Rebecca Brooker & Tristin Nyman Even before the pandemic, there was plenty for expectant mothers to worry about. Pregnant women must withstand a barrage of arguably well-intentioned, but often hyperbolic, warnings about their health and what’s to come, including concerns about everything from what to eat, to what to wear, to how to feel. Health professionals know that mothers-to-be experience predictable increases in anxiety levels before infants are born. Maternal mental health has been steadily deteriorating in the U.S., particularly among poor and minority women. The calls to “be afraid, be very afraid” are, of course, countered by the equally strong cautions for pregnant women to not worry too much, lest it lead to long-term negative outcomes for them and their infants. Such warnings are not entirely off base. Maternal stress hormones cross the placenta and affect the vulnerable fetus. Fetal exposure to the stress hormone cortisol has been linked to an array of negative outcomes, including miscarriage and preterm birth, and irritable temperament for the child and increased risk of emotional problems during childhood. One thing researchers know is that anxious mothers tend to have anxious children. This common, albeit not prescriptive, phenomenon is likely due to numerous factors, both pre- and postpartum. In our laboratory, we focus on what happens when women start their pregnancies already worried or anxious and what clues we can uncover about how to help them and their children. Our research suggests that worry during pregnancy can have long-term impacts on how mothers’ brains communicate – but also that there might be some simple steps that can help rein in the effects. © 2010–2021, The Conversation US, Inc.

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 27820 - Posted: 05.15.2021

By Lisa Sanders, M.D. “I can’t move my legs,” the 26-year-old man told his younger brother, who towered above him as he lay sprawled on the floor. He’d been on his computer for hours, he explained, and when he tried to stand up, he couldn’t. His legs looked normal, felt normal, yet they wouldn’t move. At first, he figured his legs must have fallen asleep. He pulled himself up, leaning on his desk, and slowly straightened until he was standing. He could feel the weight on his feet and knees. He let go of the desk and commanded his legs to move. Instead, they buckled, and he landed on the floor with a thud. His brother awkwardly pulled him onto the bed. Then they waited. Surely this weird paralysis would disappear just as suddenly as it came. An hour passed, then two. I’m calling an ambulance, the younger brother announced finally. Reluctantly, the elder agreed. He was embarrassed to be this helpless but worried enough to want help. When the E.M.T.s arrived, they were as confused as the brothers. The medics asked what the young man had been up to. Nothing bad, he assured them. For the past few weeks he had been getting back into shape. He changed his diet, cut out the junk and was drinking a protein concoction that was supposed to help him build muscle. And he was working out hard every day. He’d lost more than 20 pounds, he added proudly. © 2021 The New York Times Company

Keyword: Movement Disorders; Hormones & Behavior
Link ID: 27813 - Posted: 05.12.2021

By Lisa Sanders, M.D. It was dark by the time the 41-year-old woman was able to start the long drive from her father’s apartment in Washington, D.C., to her home in Westchester County, N.Y. She was eager to get back to her husband and three children. Somewhere after she crossed the border into Maryland, the woman suddenly developed a terrible itch all over her body. She’d been a little itchy for the past couple of weeks but attributed that to dry skin from her now-faded summertime tan. This seemed very different: much stronger, much deeper. And absolutely everywhere, all at the same time. The sensation was so intense it was hard for the woman to pay attention to the road. She found herself driving with one hand on the steering wheel and the other working to respond to her skin’s new need. There was no rash — or at least nothing she could feel — just the terrible itch, so deep inside her skin that she felt as if she couldn’t scratch hard enough to really get to it. By the light of the Baltimore Harbor Tunnel she saw that her nails and fingers were dark with blood. That scared her, and she tried to stop scratching, but she couldn’t. It felt as if a million ants were crawling all over her body. Not on her skin, but somehow under it. The woman had gone to Washington to help her elderly father move. His place was a mess. Many of his belongings hadn’t been touched in years. She figured that she was having a reaction to all the dust and dirt and who knows what else she encountered while cleaning. As soon as she got home, she took a long shower; the cool water soothed her excoriated skin. She lathered herself with moisturizer and sank gratefully into her bed. But the reprieve didn’t last, and from that night on she was tormented by an itch that no scratching could satisfy. © 2021 The New York Times Company

