By Laurie McGinley and  Lenny Bernstein Rachel Graham has battled excess weight for years, cycling through trendy diets, various drugs, even bariatric surgery. Nothing worked for long. But last summer, she started a new medication, and today is 40 pounds lighter — and still shedding weight. “It used to be that if I saw food, I would want to eat it,” said the 54-year-old Graham, who is 5-foot-7 and 190 pounds. “Now, if I have three or four bites of food, I don’t want to eat more.” The drug she’s taking, Mounjaro by Eli Lilly, is part of a new crop of therapies that experts are hailing as a medical milestone — a long-sought way to transform the treatment of obesity, one of the nation’s most serious health threats. Designed for diabetes but used for obesity at higher doses, the medications induce loss of 15 to 22 percent of body weight on average — more than enough to significantly reduce cardiovascular and other health risks. That makes them far superior to old-style diet pills that delivered smaller benefits along with nasty side effects such as high blood pressure and loose stools. But during the past year, soaring demand for the drugs has ignited a mad scramble, exposing some of the most persistent problems in the nation’s health-care system, including supply shortages, high costs and health-care inequities. Tensions are surging as patients with diabetes and those with weight problems sometimes compete for the same medications, which are self-administered in weekly injections. Some doctors worry that the drugs, which might have to be taken for life, will overshadow the need for lifestyle changes involving diet and exercise.

Keyword: Obesity
Link ID: 28606 - Posted: 12.21.2022

By Anthea Rowan To many, the word “hobby” signifies something lightweight or trivial. Yet taking on a new hobby as one ages might provide an important defense against dementia, some experts say. About 5.8 million adults over 65 in the United States live with Alzheimer’s disease or other dementia disorders, according to the Centers for Disease Control and Prevention. One in 9 Americans over 65 has Alzheimer’s, according to the Alzheimer’s Association. And although the rate of dementia may be falling thanks to lifestyle changes, more of us are living longer, which means the societal burden of dementia is rising. David Merrill, an adult and geriatric psychiatrist and director of the Pacific Brain Health Center in Santa Monica, Calif., suggests we use the word “pursuit” instead of “hobby,” as it elevates the concept of an activity to something demanding, something requiring concentration or collaboration. Something we ought to chase down. Activities that demand focus and industry are the whetstone to keeping cognition sharp, Merrill says. Our brains, he continues, are like any other part of our body. “‘Use it or lose it’ is not just a hypothesis, it’s a basic biologic fact that holds as true for our brains as our muscles or our bones.” While there is as yet no surefire way to prevent dementia or cure it, the Lancet in 2020 identified 12 potentially modifiable risk factors for the condition; they include physiological (blood pressure, diabetes, hearing loss), lifestyle choices (smoking, drinking, physical inactivity), environmental (air pollution) depression, social isolation and a lower level of education. The Alzheimer Society of Canada is also clear about what we can do to help minimize our dementia risk: keep cognitively engaged, learn new things, meet new people, keep a diary, remain curious and engage in conversations.

Keyword: Alzheimers; Learning & Memory
Link ID: 28605 - Posted: 12.21.2022

Patrick Barkham Three species of cetacean stranded off the coast of Scotland, including a bottlenose dolphin and a long-finned pilot whale, have been found to have the classic markers of Alzheimer’s disease, according to a study. Although types of dementia have been fairly widely detected in other animals, Alzheimer’s disease has not been found to occur naturally in species other than humans. But researchers from the University of Glasgow, the universities of St Andrews and Edinburgh and the Moredun Research Institute in Scotland were surprised to find that postmortem tests of 22 toothed whales, or odontocetes, detected three key brain changes associated with human Alzheimer’s disease in three animals. Scientists do not know the cause of this brain degeneration but it could support one theory about why some groups or pods of whales and dolphins run aground in shallow water. Some mass strandings have been linked to increasing anthropogenic noise in the oceans, but Alzheimer’s-like signs in the brain could support a “sick leader” theory, whereby mostly healthy cetaceans are stranded because they follow a group leader that has become confused or lost. The researchers found signs of Alzheimer’s in three of 22 stranded odontocetes: a white-beaked dolphin, a bottlenose dolphin and a long-finned pilot whale, also a member of the dolphin family.

