Pam Belluck A research team analyzed records of nearly a million women in Sweden’s national medical registries from 2001 through 2017, comparing 86,551 women who had perinatal depression with 865,510 women who did not. The groups were matched by age and year they gave birth. In two studies, the team found that depression that begins in pregnancy or soon after can have troubling implications for as long as 18 years. One study, published on Tuesday in JAMA Network Open, found that women with perinatal depression had three times the risk of suicidal behavior, defined as attempted or completed suicide, than women who did not experience perinatal depression. Risks were greatest in the year following their diagnosis, but, while they lessened over time, years later the risks were still twice as high compared with women without the disorder. The other study, published on Wednesday in BMJ, found that women with perinatal depression were more than six times at risk of dying by suicide as those without that diagnosis. The number of suicides was small, but it accounted for a large share of the deaths of women diagnosed with perinatal depression: 149 of the 522 deaths in that group, or 28.5 percent. For women without perinatal depression, there were 117 suicides out of 1,568 deaths or 7.5 percent. Suicide was a major reason women with perinatal depression were twice as likely to die from any cause over the 18-year period of the study compared with women without the disorder. The researchers also compared more than 20,000 women with perinatal depression to their biological sisters who gave birth during the same time frame and did not have the disorder. The risk of suicidal behavior for the sisters with perinatal depression was nearly three times that of their sisters without the diagnosis — almost as high as the difference between women with the illness and those without it to whom they were not related. That suggests depression plays a greater role in these outcomes than genetics or childhood environment, the researchers wrote. © 2024 The New York Times Company

Keyword: Depression; Hormones & Behavior
Link ID: 29089 - Posted: 01.11.2024

Jon Hamilton A new generation of blood tests is poised to change the way doctors determine whether patients with memory loss also have Alzheimer's disease. The tests detect substances in the blood that indicate the presence of sticky amyloid plaques in the brain — a hallmark of Alzheimer's. So these tests have the potential to replace current diagnostic procedures, like costly PET scans and uncomfortable spinal taps. Blood tests also promise to provide doctors with a quick way to identify patients who could benefit from new drugs that remove amyloid from the brain. But the accuracy of the tests still varies widely. "Some of them are really good, and some of them are really bad," says Dr. Suzanne Schindler, a dementia specialist at Washington University School of Medicine in St. Louis. Blood tests represent the latest advance in efforts to detect the buildup of amyloid plaques and fibrous tangles in the brain. "It used to be that the only way you could definitively diagnose someone with Alzheimer disease is by doing an autopsy," Schindler says. Then, starting in the early 2000s, scientists found ways to detect plaques and tangles using PET scans and tests of spinal fluid. There are now versions of both approaches that are approved by the Food and Drug Administration. But the scans are costly, and spinal taps are unpopular with many doctors and patients. Both also require expertise that is in short supply. So Schindler and her colleagues got a lot of attention in 2019 when they published a paper showing that amyloid plaques could be revealed by a blood test. © 2024 npr

Keyword: Alzheimers
Link ID: 29088 - Posted: 01.11.2024

By Christina Jewett and Benjamin Mueller In early 2020, the Food and Drug Administration responded to decades of escalating concerns about a commonly prescribed drug for asthma and allergies by deploying one of its most potent tools: a stark warning on the drug’s label that it could cause aggression, agitation and even suicidal thoughts. The agency’s label, which was primarily aimed at doctors, was supposed to sound an alert about the 25-year-old medication, Singulair, also known by its generic name, montelukast. But it barely dented use: The drug was still prescribed to 12 million people in the United States in 2022. Children face the greatest risks of the drug’s ill effects, and while usage by minors did decline, it was still taken by 1.6 million of them — including Nicole Sims’s son. Ms. Sims had no idea why, at 6, her son started having nightmares and hallucinations of a woman in the window. When he told her that he wanted to die, Ms. Sims went online, desperate for answers. Only then did she learn about the F.D.A. warning. She also found a Facebook support group with 20,000 members for people who had experienced side effects of the drug. Members of the group recounted a haunting toll that they linked to the drug with the help of peers, not their doctors. “It’s a mental health crisis that nobody is recognizing,” said Anna Maria Rosenberg, an administrator of the group. The F.D.A.’s handling of Singulair illustrates systemic gaps in the agency’s approach to addressing troubling side effects from medicines approved long ago — and to warning the public and doctors when serious issues arise. The agency had flagged the 2020 warning label, known as a “boxed warning,” to physicians’ groups, but it had not required that doctors be educated about the drug’s side effects. Federal regulators in 1998 initially dismissed evidence that emerged during the approval process about the drug’s potential to affect the brain and did not revise their assessment until two decades later. The F.D.A. was slow to alert the public as reports of psychiatric problems surfaced, highlighting deficiencies of a drug-monitoring system that puts the onus on drugmakers to report problems. © 2024 The New York Times Company

