Chapter 5. Hormones and the Brain

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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

Nell Greenfieldboyce Shepherds in Christmas Nativity scenes that were painted, carved or sculpted hundreds of years ago sometimes have throats with large, abnormal growths. These are realistic depictions of goiter, an enlargement of the thyroid gland caused by iodine deficiency. The condition was common in those days in northern Italy, where the soil and water are depleted of iodine. "Goiter is more often seen in poor people," says retired surgeon Renzo Dionigi of the University of Insubria in Varese, Italy, who notes that the working classes in this region would historically not have a varied diet that might supply this vital nutrient. "That's why, probably, the poor shepherds are depicted with goiters," he says. He and his son, an endocrine surgeon named Gianlorenzo Dionigi, have for years enjoyed studying art and looking for signs of medical conditions. In the Sacri Monti ("Sacred Mountains") of Piedmont and Lombardy, they have visited chapels and churches created in the 16th and 17th centuries. "In all the Sacri Monti that I and my son visited, we have been able to observe representations of goiters very, very often," says the elder Dionigi. In one Nativity tableau from 1694, for example, a young horn player with a large goiter plays for the Holy Family. And in one fresco over the main door of the Aosta Cathedral, a shepherd with goiter plays his bagpipe for the newborn Jesus. © 2019 npr

Keyword: Hormones & Behavior
Link ID: 26913 - Posted: 12.26.2019

Nicola Slawson When Lynn Enright had a hysteroscopy to examine the inside of the womb, her searing pain was dismissed by medical professionals. She only understood why when she started working on her book on female anatomy, Vagina: A Re-education. She was looking for research on pain and women’s health, only to be shocked by how little data she found. It wasn’t just the topic of pain that was poorly researched. The lack of evidence was a problem she encountered time and time again, which is no surprise when you look at the research gap: less than 2.5% of publicly funded research is dedicated solely to reproductive health, despite the fact that one in three women in the UK will suffer from a reproductive or gynaecological health problem. There is five times more research into erectile dysfunction, which affects 19% of men, than into premenstrual syndrome, which affects 90% of women. “Women have been woefully neglected in studies on pain. Most of our understanding of ailments comes from the perspective of men; it is overwhelmingly based on studies of men, carried out by men,” Enright says. Her book is one of several in the past year about the female body and the impact a lack of knowledge can have on diagnosis and treatment. They include Emma Barnett’s Period, Eleanor Morgan’s Hormonal, and Gabrielle Jackson’s Pain and Prejudice, which draws on her experience of being diagnosed with endometriosis, a chronically underfunded condition. Given that in the US, which produces a lot of medical research, research trials weren’t required by the National Institutes of Health to include women until 1993, the lack of knowledge is perhaps no surprise. Traditionally this was justified by the idea that women’s bodies were seen to be too complex due to fluctuating hormones, so clinical trials often excluded them. © 2019 Guardian News & Media Limited

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 26898 - Posted: 12.18.2019

By Rachel E. Gross In the 1960s, manufacturers of the new birth-control pill imagined their ideal user as feminine, maternal and forgetful. She wanted discretion. She was married. And she wanted visible proof that her monthly cycle was normal and that she wasn’t pregnant. In 2019, the user of the pill is perceived as an altogether different person. She’s unwed, probably would prefer to skip her period and is more forthright about when it’s that time of the month. As such, many birth-control brands now come in brightly colored rectangular packs that make no effort to be concealed. But one part of the equation remains: the week of placebo pills, in which hormones are abruptly withdrawn and a woman experiences what looks and feels a lot like her regular period — blood, cramps and all — but isn’t. Physicians have widely described this pseudoperiod as medically unnecessary. So why do millions still endure it? That’s largely the legacy of two men: John Rock and David Wagner. First there’s Rock, a Harvard fertility expert and a developer of the pill. There’s a longstanding myth that Rock, a Catholic, designed the pill in the 1950s with the church in mind and included a week of hormonal withdrawal — and therefore bleeding — to make his invention seem more natural. In fact, the thought never crossed his mind, the Rutgers University historian Margaret Marsh says. Instead, it was Gregory (Goody) Pincus, the other developer of the pill, who suggested that the pill be given as a 20-days-on, 5-days-off regimen. Pincus wanted to provide women in his trials with reassurance that they weren’t pregnant, and to know himself that the pill was working as a contraceptive. Rock agreed. After the F.D.A. approved the pill in 1960, however, those few days of light bleeding took on a new significance. Anticipating the church’s opposition, Rock became not just a researcher but also an advocate. In his 1963 book “The Time Has Come: A Catholic Doctor’s Proposals to End the Battle Over Birth Control,” he argued that the pill was merely a scientific extension of the church-sanctioned “rhythm method.” It “completely mimics” the body’s own hormones, he wrote, to extend the “safe period” in which a woman could have intercourse and not become pregnant. © 2019 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 26892 - Posted: 12.12.2019