Keyword: Alzheimers
Link ID: 28604 - Posted: 12.21.2022

By Sandra G. Boodman The 23-year-old patient arrived in the back of a police car and was in four point restraints — hands and feet strapped to a gurney — when emergency physician Elizabeth Mitchell saw her at a Los Angeles hospital early on March 17. Chloe R. Kral was being held on a 5150, shorthand in California for an emergency psychiatric order that allows people deemed dangerous to themselves or others to be involuntarily confined for 72 hours. She had spent the previous six months at a private treatment center receiving care for bipolar disorder and depression. Chloe had improved and was set to move to transitional housing when she suddenly became combative and threatened to harm staff and kill herself. Police had taken her to the emergency room at Cedars-Sinai Marina del Rey Hospital before a planned transfer to a mental hospital. Chloe, Mitchell recalled, was “mumbling about Rosa Parks” when they met. She managed to tell the doctor that she hadn’t used drugs or alcohol, but was otherwise incoherent. “We get a lot of psychiatric patients, and they’re just waiting for placement,” Mitchell said. But something indefinable — Mitchell characterized it as “maybe gut instinct” honed by nearly two decades of practice — prompted her to order a CT scan of Chloe’s head to better assess her mental status. When she pulled up the image, Mitchell gasped. “I had never seen anything like it,” she said. She rounded up her colleagues and “made everyone in the whole ER come look.” “I was speechless,” she said. “All I could think was ‘How did no one figure this out?’ ”

Keyword: Depression; Schizophrenia
Link ID: 28603 - Posted: 12.21.2022

By Claudia López Lloreda Learning lots of new information as a baby requires a pool of ready-to-go, immature connections between nerve cells to form memories quickly. Called silent synapses, these connections are inactive until summoned to help create memories, and were thought to be present mainly in the developing brain and die off with time. But a new study reveals that there are many silent synapses in the adult mouse brain, researchers report November 30 in Nature. Neuroscientists have long puzzled over how the adult human brain can have stable, long-term memories, while at the same time maintaining a certain flexibility to be able to make new memories, a concept known as plasticity (SN: 7/27/12). These silent synapses may be part of the answer, says Jesper Sjöström, a neuroscientist at McGill University in Montreal who was not involved with the study. “The silent synapses are ready to hook up,” he says, possibly making it easier to store new memories as an adult by using these connections instead of having to override or destabilize mature synapses already connected to memories. “That means that there’s much more room for plasticity in the mature brain than we previously thought.” In a previous study, neuroscientist Mark Harnett of MIT and his colleagues had spotted many long, rod-shaped structures called filopodia in adult mouse brains. That surprised Harnett because these protrusions are mostly found on nerve cells in the developing brain. “Here they were in adult animals, and we could see them crystal clearly,” Harnett says. So he and his team decided to examine the filopodia to see what role they play, and if they were possibly silent synapses. The researchers used a technique to expand the brains of adult mice combined with high-resolution microscopy. Since nerve cell connections and the molecules called receptors that allow for communication between connected cells are so small, these methods revealed synapses that past research missed. © Society for Science & the Public 2000–2022.