Keyword: Depression
Link ID: 29087 - Posted: 01.09.2024

By Amber Dance 01.08.2024 We all want to be happy — and for decades, psychologists have tried to figure out how we might achieve that blissful state. The field’s many surveys and experiments have pointed to a variety of approaches, from giving stuff away to quitting Facebook to forcing one’s face into a toothy grin. But psychology has undergone serious upheaval over the last decade, as researchers realized that many studies were unreliable and unrepeatable. That has led to a closer scrutiny of psychological research methods, with the study of happiness no exception. So — what really makes us happy? Under today’s more careful microscope, some routes to happiness seem to hold up, while others appear not to, or have yet to re-prove themselves. Here’s what we know so far, and what remains to be reassessed, according to a new analysis in the Annual Review of Psychology. One long-standing hypothesis is that smiling makes you feel happier. In a classic 1988 study, researchers asked 92 Illinois undergraduates to hold a felt tip pen in their mouth either with their teeth, forcing an unnatural grin, or with their lips, making them pout. The students then looked at four examples of The Far Side comics. On average, those with the forced smiles found the one-panel comics slightly funnier than those with the forced pouts. But when 17 different research labs got together to retest the pen-clench smile’s effects on 1,894 new participants, the finding failed to hold up, the researchers reported in 2016. The repetition study was part of a broader effort to counter psychology’s reproducibility crisis, which in part has been attributed to the variety of ways in which researchers could examine and reanalyze their data until they arrived at publishable results. “It’s kind of like shooting a bunch of arrows at the wall and drawing the bullseye on after,” says Elizabeth Dunn, a social psychologist at the University of British Columbia in Vancouver and coauthor of the new Annual Review of Psychology paper.

Keyword: Emotions
Link ID: 29086 - Posted: 01.09.2024

By Mark Johnson In the first study of its kind in humans, researchers have discovered that it is safe to use sound waves fired into specific areas of the brain to open a protective barrier and clear the way for Alzheimer’s medications. The study, reported in the New England Journal of Medicine, involved just three patients, but it raises hope about the long-term potential of the treatment strategy known as focused ultrasound. “We want to be very cautious. This is the first three people in the world that have had this [treatment]. What we’ve learned from this, I think, can help us,” said Ali Rezai, lead author of the study and executive chair and director of the Rockefeller Neuroscience Institute at West Virginia University. Rezai stressed that the goal of the research is not to replace pharmaceutical treatments but to improve their benefits by helping more of the drug penetrate the brain. Nature has provided humans with a barrier made of tightly packed cells that blocks harmful toxins, such as viruses, bacteria and fungi, from reaching the brain. Known as the blood-brain barrier, this shield has for decades presented a major challenge to scientists trying to treat neurodegenerative diseases such as Alzheimer’s and Parkinson’s, which afflict at least 7 million Americans. The barrier is a locked door that stops about 98 percent of treatments from reaching the brain. With focused ultrasound, Rezai explained, “what we want to do is push individuals toward the milder stages of Alzheimer’s with less plaques to give them a fighting chance.” Two men and a woman suffering from mild loss of memory, learning, concentration and decision-making skills due to Alzheimer’s took part in the study. The patients, who ranged in age from 59 to 77, were given six monthly doses of the federally approved — if somewhat controversial — lab-made antibody aducanumab, sold under the brand name Aduhelm. The antibody, which is administered directly into a patient’s vein, reduces a sticky substance in the brain called amyloid beta, which clumps between neurons and disrupts their function.