Keyword: Pain & Touch; Hormones & Behavior
Link ID: 27775 - Posted: 04.17.2021

by Peter Hess Mice missing a copy of the autism-linked gene MAGEL2 have trouble discerning between a familiar mouse and an unfamiliar one, but treating them with the social hormone vasopressin reverses this deficit, according to a new study. Mutations in or deletions of MAGEL2 are linked to autism and several related conditions, including Prader-Willi syndrome, which is characterized by intellectual disability, poor muscle tone, difficulty feeding and problems with social interactions. The new findings suggest that these social issues in people stem from impairments in vasopressin’s function in a brain region called the lateral septum, which relays signals between the hippocampus and the ventral tegmental area. They also hint that vasopressin treatment could remedy those issues, says Elizabeth Hammock, assistant professor of psychology and neuroscience at Florida State University in Tallahassee, who was not involved with the study. A 2020 study showed that low levels of vasopressin in cerebrospinal fluid can flag many infants who are later diagnosed with autism. But clinical trials have shown that either providing vasopressin or blocking its effects can improve social communication in autistic children. Because of these seemingly contradictory results, “a better understanding of how alterations in the vasopressinergic system leads to social deficits and how vasopressin administration could resolve some of these problems was needed,” says co-lead researcher Freddy Jeanneteau, professor of neuroscience at Montpellier University in Montpellier, France. © 2021 Simons Foundation

Keyword: Autism; Hormones & Behavior
Link ID: 27665 - Posted: 01.27.2021

by Peter Hess Two types of neurons process social information, a new mouse study suggests, but only one is disrupted in mice missing the autism-linked gene FMR1. The neurons reside in a brain region called the hypothalamus, and both send signals via the hormone oxytocin. The deletion of FMR1, however, affects these cells differently: The loss of FMR1 in the smaller, ‘parvocellular’ neurons diminishes the mice’s interest in social interactions — but only those involving peers, the new work shows. The gene’s loss from the larger, ‘magnocellular’ neurons, by contrast, does not disrupt the animals’ interactions with either peers or parents. “There are a lot of different types of social behaviors, and not all of them are impaired in autism,” says lead investigator Gül Dölen, assistant professor of neuroscience at Johns Hopkins University in Baltimore, Maryland. Whereas peer-to-peer social interactions are troublesome for many autistic people, other social interactions — such as parental connections — are on par with those seen in non-autistic people, she says. This new understanding of the different neurons’ functions could help explain why clinical trials of oxytocin for treating autism traits have shown mixed results. It could also help scientists develop more effective treatments, experts say. “There are these two different kinds of neurons that we’ve known about for a really long time, and each of their contributions to social behavior has never really been dissected out,” says Larry Young, chief of behavioral neuroscience and psychiatric disorders at Emory University in Atlanta, Georgia, who was not involved with the study. “It’s really important for the future of drug development.” © 2020 Simons Foundation

Keyword: Autism; Hormones & Behavior
Link ID: 27632 - Posted: 12.19.2020

By Sally Satel For over a half-century, steroid drugs have been a mainstay of medical care, widely used to treat inflammatory illness such as asthma, skin conditions and autoimmune diseases. Less is known about their dramatic and sometimes frightening long-term effects on mood, personality and thinking. I took steroids years ago, and the side effects changed my life. Steroid medications mimic a natural hormone in the body called glucocorticoid, which suppresses immune system processes that trigger inflammation, the sources of many autoimmune and chronic disease. In 1948, glucocorticoid was first used for a chronic inflammatory disease, rheumatoid arthritis, which causes joint deformity and chronic pain. Two years later, the American physician behind the breakthrough therapy was one of the winners of the Nobel Prize. Steroids have been prescribed for many other conditions since then. One steroid, dexamethasone, has been used for people with severe cases of covid-19 and President Trump was given it when he was hospitalized for the disease in October. My story starts in 1977. I was finishing my senior year as a biology major at Cornell University when I was diagnosed with Crohn’s disease, a form of inflammatory disease in which the body’s immune system attacks the gastrointestinal tract. I had a relatively mild case — transient pain, causing me to rush to the nearest ladies’ room, and find some blood in the bowl — and so I was able to finish my final year on time and begin a PhD program in evolutionary biology that summer. My predoctoral project entailed measuring the jaw muscles of tadpoles using jewelers’ tools and a dissecting microscope. Within weeks, though, I had a “flare” in the parlance of gastroenterology — I felt weak and was having increased bouts of blood-streaked diarrhea. In mid-October, I spent five days at the hospital where my symptoms resolved on a daily regimen of 60 mg of the potent steroid prednisone. I was discharged on 60 mg per day and felt fine for a week. But soon my brain began to feel like cotton wrapped in yards of gauze. I tried to study for an upcoming quiz but I couldn’t concentrate. © 1996-2020 The Washington Post