Keyword: Learning & Memory
Link ID: 28602 - Posted: 12.17.2022

By Gary Stix  Can the human brain ever really understand itself? The problem of gaining a deep knowledge of the subjective depths of the conscious mind is such a hard problem that it has in fact been named the hard problem. The human brain is impressively powerful. Its 100 billion neurons are connected by 100 trillion wirelike fibers, all squeezed into three pounds of squishy flesh lodged below a helmet of skull. Yet we still don’t know whether this organ will ever be able to muster the requisite smarts to hack the physical processes that underlie the ineffable “quality of deep blue” or “the sensation of middle C,” as philosopher David Chalmers put it when giving examples of the “hard problem” of consciousness, a term he invented, in a 1995 paper. This past year did not uncover a solution to the hard problem, and one may not be forthcoming for decades, if ever. But 2022 did witness plenty of surprises and solutions to understanding the brain that do not require a complete explanation of consciousness. Such incrementalism could be seen in mid-November, when a crowd of more than 24,000 attendees of the annual Society for Neuroscience meeting gathered in San Diego, Calif. The event was a tribute of sorts to reductionism—the breaking down of hard problems into simpler knowable entities. At the event, there were reports of an animal study of a brain circuit that encodes social trauma and a brain-computer interface that lets a severely paralyzed person mentally spell out letters to form words. Your Brain Has a Thumbs-Up–Thumbs-Down Switch When neuroscientist Kay Tye was pursuing her Ph.D., she was told a chapter on emotion was inappropriate for her thesis. Emotion just wasn’t accepted as an integral, intrinsic part of behavioral neuroscience, her field of study. That didn’t make any sense to Tye. She decided to go her own way to become a leading researcher on feelings. This year Tye co-authored a Nature paper that reported on a kind of molecular switch in rodents that flags an experience as either good or bad. If human brains operate the same way as the brains of the mice in her lab, a malfunctioning thumbs-up–thumbs-down switch might explain some cases of depression, anxiety and addiction.

Keyword: Consciousness
Link ID: 28601 - Posted: 12.17.2022

By Susan Coll Last summer, my husband had gone hiking with our two dogs when one of them — a year-old rescue who weighs in at over 50 pounds, can scale steep inclines like a mountain goat and has the speed and grace of an Olympic athlete — suddenly collapsed. Unable to stand, Dafna was disoriented and had also become incontinent. Was it a seizure? A stroke? A snake bite? We piled into our car and headed to an emergency veterinary clinic. I held Dafna’s head in my lap, convinced the end was near. This puppy had destroyed two pairs of my prescription eyeglasses, a new leather wallet, and had torn gashes in my clothes. She’d chewed through my daughter’s internet cords. Still, I loved her like no other. At the clinic, the staff rushed Dafna to a back room with the professionalism expected in a life-or-death situation. But we thought we also noticed a hint of amusement? Even a smirk? A few moments later, we learned why. The vet explained that while they were running a urine test to confirm their suspicions, they were pretty sure Dafna had ingested THC, maybe from a marijuana plant growing wild along the trail, or perhaps she’d eaten a discarded pot roach. Basically, our dog was stoned. It turns out that’s not so unusual these days. In Vermont, where we were and where possession and use of marijuana was legalized in 2018, the vet said she now sees as many as 10 cases per week of pot intoxication. According to ASPCApro and local vets, that’s happening across the country. © 1996-2022 The Washington Post

Keyword: Drug Abuse
Link ID: 28599 - Posted: 12.17.2022

Ari Daniel Fred Crittenden, 73, lost his sight to retinitis pigmentosa when he was 35 years old. Today he has no visual perception of light. "It's total darkness," he says. Still, he has cells in his eyes that use light to keep his internal clock ticking along nicely. Marta Iwanek for NPR Every baseball season, 73-year-old Fred Crittenden plants himself in front of his television in his small one-bedroom apartment an hour north of Toronto. "Oh, I love my sports — I love my Blue Jays," says Crittenden. "They need me to coach 'em — they'd be winning, I'll tell ya." He listens to the games in his apartment. He doesn't watch them, because he can't see. "I went blind," Crittenden recalls, when "I was 35 years young." Crittenden has retinitis pigmentosa, an inherited condition that led to the deterioration of his retinas. He lost all his rods (the cells that help us see in dim light) and all his cones (the cells that let us see color in brighter light). Within a single year, in 1985, Crittenden says he went from perfect vision to total blindness. Certain cells within Crittenden's retinas that contain melanopsin help his brain to detect light, even if what he sees is darkness. Among other things, these light-detecting cells help his body regulate his sleep cycles. Marta Iwanek for NPR "The last thing I saw clearly," he says, thinking back, "it was my daughter, Sarah. She was 5 years old then. I used to go in at night and just look at her when she was in the crib. And I could just barely still make her out — her little eyes or her nose or her lips or her chin, that kind of stuff. Even to this day it's hard." © 2022 npr