Keyword: Alzheimers; Brain imaging
Link ID: 29085 - Posted: 01.09.2024

By Bill Sullivan Schizophrenia can produce persistent delusions, hallucinations, and disorganized thinking. The precise cause is unknown but seems to involve a combination of genetics and environmental risk factors. One environmental factor may be an infectious agent, such as the common parasite Toxoplasma gondii, which causes toxoplasmosis. Since cats can transmit Toxoplasma to humans, scientists have been investigating whether there is a link between cat ownership and schizophrenia. Many studies have tried to answer this question over the past 50 years; some studies show an association, but others do not. Researchers at the University of Queensland in Australia recently reanalyzed all these studies to determine the current consensus. What Is Toxoplasma? Toxoplasma is a single-celled parasite that infects all warm-blooded animals, including up to one-third of the human population. Cats are the only animals that support the sexual stage of the parasite’s life cycle, which culminates in the expulsion of infectious parasites in the feces. These fecal parasites are housed in sturdy containers called oocysts, which are stable in the environment for years and can spread the infection to a new individual if inhaled or ingested. In addition to litter boxes, people can pick up oocysts wherever a cat may have defecated, for example in the yard, sandbox, or garden (including unwashed fruits and vegetables). Oocysts have also made their way into streams and seawater, where they can infect people though shellfish. Up to 40 million people in the U.S. are infected with Toxoplasma. While a healthy immune system can control the parasite’s growth, it cannot get rid of the infection entirely. Toxoplasma parasites remain in the brain and other tissues as latent cysts, which can resume growth if the immune system is weakened.

Keyword: Schizophrenia
Link ID: 29084 - Posted: 01.09.2024

By Aimee Cunningham Ask thousands of teens whether frequent use of certain substances brings a high risk of harm, and they mostly nail it: a majority say yes for cigarettes, alcohol, cocaine and heroin. But there’s one substance that many skip over — cannabis. Only 35 percent of 12- to 17-year-olds perceive a “great risk of harm” from smoking marijuana once or twice a week, according to the National Survey on Drug Use and Health. It’s a sentiment that some of their parents may share. Parents often don’t understand that the products used today “are not what they knew when they were in high school,” says Kelly Young-Wolff, a licensed clinical psychologist and research scientist at Kaiser Permanente Northern California Division of Research in Oakland. If their children are using cannabis, parents may think, “‘it’s not that bad, at least they’re not using this other drug that’s worse.’” But the cannabis products available now are leaps and bounds more potent — which may increase the risks for addiction and psychosis — than in the past. Marijuana plants have been bred to contain more delta-9-tetrahydrocannabinol, or THC, the main psychoactive chemical. In 1995, the total percent of THC by weight of marijuana plant material was around 4 percent; now marijuana with a THC potency of 20 percent or more is available. Trouncing that are concentrated cannabis products, including wax, budder and shatter, which can have a THC potency as high as 95 percent. Cannabis is legal for adults to use recreationally in 24 states and Washington, D.C., and is allowed for medical use in 38 states and D.C. The widespread availability of cannabis “promotes the idea that it’s safe,” says pediatrician Beth Ebel of the University of Washington School of Medicine and Seattle Children’s Hospital. But that “is an incorrect assumption.” THC can impact brain chemistry “in a way that wasn’t intended,” Ebel says. “Some of the worst effects can have lifelong health consequences, especially for a young person.” © Society for Science & the Public 2000–2024.

Keyword: Drug Abuse; Development of the Brain
Link ID: 29083 - Posted: 01.06.2024

By Max Kozlov Shredded iboga root, the main ingredient in the psychedelic drug ibogaine, is prepared for use in a traditional ceremony in Gabon.Credit: Rachel Nuwer Psychedelic drugs such as MDMA and psilocybin, the hallucinogenic compound found in magic mushrooms, have promised to revolutionize psychiatric treatments. Now, a small trial in military veterans suggests that a lesser-known, potent psychedelic drug called ibogaine could be used to treat traumatic brain injury (TBI). One month after ibogaine treatment, the veterans reported that TBI symptoms such as post-traumatic stress disorder (PTSD) and depression had decreased by more than 80%, on average1. “The drug seems to have a broad, dramatic and consistent effect,” says Nolan Williams, a neuroscientist at Stanford University in California and a co-author of the study. The results of the trial, which did not include a control group, are published today in Nature Medicine. These data support launching rigorous trials to test the drug, says Alan Davis, a clinical psychologist at the Ohio State University in Columbus. However, they note that MDMA and psilocybin, which are already in late-stage trials, will be “much better candidates for meeting the needs of this community”. Ibogaine will require years of study to determine its efficacy and safety, Davis says. Warfare’s lasting effects Ibogaine is made from the bark of a shrub (Tabernanthe iboga) native to Central Africa, where it is used for ceremonial purposes. Researchers have tended to shy away from exploring the use of ibogaine for the treatment of conditions other than opioid dependence and withdrawal2, because it is tightly regulated in many countries and can cause fatal heartbeat irregularities, says Maria Steenkamp, a clinical psychologist who studies PTSD in veterans at the NYU Grossman School of Medicine in New York City. But the available therapies for PTSD and other conditions don’t help everybody, Steenkamp says. “We are desperately in need of new interventions.” © 2024 Springer Nature Limited

