By Rodrigo Pérez Ortega There’s clear evidence that racial discrimination negatively affects the health of people of color over the course of their lives. It’s associated with depression, anxiety, and psychological stress; it increases blood pressure; and it has been shown to weaken the immune system. However, few studies have linked single discriminatory events to immediate health effects. Now, data from a first-of-its-kind study suggest a racist attack could raise a person’s stress biomarkers almost immediately. “The big question mark, for me, has always been, how does this happen? What’s the black box that’s in the middle of discrimination, stress, and health disparities?” says Tiffany Yip, a developmental psychologist at Fordham University who was not involved with the study. “I think that this paper addresses that mechanistic question.” For the proof-of-concept study, Soohyun Nam at Yale University’s School of Nursing and her team collaborated with Black churches and their communities to recruit 12 Black people between the ages of 30 and 55 living in the northeastern United States. After accounting for the participants’ baseline stress levels, the research team adapted standardized survey questions about discrimination and microaggressions—such as whether they believed they had been mistaken for a service worker because of their race—and asked participants to share any occurrences of these experiences through a smartphone app. The method, known as ecological momentary assessment (EMA), has previously been used to study physical activity and behavior—such as alcohol intake reduction or smoking frequency. But this is one of the first studies correlating stress biomarkers and racist experiences using this precise monitoring technique. Researchers also asked the participants to describe their mood five times a day over the course of a week using the same phone app. To measure their biological response, participants spat into a tube four times a day over 4 days and froze the samples until research staff collected them. The researchers then had the samples analyzed in the lab to measure levels of cortisol, a hormone released during emotional distress, and alpha amylase, an enzyme that breaks down sugars and is secreted in stressful situations.

Keyword: Stress; Hormones & Behavior
Link ID: 28481 - Posted: 09.17.2022

Short ribs glazed in a sweet sticky sauce and slow-cooked to perfection, potato chips hand-fried and tossed with a generous coating of sour cream, chicken wings battered and double-fried so that they stay crispy for hours. What is it about these, and other, mouth-watering — but incredibly fatty — foods that makes us reach out, and keep coming back for more? How they taste on the tongue is one part of the story, but to really understand what drives “our insatiable appetite for fat,” we have to examine what happens after fat is consumed, says Columbia University’s Charles Zuker, a neuroscientist and molecular geneticist who has been a Howard Hughes Medical Institute (HHMI) Investigator since 1989. Two years ago, Zuker and his team reported how sugar, upon reaching the gut, triggers signals that are sent to the brain, thus fueling cravings for sweet treats. Now, in an article published in Nature on September 7, 2022, they describe a similar gut-to-brain circuit that underlies a preference for fat. “The gut is the source of our great desire for fat and sugar,” says Zuker. The topic in question is an incredibly timely one, given the current global obesity epidemic. An estimated 13 percent of adults worldwide are obese — thrice that in 1975. In the US, that figure is even higher — at a staggering 42 percent. “It’s a very significant and important health problem,” says Zuker. Having a high body-mass index is a risk factor for stroke, diabetes, and several other diseases. “It’s clear that if we want to help make a difference here, we need to understand the biological basis for our strong appetite for fat and sugar,” he says. Doing so will help us design interventions in the future to “suppress this strong drive to consume” and combat obesity.

Keyword: Obesity; Hormones & Behavior
Link ID: 28468 - Posted: 09.10.2022

By Gina Kolata Are you a man worried about your testosterone levels? Hoping to give them a boost? Tucker Carlson, the Fox News host, has a solution. A promotional video for a new installment in a video series by Mr. Carlson describes a “total collapse of testosterone levels in American men,” positing an explanation for what he and many conservatives see as a creeping loss of masculinity in today’s society. Chock-full of oiled, shirtless men performing vaguely masculine tasks, like turning over giant tires and throwing a javelin, the video has already been widely remarked upon on social media for its bizarre erotic imagery. But one shot in particular stands out: a naked man atop a rock pile, limbs outflung, exposing his genitals to the red light issuing from what appears to be a waist-high air purifier. Something very like the theme from “2001: A Space Odyssey” plays in the background. This is the treatment proposed by Mr. Carlson’s “documentary”: Revive your underperforming testicles with red light, in particular a device made by a little known company called Joovv. A leading endocrinologist says — no surprise — the whole thing is ridiculous, and not just because of the man receiving light therapy atop a pile of stone slabs in the dead of night. First, there is precious little evidence that testosterone “levels are declining by roughly 10 percent per decade, completely changing the way people are at the most fundamental level,” as Mr. Carlson has said. Studies examining changes in testosterone over time are challenging for several reasons, including difficulties in recruiting large populations of normal subjects, daily circadian changes in testosterone, and differences in testing methods over time, noted Dr. John Amory, an expert on male reproductive health at the University of Washington. © 2022 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 28298 - Posted: 04.23.2022