Keyword: Biological Rhythms; Vision
Link ID: 28598 - Posted: 12.17.2022

By Yasemin Saplakoglu Memory and perception seem like entirely distinct experiences, and neuroscientists used to be confident that the brain produced them differently, too. But in the 1990s neuroimaging studies revealed that parts of the brain that were thought to be active only during sensory perception are also active during the recall of memories. “It started to raise the question of whether a memory representation is actually different from a perceptual representation at all,” said Sam Ling, an associate professor of neuroscience and director of the Visual Neuroscience Lab at Boston University. Could our memory of a beautiful forest glade, for example, be just a re-creation of the neural activity that previously enabled us to see it? “The argument has swung from being this debate over whether there’s even any involvement of sensory cortices to saying ‘Oh, wait a minute, is there any difference?’” said Christopher Baker, an investigator at the National Institute of Mental Health who runs the learning and plasticity unit. “The pendulum has swung from one side to the other, but it’s swung too far.” Even if there is a very strong neurological similarity between memories and experiences, we know that they can’t be exactly the same. “People don’t get confused between them,” said Serra Favila, a postdoctoral scientist at Columbia University and the lead author of a recent Nature Communications study. Her team’s work has identified at least one of the ways in which memories and perceptions of images are assembled differently at the neurological level. When we look at the world, visual information about it streams through the photoreceptors of the retina and into the visual cortex, where it is processed sequentially in different groups of neurons. Each group adds new levels of complexity to the image: Simple dots of light turn into lines and edges, then contours, then shapes, then complete scenes that embody what we’re seeing. Simons Foundation © 2022

Keyword: Attention; Vision
Link ID: 28597 - Posted: 12.15.2022

ByElizabeth Pennisi Willpower might be key to getting off the couch to exercise, but bacteria may lend a helping hand. Studies in mice reported today in Nature suggest microbes in the gut may be behind differences in the desire to work out. A research team has homed in on specific microbial molecules that stimulate a rodent’s desire to run—and keep running. By revealing exactly how these molecules talk to the brain, this group has set the stage for finding out whether similar signals help keep humans active. The work “establishes just how critical the microbiome is for exercise and goes incredibly deep in providing a new gut-brain [connection],” says Aleksandar Kostic, a microbiologist at Harvard Medical School who is co-founder of FitBiomics, a company developing probiotics to improve fitness. Kostic, who wasn’t involved in the research, and others speculate that exercise-inducing commands from the microbes might one day be packaged into pills people could take. To explore why some people like to exercise and others don’t, University of Pennsylvania microbiologist Christoph Thaiss studied mice bred to have a lot of genetic and behavioral variation. His team found more than a fivefold difference in how far the mice ran on wheels in their cages—some covered more than 30 kilometers in 48 hours, whereas others rarely moved in their wheels. The active and lazy mice didn’t show any significant differences in their genetics or biochemistry. But the researchers did notice one clue: When treated with antibiotics, mice that were normally highly energetic tended to exercise less. Follow-up studies showed the antibiotic treatment affected the brains of the formerly active mice. The activity of certain brain genes declined, along with levels of dopamine, a neurotransmitter that has been linked to “runner’s high”—that sense of wellbeing that comes with prolonged exercise.