Keyword: Stress; Drug Abuse
Link ID: 29082 - Posted: 01.06.2024

By Cara Giovanetti The human brain's billions of neurons represent a menagerie of cells that are among both the most highly specialized and variable ones in our bodies. Neurons convert electrical signals to chemical signals, and in humans, their lengths can be so tiny as to span just the tip of a sharpened pencil or, in some cases, even stretch the width of a doorway. Their flexible control of movement and decision-making explains why they are so key to survival in the animal kingdom. Most animals depend on their allotment of neurons for survival. It might stand to reason, then, that the common ancestor of all of these animals also moved about the Earth millions of years ago under the guidance of electrochemical signals transmitted and received by networks of neurons. The idea that these pivotal cells evolved multiple times seems implausible because neurons are highly complex cells, and they are also quite similar among animal lineages. But a series of recent evolutionary biology studies are straining the assumption that all animal neurons have a single origin. These findings are the culmination of several years’ worth of research on and debate about early evolutionary animal lineages and the cells and systems present in those species. The first such finding came from studying relationships among early animals, with a focus on two particular types of organisms: sponges (including sea sponges and freshwater varieties) and ctenophores, invertebrates often known as comb jellies, though they are unrelated to jellyfish. For roughly 15 years, evolutionary biologists have been divided over whether ctenophores or sponges were the first animals to branch from all other animals in the evolutionary tree. Hundreds of millions of years ago the common ancestor to all living animals branched into two species. On one side was the common ancestor of all groups of animals except for one. On the other side was that “one”—the “sister group” that was the first to diverge from all other animals. A persistent question has been whether the sister group was the sponges or ctenophores. A compelling paper published last year lends strong support to the hypothesis that ctenophores are, in fact, the long-sought sister group. Ctenophores, the researchers found, branched off before sponges and are therefore the group most distantly related to all other animals. Yet despite the new evidence, what exactly happened in evolutionary history is still unsettled because of the puzzle it poses in explaining the evolution of neurons. © 2023 SCIENTIFIC AMERICAN,

Keyword: Evolution
Link ID: 29081 - Posted: 01.06.2024

By Rodrigo Pérez Ortega Politically and ethically fraught, research into what leads to bisexual behavior or exclusive homosexuality typically sparks controversy. The latest study, published today in Science Advances, is no exception. By mining a DNA database of some 450,000 people in the United Kingdom, a research team has concluded that the genes underlying bisexual behavior are distinct from those driving exclusive same-sex behavior, and may be intertwined with a propensity for taking risks. This connection to risk-taking, the authors suggest, may also explain why men with a history of bisexual behavior still have a reasonably high number of offspring, albeit fewer than heterosexual men, possibly explaining why the genes driving such sexual behavior have persisted. The work has drawn a mix of strong reactions. Some scientists called the findings valuable, whereas others found fault with the underlying data. Still others argued the research could potentially stigmatize sexual minorities. The result that bisexuality is tied with risky behavior, some scientists say, could be used by others to discriminate against, and further perpetuate false narratives about, bisexual people. However, study co-author Jianzhi Zhang, an evolutionary geneticist at the University of Michigan (UM), counters that the association between bisexual behavior and risk-taking “is an empirical observation. … We hold no moral judgement on risk-taking and believe [it] has pros and cons (depending on the situation), as almost any trait.” He also pushes back at the idea such research should be taboo or off limits. “We should welcome more studies of bisexuality and homosexuality. … This is partly a biological question, so we should understand it.” From one stark evolutionary perspective, sex without the prospect of producing children could be seen as waste of time and energy—behavior that might be selected against. Yet population surveys have consistently found that about 2% to 10% of people engage in sex with others of the same sex. Studies of twins have suggested such sexual activity is at least partly heritable, and therefore has a genetic component. And scientists have proposed several evolutionary theories explaining why same-sex sexual behavior may persist.