Keyword: Hormones & Behavior
Link ID: 27609 - Posted: 12.07.2020

Moles have a pretty tough life. They live underground, in the dark, burrowing through heavy dirt. And when faced with an enemy, there's nowhere to turn — they have to fight. In most mammals, females tend to be at a disadvantage when it comes to face-to-face combat, because they tend to be smaller and less aggressive than males. But female moles have evolved a secret weapon: a hybrid organ made up of both ovarian and testicular tissue. This effectively makes them intersex, giving them an extra dose of testosterone to make them just as muscular and aggressive as male moles. "As a consequence, basically the whole body of the female, they get masculinized," geneticist Darío Lupiáñez told Quirks & Quarks host Bob McDonald. "They become the body builders of nature." Lupiáñez co-led a study to understand how the moles' genes facilitated this advantage, which was recently published in the journal Science. The research was part of a collaboration between the Max Planck Institute for Molecular Genetics and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association in Germany. Same genes, different instructions The team worked with Iberian moles, commonly found in Spain and Portugal, however this intersex adaptation has been documented in at least six mole species. "We know that intersexuality happens in species like humans, dogs or cats. But the difference actually in moles, it happens all the time, so all the females are intersexual. And this is really something unique among mammals," said Lupiáñez. To understand how moles evolved these intersexual traits, researchers fully mapped the genome of the Iberian mole, commonly found in Spain and Portugal. (David Carmona, Department of Genetics, University of Granada, Spain ) ©2020 CBC/Radio-Canada.

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 27530 - Posted: 10.19.2020

By Lisa Sanders, M.D. The waiter had barely put the plate in front of her when the 46-year-old woman felt the color drain from her face. She was in Fresno, Calif., on a work trip and had come to a restaurant to meet an old friend for dinner. But all of a sudden her stomach dropped — the way it might on a roller-coaster ride. A sudden coolness on her face told her she’d broken out in a sweat. She felt dizzy and a little confused. She saw the alarmed face of her friend and knew she looked as bad as she felt. She excused herself and carefully made her way to the bathroom. She sat in front of the vanity and supported her head on her arms. There was the now-familiar stabbing pain in her stomach. She wasn’t sure how long she stayed like that. Was it 10 minutes? 15? At last she felt as if she could get up. As she hurried to meet her friend at the entrance, she felt the contents of her stomach surging upward. She covered her mouth as vomit shot between her fingers. She lowered her head and bolted through the doorway, trying not to see the horrified faces of the diners. In the parking lot, the rush of stomach contents continued until she was completely empty. Exhausted, she sank into the seat of her friend’s car. She was too sick to go back to her hotel, her friend said. Instead the friend would take her to her house, until she felt better. The next thing the woman remembered was that she was sitting on the floor of her friend’s shower, hot water pounding her back. When she could, she crawled into bed. She slept until late the next morning. She thanked her friend, canceled her morning meetings and later that day headed home to Stockton, Calif. © 2020 The New York Times Company

Keyword: Hormones & Behavior
Link ID: 27498 - Posted: 09.30.2020

David Cox Gérard Karsenty was a young scientist trying to make a name for himself in the early 1990s when he first stumbled upon a finding that would go on to transform our understanding of bone, and the role it plays in our body. Karsenty had become interested in osteocalcin, one of the most abundant proteins in bone. He suspected that it played a crucial role in bone remodelling – the process by which our bones continuously remove and create new tissue – which enables us to grow during childhood and adolescence, and also recover from injuries. Intending to study this, he conducted a genetic knockout experiment, removing the gene responsible for osteocalcin from mice. However to his dismay, his mutant mice did not appear to have any obvious bone defects at all. “For him, it was initially a total failure,” says Mathieu Ferron, a former colleague of Karsenty who now heads a research lab studying bone biology at IRCM in Montreal. “In those days it was super-expensive to do modification in the mouse genome.” But then Karsenty noticed something unexpected. While their bones had developed normally, the mice appeared to be both noticeably fat and cognitively impaired. “Mice that don’t have osteocalcin have increased circulating glucose, and they tend to look a bit stupid,” says Ferron. “It may sound silly to say this, but they don’t learn very well, they appear kind of depressed. But it took Karsenty and his team some time to understand how a protein in bone could be affecting these functions. They were initially a bit surprised and terrified as it didn’t really make any sense to them.” © 2020 Read It Later, Inc.