Andrew Anthony Katrina Karkazis, a senior research fellow at Yale University, is a cultural anthropologist working at the intersection of science, technology, gender studies and bioethics. With Rebecca Jordan-Young, a sociomedical scientist, she has written Testosterone: An Unauthorised Biography. It is a critique of both popular and scientific understandings of the hormone, and how they have been used to explain, or even defend, inequalities of power. You suggest that testosterone is understood as an exclusively male hormone, even though it’s also found in women. But surely no scientist believes this. No, what we’re saying is that the hormone has a century-long biography and identity that continues to be that of a male sex hormone. That language is used by authoritative sources in the US like the National Library of Medicine, but also in many media articles. It’s an argument that has to do with how the hormone is understood, which then shapes the kinds of research questions that get asked, what kinds of research get done or not done. There’s actually almost no research on the relationship between testosterone and aggression in women. That is a consequence of the framing of the hormone as having to do with men, masculinity, behaviours understood and framed as masculine. It’s the idea that because men generally have more testosterone, somehow that makes it more relevant in men. But the truth is we know very little about it. You write that testosterone’s authorised biography is about libido, aggression and masculinity. Does this mean that testosterone is not about these things? I think that it’s still very widely understood as the driver of all things masculine. When people think about testosterone, aggression is one of the first things that comes to mind. But when you look at the evidence, there’s not good evidence at all. In fact, it’s very weak regarding the relationship between endogenous testosterone [ie testosterone that originates within an organism] and aggression. So it’s an artefact of the ideology of testosterone that we continue to believe that it drives aggression, because aggression has been framed as a masculine behaviour and testosterone has been framed as a masculine hormone. © 2019 Guardian News & Media Limited

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 26883 - Posted: 12.09.2019

By Lisa Sanders, M.D. “Please find something wrong with me,” the 28-year-old woman pleaded. For nearly a year, she’d been looking for a reason for the strange symptoms that now dominated her life. Dr. Raphael Sung, a cardiologist specializing in finding and fixing abnormal heart rhythms at National Jewish Health hospital in Denver, was surprised by her reaction to the news that her heart was normal. Most patients are happy to get that report. For this patient, it seemed like just one more dead end. The patient’s symptoms started right after her baby was born 10 months earlier. Out of nowhere, her heart would start beating like crazy. At first, she assumed that these were anxiety attacks, triggered by the stress of bringing her premature daughter home. Her baby spent her first week of life in the newborn intensive care unit. When she was big enough to come home, she still weighed only four pounds, nine ounces. The new mother worried that without the doctors and nurses and equipment that had kept her alive, her tiny baby might die. But she didn’t. She seemed to thrive at home. Despite that, her mother’s heart continued to take off like a spooked horse several times a day. After a couple of weeks, her symptoms worsened. Sometimes her racing heart would set off terrible headaches, the worst she’d ever had. It was as if someone had thrust a sharp stick deep into her brain. The knife of pain quickly turned into a sense of pressure so intense it felt as if the back of her skull would blow off. Minutes later, she would feel the blood drain from her face; she’d be suddenly drenched in sweat. Her hands would curl into tight fists, and vomit would shoot out of her mouth like a geyser. Her husband joked (though only once) that she looked like the girl in “The Exorcist.” © 2019 The New York Times Company

Keyword: Hormones & Behavior
Link ID: 26767 - Posted: 10.30.2019

Zoë Corbyn At a time when women’s reproductive freedoms are under attack, any suggestion that the birth control pill could be problematic feels explosive. But Sarah E Hill, a professor of social psychology at the Texas Christian University in Fort Worth, Texas argues we need to talk about how oral contraceptives are affecting women’s thinking, emotions and behaviour. How the Pill Changes Everything: Your Brain on Birth Control is her new book about the science behind a delicate subject. Some US states have recently made it harder to get an abortion and the Trump administration is doing its best to chisel away at access to birth control. Is your book trying to dissuade women from using the pill? My institution was founded as a Christian school, but it doesn’t have a particular religious bent now. My goal with this book is not to take the pill away or alarm women. It is to give them information they haven’t had up until now so they can make informed decisions. The pill, along with safe, legalised abortions, are the two biggest keys to women’s rights. But we also have a blind spot when it comes to thinking about how changing women’s sex hormones – which is what the pill does – influences their brains. For a long time, women have been experiencing “psychological” side-effects on the pill but nobody was telling them why. The backlash we are seeing against the pill, particularly with millennial women walking away from it, I think is because women haven’t felt right on it and have grown weary of doctors patting them on their heads and telling them they are wrong. The more information women have, the more it will bring them back to the pill. © 2019 Guardian News & Media Limited