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 29080 - Posted: 01.06.2024

Allison Aubrey Among the roughly 40 million adults in the U.S. who have hearing loss, most don't use hearing aids. This means they may be missing out on more than just good hearing. Research shows hearing loss, if left untreated, can increase the risk of frailty, falls, social isolation, depression and cognitive decline. One study from scientists at Johns Hopkins University found that even people with mild hearing loss doubled their risk of dementia. Now a new study finds that restoring hearing loss with hearing aids may lengthen people's lives. Dr. Janet Choi, an otolaryngologist with Keck Medicine of USC, wanted to evaluate whether restoring hearing with hearing aids may increase the chances of living longer. Using data from the the National Health and Nutrition Examination Survey, a large, national study, Choi and her colleagues tracked the status of nearly 1,900 adults who had been shown to have hearing loss during screenings. The participants completed questionnaires about their use of hearing aids. "The group of patients who were using hearing aids regularly had a 24% lower risk of mortality compared to the group who never use hearing aids," Choi says. Meaning, the participants who were in the habit of wearing hearing aids were significantly less likely to die early. The researchers had hypothesized this would be the case given all the studies pointing to the negative impacts of untreated hearing loss. But Choi says they did not expect such a big difference in mortality risk. "We were surprised," she says. Prior research has shown that age-related hearing loss – if untreated – can take its toll on physical and mental health. And a recent study found restoring hearing with hearing aids may slow cognitive decline among people at high risk. © 2024 npr

Keyword: Hearing
Link ID: 29079 - Posted: 01.06.2024

By Gina Kolata People taking the wildly popular drugs Ozempic, to treat diabetes, and Wegovy, to combat obesity, are slightly less likely to have suicidal thoughts than people who are not taking them, researchers reported on Friday. Millions of people take Ozempic and Wegovy, which are considered to be among the biggest blockbusters in medical history. But last year a European drug safety agency said it was investigating whether the drugs cause suicidal thoughts. The new study, published in the journal Nature Medicine, was funded by the National Institutes of Health and used a huge population. The findings provide data that may potentially reassure people who take the drugs. Novo Nordisk, maker of the drugs, had no role in the study, and the study’s investigators had no conflicts of interest. The investigators used anonymized electronic health records from a database of 100.8 million people. That allowed them to look at two groups: 240,618 who were prescribed Wegovy or other weight loss drugs, and 1,589,855 who were prescribed Ozempic or other medicines to lower their blood sugar. Suicidal thoughts were included in patients’ records as part of routine monitoring of their health. The investigators compared the incidence of suicidal thoughts in people who were taking the drugs with the incidence among similar people who were not taking them but were taking other weight loss and anti-diabetes medications. They also asked if there was an increase in the recurrence of suicidal thoughts among those taking the drugs who had previously reported thoughts of suicide. The database’s size allowed the researchers to look at subgroups such as sex, race and age groups. “No matter how hard we tried we did not see any increased risk,” said Rong Xu, director of the Center for Artificial Intelligence in Drug Discovery at Case Western Reserve University in Cleveland. Dr. Xu conceived the study and interpreted the data with Dr. Nora D. Volkow, director of the National Institute on Drug Abuse. But it was an observational study, so it is impossible to draw conclusions about cause and effect. Such studies can only show associations. “More studies are absolutely needed,” Dr. Volkow said. © 2024 The New York Times Company