Keyword: Obesity
Link ID: 28596 - Posted: 12.15.2022

By Yasemin Saplakoglu It’s often subtle at first. A lost phone. A forgotten word. A missed appointment. By the time a person walks into a doctor’s office, worried about signs of forgetfulness or failing cognition, the changes to their brain have been long underway — changes that we don’t yet know how to stop or reverse. Alzheimer’s disease, the most common form of dementia, has no cure. “There’s not much you can do. There are no effective treatments. There’s no medicine,” said Riddhi Patira, a behavioral neurologist in Pennsylvania who specializes in neurodegenerative diseases. That’s not how the story was supposed to go. Three decades ago, scientists thought they had cracked the medical mystery of what causes Alzheimer’s disease with an idea known as the amyloid cascade hypothesis. It accused a protein called amyloid-beta of forming sticky, toxic plaques between neurons, killing them and triggering a series of events that made the brain waste away. The amyloid cascade hypothesis was simple and “seductively compelling,” said Scott Small, the director of the Alzheimer’s Disease Research Center at Columbia University. And the idea of aiming drugs at the amyloid plaques to stop or prevent the progression of the disease took the field by storm. Decades of work and billions of dollars went into funding clinical trials of dozens of drug compounds that targeted amyloid plaques. Yet almost none of the trials showed meaningful benefits to patients with the disease. That is, until September, when the pharmaceutical giants Biogen and Eisai announced that in a phase 3 clinical trial, patients taking the anti-amyloid drug lecanemab showed 27% less decline in their cognitive health than patients taking a placebo did. Last week, the companies revealed the data, now published in the New England Journal of Medicine, to an excited audience at a meeting in San Francisco. Simons Foundation © 2022

Keyword: Alzheimers
Link ID: 28595 - Posted: 12.15.2022

By Jake Buehler Female snakes have clitorises too, a new study finds. The research raises the possibility that the sex lives of snakes are more complicated and diverse than previously understood, researchers report December 14 in Proceedings of the Royal Society B. Clitorises are found in a wide range of vertebrate life, from crocodiles to dolphins (SN: 1/10/22). One exception is birds, which lost their clitorises over the course of their evolution. Female snakes appeared to have lost the sex organ too, which was puzzling, since their close lizard relatives possess paired clitorises, called hemiclitorises. Male lizards and snakes have accompanying paired phalli, or hemipenises.  This element of female snakes’ sexual anatomy went unexamined in detail for so long partly because hemiclitorises can be fragile and easy to miss, but also because female genitalia have historically been considered “quite taboo,” says evolutionary biologist Megan Folwell of the University of Adelaide in Australia. “Even in humans, the proper function and significance of the human clitoris was still being discussed in 2006,” she says. Conflicting accounts of snake hemiclitorises in some scientific papers led Folwell to take a detailed look. She first examined a euthanized female common death adder (Acanthophis antarcticus). “I just started with dissecting the tail and going into it with a really open mind of what I might find,” she says. She was “pleasantly surprised” to find dual organs within that were completely different from the hemipenises found in male snakes. Also, unlike lizard hemiclitorises, the snake’s couldn’t turn out externally. © Society for Science & the Public 2000–2022.

Keyword: Sexual Behavior; Evolution
Link ID: 28594 - Posted: 12.15.2022

By Ellen Barry BETHESDA, Md. — The psychiatrist E. Fuller Torrey is 85 years old and has Parkinson’s disease, the tremors at times so strong that his hand beats like a drum on the table. Still, every morning when he reads the newspapers, he looks for accounts of violent behavior by people with severe mental illness, to add to an archive he has maintained since the 1980s. His records include reports of people who, in the grip of psychosis, assaulted political figures or pushed strangers into the path of subway trains; parents who, while delusional, killed their children by smothering, drowning or beating them; adult children who, while off medication, killed their parents with swords, axes or hammers. Dr. Torrey, who has done pioneering research into the biological basis of schizophrenia, has used these stories in service of an argument: that it was a mistake for the United States to shut down its public psychiatric hospitals without adequate follow-up care. And that to remedy this, the government should create systems to compel seriously mentally ill people in the community to get treatment. For much of his career, Dr. Torrey was a lonely voice on this issue, disavowed by patient advocacy groups and by organized psychiatry. But his ideas are now animating major policy shifts, including the announcement by Mayor Eric Adams of New York last month that city officials would send people with untreated mental illnesses to hospitals, even if they posed no threat to others. Dr. Torrey’s influence on New York City’s policy is profound. The mayor’s adviser on this matter is Brian Stettin, who was thrust into mental health policy in 1999 when, as a lawyer in the office of Attorney General Eliot Spitzer of New York, he was asked to draft Kendra’s Law, named for a woman who was pushed in front of a subway train by a man with schizophrenia. The law allows a court to order a person with mental illness to comply with an outpatient treatment plan, risking involuntary commitment if the person refuses. © 2022 The New York Times Company