Keyword: Hormones & Behavior; Obesity
Link ID: 27473 - Posted: 09.16.2020

Sean Ingle The double Olympic 800m champion Caster Semenya appears to have lost her long-running legal battle against regulations requiring women with high testosterone to take medication to compete internationally between 400m and a mile. A Swiss federal tribunal said on Tuesday that it supported a decision by the court of arbitration for sport last year that track and field’s policy for athletes with differences in sex development (DSD) was “necessary, reasonable and proportionate” to ensure fair competition in women’s sport. Charley Hull withdraws from ANA Inspiration after positive Covid-19 test Read more “Based on these findings, the Cas decision cannot be challenged,” the tribunal said. “Fairness in sport is a legitimate concern and forms a central principle of sporting competition. It is one of the pillars on which competition is based.” It now looks impossible for Semenya, the London 2012 and Rio 2016 gold medallist, to defend her title in Tokyo. She responded to the news by accusing World Athletics of being on the “wrong side of history”. “I am very disappointed by this ruling, but refuse to let World Athletics drug me or stop me from being who I am,” she said. “Excluding female athletes or endangering our health solely because of our natural abilities puts World Athletics on the wrong side of history. I will continue to fight for the human rights of female athletes, both on the track and off the track, until we can all run free the way we were born.” The South African was almost unstoppable until World Athletics implemented a new policy for DSD athletes, including Semenya, that compelled them to reduce their testosterone levels to less than 5 nmol/L if they wanted to compete in elite events between 400m and a mile. © 2020 Guardian News & Media Limited

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 27462 - Posted: 09.09.2020

by Chloe Williams A new wireless device activates a mouse’s neurons as it navigates a cage with food, hiding places and other mice, allowing researchers to study social behavior in a realistic environment1. Experiments using this setup suggest that oxytocin has distinct effects in different contexts — which may be particularly important as researchers explore the hormone’s value as a potential treatment for autism. The device makes use of optogenetics, a technique in which researchers use pulses of light to activate or silence neurons. Autism researchers have used the approach to manipulate neural circuits in mice, but traditional optogenetic devices involve a fiber-optic cable, which tethers the animal and interferes with social interactions. Other wireless devices have been able to activate neurons without a tether, but researchers have mostly used them to study social behavior involving just two mice interacting for only about 15 minutes in an otherwise empty cage — a scenario that fails to capture a full range of mouse behaviors2. The new wireless device, powered by two watch batteries, consists of a light-emitting diode attached to an optical fiber that is implanted into the brain. It has an on-off switch that allows researchers to control it remotely using a magnet placed inside the cage. Using this setup, researchers can modulate brain activity in a group of mice as they roam for days through a cage that has hiding places, platforms, a nest, food and water. The device’s designers tested it in mice engineered to express light-sensitive proteins in part of the hypothalamus. This region produces the hormone oxytocin, generally thought to reduce aggression and enhance social bonds. When delivered as a nasal spray, it improves social skills in some people with autism. © 2020 Simons Foundation

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 27369 - Posted: 07.16.2020

By Gretchen Reynolds Exercise may help change exercisers’ brains in surprising ways, according to a new study of physical activity and brain health. The study, which included both mice and people, found that exercise prompts the liver to pump out a little-known protein, and that chemically upping the levels of that protein in out-of-shape, elderly animals rejuvenates their brains and memories. The findings raise provocative questions about whether the brain benefits of exercise might someday be available in a capsule or syringe form — essentially “exercise in a pill.” We already have considerable evidence, of course, that physical activity protects brains and minds from some of the declines that otherwise accompany aging. In past rodent studies, animals that ran on wheels or treadmills produced more new neurons and learned and remembered better than sedentary mice or rats. Similarly, older people who took up walking for the sake of science added tissue volume in portions of their brains associated with memory. Even among younger people, those who were more fit than their peers tended to perform better on cognitive tests. But many questions remain unanswered about how, at a cellular level, exercise remodels the brain and alters its function. Most researchers suspect that the process involves the release of a cascade of substances inside the brain and elsewhere in the body during and after exercise. These substances interact and ignite other biochemical reactions that ultimately change how the brain looks and works. But what the substances are, where they originate and how they meet and mingle has remained unclear. So, for the new study, which was published this month in Science, researchers at the University of California, San Francisco, and other institutions decided to look inside the minds and bloodstreams of mice. In past research from the same lab, the scientists had infused blood from young mice into older ones and seen improvements in the aging animals’ thinking. It was like “transferring a memory of youth through blood,” says Saul Villeda, a professor at U.C.S.F., who conducted the study with his colleagues Alana Horowitz, Xuelai Fan and others. © 2020 The New York Times Company