Keyword: Obesity; Depression
Link ID: 29078 - Posted: 01.06.2024

Kamal Nahas Peter Hegemann, a biophysicist at Humboldt University, has spent his career exploring interactions between proteins and light. Specifically, he studies how photoreceptors detect and respond to light, focusing largely on rhodopsins, a family of membrane photoreceptors in animals, plants, fungi, protists, and prokaryotes.1 Early in his career, his curiosity led him to an unknown rhodopsin in green algae that later proved to have useful applications in neuroscience research. Hegemann became a pioneer in the field of optogenetics, which revolutionized the ways in which scientists draw causal links between neuronal activity and behavior. In the early 1980s during his graduate studies at the Max Planck Institute of Biochemistry, Hegemann spent his days exploring rhodopsins in bacteria and archaea. However, the field was crowded, and he was eager to study a rhodopsin that scientists knew nothing about. Around this time, Kenneth Foster, a biophysicist at Syracuse University, was investigating whether the green algae Chlamydomonas, a photosynthetic unicellular eukaryote related to plants, used a rhodopsin in its eyespot organelle to detect light and trigger the algae to swim. He struggled to pinpoint the protein itself, so he took a roundabout approach and started interfering with nearby molecules that interact with rhodopsins.2 Rhodopsins require the small molecule retinal to function as a photoreceptor. When Foster depleted Chlamydomonas of its own retinal, the algae were unable to use light to direct movement, a behavior that was restored when he introduced retinal analogues. In 1985, Hegemann joined Foster’s group as a postdoctoral researcher to continue this work. “I wanted to find something new,” Hegemann said. “Therefore, I worked on an exotic organism and an exotic topic.” A year later, Hegemann started his own research group at the Max Planck Institute of Biochemistry where he searched for the green algae’s rhodopsin that Foster proposed should exist. © 1986–2024 The Scientist.

Keyword: Brain imaging; Vision
Link ID: 29077 - Posted: 01.03.2024

By April Dembosky Every year, an estimated 100,000 young adults or adolescents in the U.S. experience a psychotic episode. Only 10-20% of them gain access to the holistic treatment approach recommended by the National Institute of Mental Health as the gold standard of care for early psychosis, due to lack of space or because insurance won't cover it. Illustration by Anna Vignet/KQED After M graduated from high school in California, she got a job at a fast food restaurant making burgers. Her coworkers were chatting over the fryer one day when M got a weird feeling, like somehow they knew what she was thinking. It was like her coworkers could read her mind and were discussing her thoughts with each other. "I was like, are they talking about burgers or are they talking about me?" says M, now 21. NPR has agreed to identify M by her middle initial because she fears the stigma around her mental illness could disrupt her career path. There was one coworker in particular, a guy she had a crush on, and she was pretty sure he was watching her. She suspected he hacked into her phone so he could listen to her conversations, find out where she was and follow her around. If she was walking down the street, or hanging out in the park, she saw him. Her mom remembers M wanted to sleep with the lights on, repeatedly asking her through the night, "Mom, is someone here?" One day, her mom said M got so paranoid, so scared, she locked herself in the bathroom and just screamed and screamed and screamed. Her mom wanted to call for help. But she didn't have a job at the time. This was about a year into the pandemic, and the hotel where M's mom worked had been closed since the first lockdown. When she lost her job, she lost her family's health benefits, too. "My husband was like, 'What is that going to cost?'" her mom remembers. © 2024 npr

Keyword: Schizophrenia
Link ID: 29076 - Posted: 01.03.2024

By Katie Engelhart The doctors told Naomi that she could not leave the hospital. She was lying in a narrow bed at Denver Health Medical Center. Someone said something about a judge and a court order. Someone used the phrase “gravely disabled.” Naomi did not think she was gravely disabled. Still, she decided not to fight it. She could deny that she was mentally incompetent — but this would probably just be taken as proof of her mental incompetence. Of her lack of insight. She would, instead, “succumb to it.” It was early 2018. She had come to the hospital voluntarily, because she was getting so thin. In the days before, she had felt her electrolyte levels dip toward the danger zone — and she had decided that, even after everything, she did not want to be dead. By then, Naomi was 37 and had been starving herself for 26 years, and she was exquisitely attuned to her body’s corrupted chemistry. At the hospital, she was admitted to the ACUTE Center for Eating Disorders & Severe Malnutrition for medical stabilization. There, doctors began what was once called refeeding but is now more commonly called nutritional rehabilitation, using an intravenous line that fed into her neck. Reintroducing food to an emaciated body can be dangerous and even lethal if done too quickly. Physicians identified this phenomenon in the aftermath of World War II, when they observed skeletal concentration-camp survivors and longtime prisoners of war eat high-caloric foods and then drop dead of cardiac failure. “Well, here I am,” Naomi said in a video message that she recorded for her parents. “I am alive, but am I happy? I don’t know. … It’s pretty pathetic. I don’t know how I feel about the fact that I would have died had I not come.” In the video, she was wearing a hot pink tank top, even though it was cool in the hospital room, because she wanted to shiver, because shivering burned calories. A few days later, when she was not imminently dying anymore, Naomi announced that she was going home — and the hospital responded by placing her on a 72-hour mental-health hold. Clinicians then obtained what Colorado calls a short-term certification, which required, by judicial order, that Naomi be detained and treated, in her case until she reached what physicians determined to be 80 percent of her “ideal body weight.” In Colorado, as in most states, a patient can be treated against her will if she is mentally ill and found incapable of making informed decisions. That day, Naomi was transferred to a residential program at Denver’s Eating Recovery Center (E.R.C.) © 2024 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 29075 - Posted: 01.03.2024