Keyword: Schizophrenia
Link ID: 28593 - Posted: 12.13.2022

By Allison Gasparini Are you drinking enough water? The question seems like it should have a straightforward answer — a specific amount of water you need to drink daily to combat dehydration.      But the rate and way in which the human body takes in and excretes water is not as universal as you might expect. By studying more than 5,000 people living in 23 countries and ranging in age from 8 days to 96 years, researchers have found that the turnover of water in a person’s body varies widely depending on the individual’s physical and environmental factors. The results, published in the Nov. 24 Science, suggest that the idea that a person should ideally consume eight 8-ounce glasses of water a day is not a one-size-fits-all solution to peak hydration.     Even within the calculations, “individual variabilities could be huge,” says biomedical engineer Kong Chen, director of the metabolic research program at the National Institutes of Health’s Clinical Center. Yosuke Yamada, a physiologist at the National Institute of Biomedical Innovation, Health and Nutrition in Japan, and colleagues used a stable isotope of hydrogen known as deuterium to track the movement of water through people’s bodies. Drinking water accounts for only half of the total water intake by humans, with the rest coming from food. Simply measuring the amount of water that a person drinks in a day is not enough to accurately gauge water turnover or the amount of water used by the body daily. © Society for Science & the Public 2000–2022.

Keyword: Obesity
Link ID: 28592 - Posted: 12.13.2022

By Christina Jewett and Cade Metz A jumble of cords and two devices the size of soda cans protrude from Austin Beggin’s head when he undergoes testing with a team of researchers studying brain implants that are meant to restore function to those who are paralyzed. Despite the cumbersome equipment, it is also when Mr. Beggin feels the most free. He was paralyzed from the shoulders down after a diving accident eight years ago, and the brain device picks up the electrical surges that his brain generates as he envisions moving his arm. It converts those signals to cuffs on the major nerves in his arm. They allow him to do things he had not done on his own since the accident, like lift a pretzel to his mouth. “This is like the first time I’ve ever gotten the opportunity or I’ve ever been privileged and blessed enough to think, ‘When I want to open my hand, I open it,’” Mr. Beggin, 30, said. Days like that are always “a special day.” The work at the Cleveland Functional Electrical Stimulation Center represents some of the most cutting-age research in the brain-computer interface field, with the team connecting the brain to the arm to restore motion. It’s a field that Elon Musk wants to advance, announcing in a recent presentation that brain implants from his company Neuralink would someday help restore sight to the blind or return people like Mr. Beggin to “full-body functionality.” Mr. Musk also said the Neuralink device could allow anyone to use phones and other machines with new levels of speed and efficiency. Neuroscientists and Mr. Beggin alike see such giant advances as decades away, though. Scientists who have approval to test such devices in humans are inching toward restoring normal function in typing, speaking and limited movements. Researchers caution that the goal is much harder and more dangerous than it may seem. And they warn that Mr. Musk’s goals may never be possible — if it is even worth doing in the first place. © 2022 The New York Times Company