Keyword: Hormones & Behavior
Link ID: 27368 - Posted: 07.16.2020

By Anna Goldfarb It’s understandable that you may be struggling to fall asleep these days. Our world has been turned upside down, so it is especially hard to unplug from the day and get the high-quality sleep your body needs. “Almost every single patient I’m speaking with has insomnia,“ said Dr. Alon Y. Avidan, a professor and vice chair in the department of neurology at the David Geffen School of Medicine at the University of California, Los Angeles, and director of the U.C.L.A. Sleep Disorders Center. “Especially now with Covid-19, we have an epidemic of insomnia. We call it Covid-somnia.” An increase in anxiety in both children and adults is affecting our ability to fall asleep. Additionally, our lifestyles have changed drastically as people observe sheltering in place guidelines. With more people staying indoors, it can mean they are not getting enough light exposure. “Without light exposure in the morning,” Dr. Avidan said, people “lose the circadian cues that are so fundamentally important in setting up appropriate and normal sleep-wake time.” There are nonmedical ways to help you sleep better: Meditation, turning off screens early in the night, warm showers and cool bedrooms can help your body rest better. But if these options don’t work, or if you are ready for the next step, you may have considered trying melatonin supplements. These pills are commonplace enough that you have most likely heard of them and seen them in your local pharmacy. Here’s what you need to know about the pros and cons of using melatonin supplements for sleeping difficulties. What is melatonin? Melatonin is a hormone that helps regulate sleep timing. It is produced in the pea-size pineal gland, which is nestled in the middle of your brain and syncs melatonin production with the rising and setting of the sun. According to the National Sleep Foundation, the gland remains inactive during the day but switches on around 9 p.m. (when it’s generally dark) to flood the brain with melatonin for the next 12 hours. © 2020 The New York Times Company

Keyword: Sleep; Biological Rhythms
Link ID: 27360 - Posted: 07.14.2020

By Yasmin Anwar, Media Relations Stephen Glickman, a pioneer in behavioral endocrinology and founder of the world’s first colony of captive spotted hyenas — he raised generations of them in a UC Berkeley research facility — died at his home in Berkeley on May 22 from pancreatic cancer. He was 87. A professor emeritus of psychology and of integrative biology, whose lifelong bond with animals began during his boyhood near the Bronx Zoo in New York, Glickman joined the UC Berkeley faculty in 1968. Over the next five decades, he conducted studies of creatures great and small, authoring more than 100 research papers. His sharp intellect, warm wit and overall lovability engaged peers and protégés in scientific and social justice pursuits, colleagues said. “Steve was a giant in the field of animal behavior,” said UC Berkeley psychology chair Ann Kring. “He studied a wide variety of species in the wild, at the zoo and, perhaps most famously, at the field station where he conducted work with hyenas for more than 30 years.” Glickman’s standout legacy is his ardent stewardship of a colony of spotted hyenas at UC Berkeley’s Field Station for the Study of Behavior, Ecology and Reproduction. The hyena compound in the Berkeley hills, above the campus, closed in 2014 when funding dried up, but not before yielding seminal discoveries about endocrinology, fertility and other medical conditions that affect humans. Hormone-driven matriarchy By studying female hyenas, who use a long, phallic clitoris, instead of a vagina, for mating and giving birth, Glickman and fellow researchers found that high levels of androgens produced in their ovaries masculinized their sex organs and boosted their aggression and dominance in the pack. Copyright © 2020 UC Regents; all rights reserved