By Regina G. Barber Human brains aren't built to comprehend large numbers, like the national debt or how much to save for retirement. But with a few tools — analogies, metaphors and visualizations — we can get better at it. erhui1979/Getty Images Imagine a horizontal line. The very left is marked one thousand and the very right is marked one billion. On this line, where would you add a marker to represent one million? If you said somewhere in the middle, you answered the same as the roughly 50 percent of people who have done this exercise in a number line study. But the answer is actually much closer to one thousand since there are one thousand millions in one billion. This error makes sense because "our human brains are pretty bad at comprehending large numbers," says Elizabeth Toomarian, an educational neuroscientist at Stanford University. She studies how the brain makes sense of numbers. Or doesn't. "Our brains are evolutionarily very old and we are pushing them to do things that we've only just recently conceptualized," says Toomarian. Instead, the human brain is built to understand how much of something is in its environment. For example, which bush has more berries or how many predators are in that clearing? But comprehending the national debt or imagining the size of our universe? "We certainly can use our brains in that way, but we're recycling these sort of evolutionarily old brain architectures to do something really new," she says. In other words, it's not our fault that we have trouble wrapping our heads around big numbers. © 2024 npr

Keyword: Attention
Link ID: 29074 - Posted: 01.03.2024

By Fletcher Reveley One afternoon in May 2020, Jerry Tang, a Ph.D. student in computer science at the University of Texas at Austin, sat staring at a cryptic string of words scrawled across his computer screen: “I am not finished yet to start my career at twenty without having gotten my license I never have to pull out and run back to my parents to take me home.” The sentence was jumbled and agrammatical. But to Tang, it represented a remarkable feat: A computer pulling a thought, however disjointed, from a person’s mind. For weeks, ever since the pandemic had shuttered his university and forced his lab work online, Tang had been at home tweaking a semantic decoder — a brain-computer interface, or BCI, that generates text from brain scans. Prior to the university’s closure, study participants had been providing data to train the decoder for months, listening to hours of storytelling podcasts while a functional magnetic resonance imaging (fMRI) machine logged their brain responses. Then, the participants had listened to a new story — one that had not been used to train the algorithm — and those fMRI scans were fed into the decoder, which used GPT1, a predecessor to the ubiquitous AI chatbot ChatGPT, to spit out a text prediction of what it thought the participant had heard. For this snippet, Tang compared it to the original story: “Although I’m twenty-three years old I don’t have my driver’s license yet and I just jumped out right when I needed to and she says well why don’t you come back to my house and I’ll give you a ride.” The decoder was not only capturing the gist of the original, but also producing exact matches of specific words — twenty, license. When Tang shared the results with his adviser, a UT Austin neuroscientist named Alexander Huth who had been working towards building such a decoder for nearly a decade, Huth was floored. “Holy shit,” Huth recalled saying. “This is actually working.”

Keyword: Brain imaging; Language
Link ID: 29073 - Posted: 01.03.2024

By Laura Sanders In this busy holiday season, many of us multitask. Arctic reindeer are no exception. Reindeer can eat and sleep at the same time, a new study suggests. This timesaving strategy, described December 22 in Current Biology, adds to the number of ingenious ways animals can catch some z’s under tough conditions (SN: 11/30/23). Arctic reindeer are quite busy in the summer — eating when the sun shines around the clock and the food is abundant. Like other ruminants, reindeer spend a considerable amount of time chewing on regurgitated food, making it smaller and easier to digest. Finding time to sleep amid all this cud chewing might be tough. But not if the reindeer could sleep while they chewed. To find out if the reindeer could actually sleep-eat, neuroscientist Melanie Furrer and chronobiologist Sara Meier, along with their colleagues, trained four female Eurasian tundra reindeer (Rangifer tarandus tarandus) to tolerate a pen and electrodes on shaved patches of skin. The process involved some kicks and lots of lichen treats, “which is like candy to them,” says Meier, of the University of Zurich. The researchers were looking for the brain waves that appear during non-REM sleep, a deep, restorative sleep phase. These waves appeared when the reindeer were chewing cud, though the chewing motion itself made it hard to say whether the signal was identical to that of a regular sleep session. “We couldn’t go into detail by looking only at the brain waves, because we have this chewing in there that disturbs it a bit,” says Furrer, also of the University of Zurich. Still, other signs also pointed to sleep while chewing. The reindeer were calm while chewing, often with their eyes closed. “They were in a very relaxed state that resembles the body position of non-REM sleep,” Furrer says. Ruminating reindeer were also harder to disturb; rustling from neighboring reindeer was less likely to get a look from a ruminating reindeer. When reindeer are kept awake, they need catch-up recovery sleep. But time spent chewing decreased this time spent in recovery sleep, the researchers found. © Society for Science & the Public 2000–2023.