Keyword: Robotics
Link ID: 28591 - Posted: 12.13.2022

Kristine Zengeler Many neurodegenerative diseases, or conditions that result from the loss of function or death of brain cells, remain largely untreatable. Most available treatments target just one of the multiple processes that can lead to neurodegeneration, which may not be effective in completely addressing disease symptoms or progress, if at all. But what if researchers harnessed the brain’s inherent capabilities to cleanse and heal itself? My colleagues and I in the Lukens Lab at the University of Virginia believe that the brain’s own immune system may hold the key to neurodegenerative disease treatment. In our research, we found a protein that could possibly be leveraged to help the brain’s immune cells, or microglia, stave off Alzheimer’s disease. No available treatments for neurodegenerative diseases stop ongoing neurodegeneration while also helping affected areas in the body heal and recuperate. In terms of failed treatments, Alzheimer’s disease is perhaps the most infamous of neurodegenerative diseases. Affecting more than 1 in 9 U.S. adults 65 and older, Alzheimer’s results from brain atrophy with the death of neurons and loss of the connections between them. These casualties contribute to memory and cognitive decline. Billions of dollars have been funneled into researching treatments for Alzheimer’s, but nearly every drug tested to date has failed in clinical trials.

Keyword: Alzheimers; Neuroimmunology
Link ID: 28590 - Posted: 12.13.2022

By Emily Anthes In creating modern dog breeds, humans sculpted canines into physical specimens perfectly suited for a wide variety of tasks. Bernese mountain dogs have solid, muscular bodies capable of pulling heavy loads, while greyhounds have lean, aerodynamic frames, ideal for chasing down deer. The compact Jack Russell terrier can easily shimmy into fox or badger dens. Now, a large study, published in Cell on Thursday, suggests that behavior, not just appearance, has helped qualify these dogs for their jobs. Breeds that were created for similar roles — whether rounding up sheep or flushing birds into the air — tend to cluster into distinct genetic lineages, which can be characterized by different combinations of behavioral tendencies, the researchers found. “Much of modern breeding has been focused predominantly on what dogs look like,” Evan MacLean, an expert on canine cognition at the University of Arizona who was not involved in the study, said in an email. But, he emphasized, “Long before we were breeding dogs for their appearances, we were breeding them for behavioral traits.” The study also found that many of the genetic variants that set these lineages apart from each other appear to regulate brain development, and many seem to predate modern breeds. Together, the results suggest that people may have created today’s stunning assortment of breeds, in part, by harnessing and preserving desirable behavioral traits that already existed in ancient dogs, the researchers said. “Dogs have fundamentally the same blueprint, but now you’ve got to emphasize certain things to get particular tasks done,” said Elaine Ostrander, a dog genomics expert at the National Human Genome Research Institute and the senior author of the study. “You’re going to tweak a gene up, you’re going to tweak it down.” In an email, Bridgett vonHoldt, an evolutionary biologist at Princeton University who was not involved in the research, called the new paper “a major landmark in the field of dog genomics and behavior. We know it is complicated. This study not only gives us hope, it will be viewed as an inspiration for all in the field.” © 2022 The New York Times Company

Keyword: Genes & Behavior; Evolution
Link ID: 28589 - Posted: 12.10.2022

By Bonnie Berkowitz and  William Neff Creating a physique that can win at the highest level of professional bodybuilding requires superhuman self-discipline, intense training and genetic good fortune. Increasingly, say the people familiar with the culture and its consequences, it cannot be done without illicit drugs and a willingness to push a body to — or past — its limits. More than a dozen scientists, trainers, judges and competitors interviewed for this report said that just earning a pro card, an amateur’s ticket to the pro ranks, is very difficult without anabolic steroids. Winning a marquee title drug-free? Several people laughed at the question. “Impossible,” said Harrison Pope, one of the country’s leading anabolic-steroid researchers. The behemoths who win the best-known and most lucrative titles barely resemble the iconic, classically muscled champions of the past, such as Arnold Schwarzenegger, who won the sport’s premiere title, Mr. Olympia, seven times between 1970 and 1980. “Arnold Schwarzenegger would not win today,” said Brad Schoenfeld, a professor at Lehman College in New York and author of several books on bodybuilding and muscle growth. “He would not even get a pro card.” Although bodybuilders spend years lifting weights and honing each muscle, they don’t need to demonstrate strength for the judges beyond the ability to hold poses onstage. They only need to look strong. Some competitors — and a growing legion of young, mostly male admirers — chase that look by diving into a reckless pharmacological game of whack-a-mole that insiders say has grown more intense and dangerous as sheer size has trumped the “Greek god” ideal of previous generations.