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 26723 - Posted: 10.19.2019

Hannah Devlin Science correspondent Boosting testosterone levels significantly improves female athletic performance, according to one of the first randomised controlled trials. The findings come as the International Association of Athletics Federations (IAAF) announced on Monday it would impose an upper limit for testosterone levels on trans female athletes competing in middle-distance events. Testosterone was assumed to be performance-enhancing and a factor in explaining differences in strength and endurance between men and women. However, there was a surprising lack of evidence on the impact of testosterone in women and the question had become mired in controversy following a series of rulings in professional sport. The latest research confirmed that testosterone significantly increases endurance and lean muscle mass among young women, even when given for a relatively short period. Angelica Hirschberg, a gynaecologist for the Swedish Olympic Committee based at Karolinska University Hospital and the study’s first author, said the results were the first to show a causal effect of testosterone on physical performance in women. “This has not been demonstrated previously because most studies have been performed in men,” she said. “Furthermore, the study shows the magnitude of performance enhancement by testosterone. Testosterone levels increased more than four times but were still much below the male range. The improvement in endurance performance by the increased testosterone levels was more than 8% – this is a huge effect in sports.” © 2019 Guardian News & Media Limited

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 26706 - Posted: 10.16.2019

By Emily Underwood Adrenaline. The word is synonymous with any activity that gets our blood racing, whether it be encountering a rattlesnake or watching the latest horror movie. But a new study reveals that when it comes with our body’s stress response, adrenaline may be less important than another hormone, one that seeps out of our bones. Our skeleton is much more than a rigid scaffold for the body, says geneticist Gérard Karsenty of Columbia University. Our bones secrete a protein called osteocalcin, discovered in the 1970s, that rebuilds the skeleton. In 2007, Karsenty and colleagues discovered that this protein acts as a hormone to keep blood sugar levels in check and burn fat. Later, his group showed that the hormone is important for maintaining brain function and physical fitness, restoring memory in aged mice and boosting performance during exercise in old mice and people. The findings led Karsenty to hypothesize that animals evolved bony skeletons to escape danger. The new study furthers that argument. Karsenty and colleagues exposed mice to several stressors, including a mild electric shock to the foot and a whiff of fox urine, a scent that triggers an innate fear response. Then, the researchers measured the osteocalcin in the animals’ blood. Within 2 to 3 minutes of being exposed to a stressor, levels of osteocalcin in the mice quadrupled, the team reports today in Cell Metabolism. A classic stressor in people had a similar effect: When the researchers asked volunteers to speak in front of an audience, osteocalcin levels also spiked. © 2019 American Association for the Advancement of Science

Keyword: Hormones & Behavior; Stress
Link ID: 26609 - Posted: 09.13.2019

By Roni Dengler | Testosterone often gets a bad rap. The hormone responsible for male sexual development has been linked in studies to aggression and a lack of empathy. People with autism – a developmental condition that can lead to anxiety and trouble interacting with others – also have a hard time empathizing. Since the condition is four times more common in boys than girls, scientists once thought testosterone might reduce our ability to tell how others are feeling. But now, researchers find that’s not the case. “Of course, the primary suspect when we have something that is sharply differentiated by sex is testosterone,” University of Pennsylvania marketing professor Gideon Nave, who led the work, said in a press release. In the new study, Nave and colleagues report men given extra testosterone were able to read emotions just as well as those with typical hormone levels. The findings contrast a prevailing hypothesis that testosterone challenges men’s ability to empathize. Emotional Eyes In previous studies, other scientists tested whether testosterone influences empathy. They gave a few dozen women testosterone and then tested their ability to infer emotions by looking at pictures of people’s eyes. The studies concluded the testosterone lowered the women’s ability to empathize. The findings lent support for what’s known as the “extreme male brain hypothesis.” The hypothesis posits that men and women process and experience the world differently – women empathize and men systemize. Another study linking prenatal testosterone levels to autism added weight to the hypothesis.

Keyword: Hormones & Behavior; Emotions
Link ID: 26603 - Posted: 09.12.2019

Briar Stewart · A Canadian-born researcher is helping to launch the first substantial study of transgender athletes in a bid to better understand how transitioning and hormone therapy affects athletic performance. The issue of how to include transgender women in competition is centred around rules, rights and biological differences. And the debate about what constitutes an unfair advantage is heated, which is why medical physicist Joanna Harper hopes science can steer the conversation. "Until we have several of these larger-scale studies done worldwide, it's hard to be truly definitive on anything," she said. Harper, who is also an adviser to the International Olympic Committee (IOC), will be moving to the U.K. this fall to help lead the research into transgender athletes. The work will be carried out at Loughborough University, through its School of Sport, Exercise and Health Sciences. Personal motivation It was Harper's own experience that motivated her to try and track transgender athletes both before and after a gender transition. Harper, who is originally from Parry Sound, Ont, but is now based in Portland, Ore., has been a competitive runner for decades. When she was younger and racing as a male, her marathon time was a very quick two hours and 23 minutes. But once she started her transition in 2004 and began taking testosterone blockers and estrogen, her pace slowed. "Within nine months of hormone therapy, I was running 12 per cent slower," she said. "That's the difference between serious male distance runners and serious female distance runners." Harper, now in her 60s, still competes, racing alongside women. She wins some events and loses others, which is why she asserts that if trans women can become hormonally like other women, competition can be "equitable and meaningful." ©2019 CBC/Radio-Canada.

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 26444 - Posted: 07.24.2019