Keyword: Sleep; Attention
Link ID: 29072 - Posted: 12.31.2023

By Catherine Pearson Dry January sounds like a simple proposition: No alcohol. For 31 days. And some enthusiasts jump in without much planning — perhaps even hungover after a rowdy New Year’s Eve. There is no data suggesting that those folks won’t be able to abstain from drinking, said Dr. David Wolinsky, an assistant professor of psychiatry and behavioral sciences with Johns Hopkins Medicine, who specializes in addiction. But starting the month with a few strategies in your back pocket — and with a clear sense of your goals — may help you get the most out of the challenge. “Most of the benefits of Dry January are probably going to be related to the intention with which you go into Dry January,” Dr. Wolinsky said. The challenge isn’t a stand-in for treatment for people with alcohol use disorder, he stressed, but those who are looking to get a fresh start to the year may benefit from the mental and physical reset it can offer, and the opportunity to adopt new habits. For instance, a 2016 study found that six months after Dry January ended, participants were drinking less than they were before. We spoke to Dr. Wolinsky and other experts about some strategies for a successful month. One of the simplest steps is to spread the word among friends and family that you intend to take the month off, said Casey McGuire Davidson, a sobriety coach and host of “The Hello Someday Podcast,” which focuses on “sober-curious” topics. Research has shown that accountability can play a critical role in helping habits stick, and you might find a friend or partner to join you, Ms. Davidson suggested. Even if you don’t, you may be surprised by how encouraging people are of your goal (though she said you should share it only with people you trust). “Dry January gives people a period of time when they can stop drinking with community and support,” she said, “without a lot of questions.” Ms. Davidson also recommended reading books that may help you evaluate your relationship with alcohol, or listening to sobriety podcasts. © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 29071 - Posted: 12.31.2023

Rudi Zygadlo To celebrate our anniversary, my partner and I dine in a trendy London restaurant in Hackney with a Michelin star – my first time in such a place. A crispy little bonbon is introduced to us simply as “Pine, kvass lees and vin brûlé.” I watch my partner light up, the flickering candle in her eyes, as the waiter sets the thing down. The impact of the aroma has already registered on her face. With her first bite she is transported to her childhood in Massachusetts. “Gosh,” she gasps, closing her eyes as a New England virgin pine forest explodes in her mind. When she blinks open, returning to the here and now, she looks at me guiltily. I take a bite and wince. No coniferous wonderland for me. Just unpleasant bitterness, confined very much to the tongue. I am pleased for her, truly. I’m a magnanimous guy. But from that moment on, the whole evening is a bit of a spectator sport and, by the end of it, I have a feeling that she is even playing her enjoyment down, muting her reactions, as if to say, “You’re not missing out.” She finds some dishes prove more successful than others – the sweetness of cherry, an umami-rich mushroom – but I am missing out: on the nuances, the emotions, the memories. The smell. It’s been three years since I lost it. November 2020. I was living with three friends in a flat in Glasgow when we all caught Covid in the pre-vaccine days. Two of us lost our smell and never fully recovered it. We’re in good company. Around 700,000 people in the UK are believed to have total smell loss caused by the virus, with around six million still experiencing some olfactory dysfunction. I estimate mine has returned by about 30%, but it’s inconsistent and often distorted. To summarise my symptoms of anosmia, as total or partial loss of smell is known: some things have a faint odour, some don’t smell as they should and others don’t smell at all. For example: basil smells mild but good, ground coffee and a certain brand of toothpaste smell like fish and, mercifully, shit doesn’t stink at all. Apart from the latter, all bad news.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29070 - Posted: 12.31.2023