Keyword: Hormones & Behavior; Drug Abuse
Link ID: 28588 - Posted: 12.10.2022

Miryam Naddaf More than 3,500 genetic variations that potentially affect smoking and drinking behaviour have been identified in a study involving almost 3.4 million people with African, American, East Asian and European ancestry. The findings, published in Nature on 7 December1, highlight how increasing the sample size and ethnic diversity improves the power of such genome-screening analyses — called genome-wide association studies (GWASs) — to reveal how various traits are linked to genes, combinations of genes or mutations. Smoking and drinking are important risk factors for several physical and mental illnesses, including cardiovascular diseases and psychiatric disorders. Although both behaviours are influenced by environmental and social factors, there is evidence that genetics can affect tobacco and alcohol consumption. “We’re at a stage where genetic discoveries are being translated into clinical [applications],” says study co-author Dajiang Liu, a statistical geneticist at Penn State College of Medicine in Hershey, Pennsylvania. “If we can forecast someone's risk of developing nicotine or alcohol dependence using this information, we can intervene early and potentially prevent a lot of deaths.” Scientists use GWASs to find genetic ties to diseases or behaviours by comparing genetic sequences in large numbers of people. But so far, most of these studies have focused on European populations. Liu and his colleagues constructed a model that incorporated the genomic data of 3,383,199 people, 21% of whom had non-European ancestry. They identified 3,823 genetic variants that were associated with smoking or drinking behaviours. Thirty-nine of these were linked with the age at which individuals started smoking, 243 with the number of cigarettes smoked per day and 849 with the number of alcoholic drinks consumed per week.

Keyword: Drug Abuse; Genes & Behavior
Link ID: 28587 - Posted: 12.10.2022

By Ingrid Wickelgren  Recurrent intrusive memories lie at the heart of certain mental illnesses, including post-traumatic stress disorder and obsessive-compulsive disorder. Clinicians often treat these conditions with “exposure therapy.” They gradually and gently re-expose patients to feared stimuli or simulations—from reminders of active combat to germs on a toilet—teaching the brain to become accustomed to the stimuli and to decouple them from danger. But exposure therapy has drawbacks. “Facing these traumatic memories is painful to patients,” says Yingying Wang, a cognitive psychologist at Zhejiang University in China. “These treatments suffer from a very high dropout rate.” Wang and her colleagues have taken a first step toward developing a more benign way to dim traumatic memories. Their proof-of-concept study involves subliminal exposure to cues to those memories after putting the brain in a state in which it is likely to forget. The new findings present a new spin on a form of active forgetting in which people learn to suppress memories by practicing not thinking about them in the presence of reminders. In various studies, participants have memorized pairs of words such as needle-doctor or jogger-collie and then practiced either thinking or not thinking about the second word when the first word (the reminder) appears. Practicing not thinking about the second word has led to forgetting. The mechanism for this effect centers on the brain’s main memory hub, the hippocampus. Psychologists have discovered that suppressing memory retrieval puts the hippocampus in a degraded functional state. This state lasts for a small window of time—at least 10 seconds but potentially much longer—casting what researchers have dubbed an “amnesic shadow” that leads to poor memory for other things that happen within it. So when people suppress neutral word pairs, they put their brain into a state in which they are likely to forget new experiences. © 2022 Scientific American,

Keyword: Stress; Learning & Memory
Link ID: 28586 - Posted: 12.10.2022