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 27292 - Posted: 06.09.2020

By Meredith Wadman In January, one of the first publications on those sickened by the novel coronavirus in Wuhan, China, reported that three out of every four hospitalized patients were male. Data from around the world have since confirmed that men face a greater risk of severe illness and death from COVID-19 than women and that children are largely spared. Now, scientists investigating how the virus does its deadly work have zeroed in on a possible reason: Androgens—male hormones such as testosterone—appear to boost the virus’ ability to get inside cells. A constellation of emerging data supports this idea, including COVID-19 outcomes in men with prostate cancer and lab studies of how androgens regulate key genes. And preliminary observations from Spain suggest that a disproportionate number of men with male pattern baldness—which is linked to a powerful androgen—end up in hospitals with COVID-19. Researchers are rushing to test already approved drugs that block androgens’ effects, deploying them early in infection in hopes of slowing the virus and buying time for the immune system to beat it back. “Everybody is chasing a link between androgens … and the outcome of COVID-19,” says Howard Soule, executive vice president at the Prostate Cancer Foundation, who on 13 May ran a Zoom call presenting the newest research that drew 600 scientists and physicians. A second call scheduled for today will discuss incipient clinical trials. Epidemiological data from around the world have confirmed the early reports of male vulnerability. In Lombardy in Italy, for example, men comprised 82% of 1591 patients admitted to intensive care units (ICUs) from 20 February to 18 March, according to a JAMA paper. And male mortality exceeded that of women in every adult age group in another JAMA study of 5700 New York City patients hospitalized with COVID-19. © 2020 American Association for the Advancement of Science.

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 27284 - Posted: 06.04.2020

Ruth Williams Experiments in mice and observations in humans have suggested the bone protein osteocalcin acts as a hormone regulating, among other things, metabolism, fertility, exercise capacity and acute stress. That interpretation is now partially in doubt. Two independent papers published yesterday (May 28) in PLOS Genetics, each of which presents a new osteocalcin knockout mouse strain, report that glucose metabolism and fertility were unaffected in the animals. While some researchers praise the studies, others highlight weaknesses. “I thought they were very good papers. I think the authors should be congratulated for very comprehensive studies of both skeletal and extraskeletal functions of osteocalcin,” says emeritus bone researcher Caren Gundberg of Yale School of Medicine who was not involved in the research. Skeletal biologist Gerard Karsenty of Columbia University disagrees. “There have been 25 laboratories in the world . . . that have shown osteocalcin is a hormone,” says Karsenty. These two papers “do not affect the work of [those] groups,” he adds, “because they are . . . technically flawed.” This tiny protein, one of the most abundant in the body, is produced and secreted by bone-forming osteoblast cells. In the 40 or so years since osteocalcin’s discovery, its precise function, or functions—whether in the bone or endocrine system—have not been fully pinned down. Studies from Karsenty’s lab more than 10 years ago were the first to indicate that osteocalcin could act as a hormone, regulating glucose metabolism. But the suggested hormonal function has been questioned for its relevance to humans. For example, while studies in people have shown that levels of osteocalcin in the blood are correlated with diabetes, whether this is a cause or effect is unclear. © 1986–2020 The Scientist.

Keyword: Hormones & Behavior; Obesity
Link ID: 27275 - Posted: 06.03.2020

By Christina Caron For the Langstaff family, the bedtime routine had become more like a bedtime marathon. “My son has struggled with sleep from the moment he was born,” Anna Langstaff, the head of a Montessori school in Portland, Ore., said of her 6-year-old son, Henry. “We used to joke that he was like a little knight fighting a dragon called sleep.” When Henry was a toddler, dimming the lights and other bedtime cues simply sent him into “battle mode” she said. “He’d start yelling, ‘No bed! No bed!’” After years of struggling with what had become a two-hour bedtime routine, the Langstaffs turned to their pediatrician, who recommended a chocolate containing melatonin, a hormone secreted by a pea-size organ in the brain called the pineal gland that helps regulate the body’s internal clock and induces sleepiness. “It was like magic,” she said. Now Henry falls asleep at 7:30 p.m. and continues to wake up at the same time he always has, shortly before 6 a.m., Langstaff said. “Magic” — “game changer” — these are words frequently used by parents describing how melatonin helps their children fall asleep. An online survey of 933 parents with children under 18 conducted by YouGov for The New York Times in May found that only about a third had kids who were struggling with sleep issues in the past year. But among those parents, almost half had given melatonin to their children. © 2020 The New York Times Company

