Limited

Keyword: Stress; Depression
Link ID: 29592 - Posted: 12.07.2024

By Steven Strogatz Death might seem like a pure loss, the disappearance of what makes a living thing distinct from everything else on our planet. But zoom in closer, to the cellular level, and it takes on a different, more nuanced meaning. There is a challenge in simply defining what makes an individual cell alive or dead. Scientists today are working to understand the various ways and reasons that cells disappear, and what these processes mean to biological systems. In this episode, cellular biologist Shai Shaham talks to Steven Strogatz about the different forms of cell death, their roles in evolution and disease, and why the right kinds and patterns of cell death are essential to our development and well-being. STEVE STROGATZ: In the second that it took you to hit play on this episode, a million cells in your body died. Some were programmed to expire in natural, regulated processes, such as apoptosis. Some terminated their own lives after infection, to stop viral invaders from spreading. Others suffered physical damage and went through necrosis, their membranes splitting open and their contents spilling out. We know there are nearly a dozen different ways for our cells to kick the bucket. And learning how to control these processes can make all the difference in the world to a sick patient. In this episode, we ask cellular biologist Shai Shaham (opens a new tab), how can the death of a cell help other cells around it? And how do these insights help us understand life itself? Shai is a professor at The Rockefeller University (opens a new tab), where he studies programmed cell death during animal development and the complex role that glial cells play in the nervous system. There was an example near and dear to my heart, since we work on C. elegans, which is a nematode worm. And there was a recent description of a nematode that was extracted from permafrost in Siberia where it froze about 40,000 years ago and was revived back in the lab. And so you ask yourself, was that whole organism alive or dead for 40,000 years? © 2024 Simons Foundation

Keyword: Apoptosis; Development of the Brain
Link ID: 29591 - Posted: 12.07.2024

Aswathy Ammothumkandy, Charles Liu, Michael A. Bonaguidi Your brain can still make new neurons when you’re an adult. But how does the rare birth of these new neurons contribute to cognitive function? Neurons are the cells that govern brain function, and you are born with most of the neurons you will ever have during your lifetime. While the brain undergoes most of its development during early life, specific regions of the brain continue to generate new neurons throughout adulthood, although at a much lower rate. Whether this process of neurogenesis actually happens in adults and what function it serves in the brain is still a subject of debate among scientists. Past research has shown that people with epilepsy or Alzheimer’s disease and other dementias develop fewer neurons as adults than people without these conditions. However, whether the absence of new neurons contributes to the cognitive challenges patients with these neurological disorders face is unknown. We are part of a team of stem cell researchers, neuroscientists, neurologists, neurosurgeons and neuropsychologists. Our newly published research reveals that the new neurons that form in adults’ brains are linked to how you learn from listening to other people. Researchers know that new neurons contribute to memory and learning in mice. But in humans, the technical challenges of identifying and analyzing new neurons in adult brains, combined with their rarity, had led scientists to doubt their significance to brain function. To uncover the relationship between neurogenesis in adults and cognitive function, we studied patients with drug-resistant epilepsy. These patients underwent cognitive assessments prior to and donated brain tissue during surgical procedures to treat their seizures. To see whether how many new neurons a patient had was associated with specific cognitive functions, we looked under the microscope for markers of neurogenesis. © 2010–2024, The Conversation US, Inc.

Keyword: Neurogenesis; Learning & Memory
Link ID: 29590 - Posted: 12.07.2024

By Shane O’Neill In 2018, Matt Christensen kicked heroin by replacing drugs with drinking. When he stopped drinking in 2022, he turned to food. He put on 95 pounds. His doctor recommended he try Wegovy, part of a class of drugs known as GLP-1 receptor agonists, to help him lose weight. Eventually he switched to a different drug called Zepbound, which targets both GLP-1 and GIP agonists. The drugs worked. Get concise answers to your questions. Try Ask The Post AI. But a funny thing happened on his weight-loss journey: His cravings for food had diminished but so had his cravings for drugs and alcohol. Christensen, 42, started drinking at age 9 and using heroin at 17. For decades, catching a cold meant reaching for a hot toddy. Work stress meant numbing out with Xanax. Even passing through certain neighborhoods in Chicago where he used to buy drugs would lead to cravings. But after he started taking GLP-1 agonists, those triggers became, well, less triggering. “It was the weirdest thing,” he said. “It was just quiet. I just found it really easy all of a sudden.” More than that, Christensen noticed that an unease he had always felt in his body — a discomfort he perpetually tried to quell with fidgeting, food or drugs — was diminishing. “That’s a feeling that I’ve had my entire life,” he said. “Taking these drugs has toned that down. “There’s no silver bullet for addiction or mental illness, but for me, in concert with the other treatments, it has been an absolute game changer,” he said. Matt Christensen says weight-loss drugs like Ozempic and Zepbound have been “an absolute game changer” when it comes to his addiction struggles.