Keyword: Sleep; Hormones & Behavior
Link ID: 27253 - Posted: 05.18.2020

by Peter Hess Low levels of the hormone vasopressin in early infancy may presage an autism diagnosis in childhood, according to a new study1. Although preliminary, the results suggest that testing vasopressin levels — particularly in infants with high odds of having autism — could flag the condition in the first few months of life. Early identification would allow autistic children to start therapies far sooner than is currently possible, says co-lead investigator Karen Parker, associate professor of psychiatry and behavioral sciences at Stanford University in California. “By the time a child receives an autism diagnosis, they’re pretty far along the path of having these robust social impairments,” Parker says. Previous work has shown that autistic children have, on average, 66 percent less vasopressin in their cerebrospinal fluid than their neurotypical peers, and that low levels of vasopressin track with poor social skills. The new study found a similar trend in infants aged 3 months and younger. “The surprising thing is that this relationship extends to infancy,” before any observable autism traits have emerged, says Larry Young, chief of behavioral neuroscience and psychiatric disorders at Emory University in Atlanta, Georgia, who was not involved with the study. The results, if confirmed, suggest there is a direct biological connection between vasopressin release and autism, Young says. © 2020 Simons Foundation

Keyword: Autism; Hormones & Behavior
Link ID: 27243 - Posted: 05.12.2020

By Randi Hutter Epstein It was a staple of medical thinking dating to the 1910s that stress was the body’s alarm system, switching on only when terrible things happened, often leaving a person with an either-or choice: fight or flight. The neuroscientist Bruce S. McEwen trailblazed a new way of thinking about stress. Beginning in the 1960s, he redefined it as the body’s way of constantly monitoring daily challenges and adapting to them. Dr. McEwen, who died on Jan. 2 at 81, described three forms of stress: good stress — a response to an immediate challenge with a burst of energy that focuses the mind; transient stress — a response to daily frustrations that resolve quickly; and chronic stress — a response to a toxic, unrelenting barrage of challenges that eventually breaks down the body. It was Dr. McEwen’s research into chronic stress that proved groundbreaking. He and his research team at Rockefeller University in Manhattan discovered in 1968 that stress hormones had a profound effect on the brain. In studies using animals (five rats in the initial one), Dr. McEwen and his colleagues demonstrated that toxic stress atrophied neurons near the hippocampus, the brain’s memory and learning center, while expanding neurons near the amygdala, an area known for vigilance toward threats. Describing the burden of continuing stress, he coined the term “allostatic load” (derived from allostasis, the process by which the body seeks to regain stability, or homeostasis, in response to stressors). Their discoveries, first published in the journal Nature in 1968, ignited a new field of research, one that would reveal how stress hormones and other mediators change the brain, alter behavior and impact health, in some cases accelerating disease. At the time, only a few scientists were asserting that the brain remains malleable throughout life, challenging the dogma that the brain stops changing after adolescence. Dr. McEwen’s studies documenting how hormones alter neurons lent credence to this emerging idea. © 2020 The New York Times Company

Keyword: Stress; Hormones & Behavior
Link ID: 27031 - Posted: 02.11.2020

Emily Makowski Bruce McEwen, a neuroendocrinologist at Rockefeller University, died January 2 after a brief illness. He was 81 years old. McEwen is best known for his research on how stress hormones can reconfigure neural connections in the brain, according to a university statement. In 1968, McEwen and his colleagues discovered that the rat hippocampus is affected by the hormone cortisol, sparking further research into how hormones can enter the brain and affect mental functioning and mood. At the time, most scientists believed that the brain was not malleable after becoming fully developed, a line of thinking that McEwen’s research findings contradicted. In 1993, he coined the term allostatic load, which describes the physiological effects of chronic stress. With his wife, Karen Bulloch, a Rockefeller professor, he studied how immune cells in the brain increase during a person’s lifespan and can contribute to neurodegenerative disease. He also researched how sex hormones affect the central nervous system. Over the course of his career, which spanned six decades, McEwen received many accolades including the Pasarow Foundation award in neuropsychiatry, the Fondation Ipsen Neuronal Plasticity and Endocrine Regulation prizes, the Scolnick Prize in Neuroscience, and the William James Lifetime Achievement Award for Basic Research. He was a member of the National Academy of Sciences, the National Academy of Medicine, and the American Society of Arts and Sciences. “Bruce was a giant in the field of neuroendocrinology,” McEwen’s colleague Leslie Vosshall, a neuroscientist at Rockefeller, says in the statement. “He was a world leader in studying the impact of stress hormones on the brain, and led by example to show that great scientists can also be humble, gentle, and generous human beings.” © 1986–2020 The Scientist

Keyword: Stress; Hormones & Behavior
Link ID: 26942 - Posted: 01.09.2020