Keyword: Drug Abuse; Obesity
Link ID: 29589 - Posted: 12.07.2024

By Yasemin Saplakoglu Bacteria are in, around and all over us. They thrive in almost every corner of the planet, from deep-sea hydrothermal vents to high up in the clouds, to the crevices of your ears, mouth, nose and gut. But scientists have long assumed that bacteria can’t survive in the human brain. The powerful blood-brain barrier, the thinking goes, keeps the organ mostly free from outside invaders. But are we sure that a healthy human brain doesn’t have a microbiome of its own? Over the last decade, initial studies have presented conflicting evidence. The idea has remained controversial, given the difficulty of obtaining healthy, uncontaminated human brain tissue that could be used to study possible microbial inhabitants. Recently, a study published in Science Advances provided the strongest evidence yet (opens a new tab) that a brain microbiome can and does exist in healthy vertebrates — fish, specifically. Researchers at the University of New Mexico discovered communities of bacteria thriving in salmon and trout brains. Many of the microbial species have special adaptations that allow them to survive in brain tissue, as well as techniques to cross the protective blood-brain barrier. Matthew Olm (opens a new tab), a physiologist who studies the human microbiome at the University of Colorado, Boulder and was not involved with the study, is “inherently skeptical” of the idea that populations of microbes could live in the brain, he said. But he found the new research convincing. “This is concrete evidence that brain microbiomes do exist in vertebrates,” he said. “And so the idea that humans have a brain microbiome is not outlandish.” While fish physiology is, in many ways, similar to humans’, there are some key differences. Still, “it certainly puts another weight on the scale to think about whether this is relevant to mammals and us,” said Christopher Link (opens a new tab), who studies the molecular basis of neurodegenerative disease at the University of Colorado, Boulder and was also not involved in the work. © 2024 Simons Foundation

Keyword: Obesity; Brain imaging
Link ID: 29588 - Posted: 12.04.2024

Amy Fleming Nine years ago, Nikki Schultek, an active and healthy woman in her early 30s, experienced a sudden cascade of debilitating and agonising symptoms – including cognitive and breathing problems and heart arrhythmia – and was investigated for multiple sclerosis. But three brain scans and numerous X-rays later, there was still no diagnosis or treatment plan. “It was like living in a nightmare, imagining not watching my children – three and five years old – grow up,” says Schultek. Now, speaking on a video call from North Carolina, she is as bright as a button and shows no signs of degenerative brain disease. It turned out she had multiple chronic infections, including Borrelia burgdorferi bacteria, which causes Lyme disease and which had stealthily reached her brain. Antibiotics restored her health, but B burgdorferi is hard to eradicate once in the brain. She may need maintenance treatment to keep the disease at bay. Schultek is not the only person whose neurological disorder turned out to be caused by microbes in the brain. A recent paper she jointly lead-authored, published in Alzheimer’s and Dementia, compiled a long list of case reports where infectious disease was discovered to be the primary cause of dementia, meaning that, in many cases, the dementia was reversible. A few of the patients died, but most survived and saw significant improvements in cognitive function, including a man in his 70s who had been diagnosed with Alzheimer’s disease after his swift cognitive decline saw him unable to drive or, eventually, leave the house alone. A sample of his cerebrospinal fluid was taken and revealed a fungal infection caused by Cryptococcus neoformans. Within two years of taking antifungal medication, he was driving again and back at work as a gardener. Richard Lathe, a professor of infectious medicine at the University of Edinburgh and another lead author of the paper, says these patients “were by accident found to be suffering from various fungal, bacterial or viral infections, and when they treated the patient with antifungals, antivirals or antibiotics, the dementia went away”. He, among others, has been investigating the possibility that, like the gut, the brain hosts a community of microbes – an area of largely scientifically uncharted waters, but with huge life-saving potential. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Obesity
Link ID: 29587 - Posted: 12.04.2024

' 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