By Christina Caron Q: Are there any proven treatments for low libido in women? “Proven” is a strong word — and one that makes scientists squeamish. But it is safe to say that there is “very strong evidence” for increasing sexual desire through certain types of psychological interventions like cognitive behavioral therapy and mindfulness meditation, said Lori A. Brotto, a psychologist and professor at the University of British Columbia in Vancouver and a renowned expert in women’s sexual health. When it comes to medications, however, it’s a different story. In recent years, two new medications for women with low libido have been approved by the U.S. Food and Drug Administration, “though their efficacy is marginally better than a placebo,” said Dr. Stacy Tessler Lindau, a gynecologist at the University of Chicago Medicine and the creator of WomanLab, a website about sexual health. These drugs, flibanserin (a pill) and bremelanotide (an injection that is self-administered about 40 minutes before sexual activity), were approved for the “very small subset of women” who are premenopausal, have low libidos and do not have any identifiable physical, mental or relationship problems, Dr. Lindau said. “They may have modest benefit, but they also come with side effects and cost,” she added. “So far, insurance coverage has been limited.” In the end, the most beneficial solution will depend on the reason you are experiencing low libido and why you consider your libido to be a problem. For older women, loss of estrogen during menopause is commonly associated with a change in libido because it can cause vaginal dryness and tightness that can make intercourse painful. Some women also find it more difficult to get aroused. And when menopause is accompanied by hot flashes and night sweats, that can make sex seem less appealing too. © 2022 The New York Times Company

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 28235 - Posted: 03.11.2022

by Peter Hess Of all the brain chemistry that autism researchers study, few molecules have garnered as much attention as the so-called ‘social hormone,’ oxytocin. Some autistic children appear to have low blood levels of oxytocin, which has led several teams to test oxytocin delivered intranasally as an autism therapy. So far, though, such clinical trials have yielded inconsistent results. Here we explain what scientists know so far about oxytocin’s connection to autism. What does oxytocin do in the brain and body? Oxytocin serves multiple purposes, such as promoting trust between people, moderating our response to threats, and supporting lactation and mother-child bonding. The hormone is produced primarily in the hypothalamus, a brain region that mediates basic bodily functions, including hunger, thirst and body temperature. Oxytocin-producing neurons in the hypothalamus project into other parts of the brain, such as the nucleus accumbens, where the hormone regulates social-reward learning. In the brain’s sensory system, including the olfactory bulb, oxytocin seems to help balance excitatory and inhibitory signals, improving social-information processing, at least in rats. In the amygdala, oxytocin appears to help dull threat responses to negative social information and foster social recognition. The pituitary gland controls the release of oxytocin into the bloodstream. Blood oxytocin is crucial to start uterine muscle contractions during childbirth. It also supports lactation by facilitating the milk letdown reflex, stimulating the flow of milk into the nipple. © 2022 Simons Foundation

Keyword: Hormones & Behavior; Autism
Link ID: 28143 - Posted: 01.08.2022

By Pam Belluck What if something in the blood of an athlete could boost the brainpower of someone who doesn’t or can’t exercise? Could a protein that gets amplified when people exercise help stave off symptoms of Alzheimer’s and other memory disorders? That’s the tantalizing prospect raised by a new study in which researchers injected sedentary mice with blood from mice that ran for miles on exercise wheels, and found that the sedentary mice then did better on tests of learning and memory. The study, published Wednesday in the journal Nature, also found that the type of brain inflammation involved in Alzheimer’s and other neurological disorders was reduced in sedentary mice after they received their athletic counterparts’ blood. “We’re seeing an increasing number of studies where proteins from outside the brain that are made when you exercise get into the brain and are helpful for improving brain health, or even improving cognition and disease,” said Rudolph Tanzi, a professor of neurology at Massachusetts General Hospital and Harvard Medical School. He led a 2018 study that found that exercise helped the brains of mice engineered to have a version of Alzheimer’s. The most promising outcome would be if exercise-generated proteins can become the basis for treatments, experts said. The study, led by researchers at Stanford School of Medicine, found that one protein — clusterin, produced in the liver and in heart muscle cells — seemed to account for most of the anti-inflammatory effects. But several experts noted that recent studies have found benefits from other proteins. They also said more needs to be learned about clusterin, which plays a role in many diseases, including cancer, and may have negative effects in early stages of Alzheimer’s before brain inflammation becomes dominant. © 2021 The New York Times Company

Keyword: Alzheimers; Hormones & Behavior
Link ID: 28108 - Posted: 12.11.2021

by Angie Voyles Askham An intranasal form of the hormone oxytocin is no more effective than placebo at increasing social behaviors in autistic children, according to what may be the largest clinical trial of the treatment to date. The results were published today in The New England Journal of Medicine. Because of oxytocin’s role in strengthening social bonds, researchers have considered it as a candidate treatment for autism for more than a decade. Small trials hinted that the hormone could improve social skills in some autistic people, such as those with low blood levels of oxytocin or infants with Prader-Willi syndrome, an autism-related condition. But the new results, based on 250 autistic children, suggest that “oxytocin, at least in its current form, is probably not helpful for the majority of kids with autism,” says Evdokia Anagnostou, professor of pediatrics at University of Toronto in Canada, who was not involved in the new work. The null results “change things,” says lead researcher Linmarie Sikich, associate professor of psychiatry and behavioral sciences at the Duke Center for Autism and Brain Development in Durham, North Carolina. “Most people still felt like there was a good chance that this would be treatment for many people with autism.” This type of research is prone to publication bias, in which non-significant results are less likely to be published than significant ones, says Daniel Quintana, senior researcher in biological psychiatry at the University of Oslo in Norway, who was not involved in the study. For that reason, the new work is “an important contribution to the field,” he says, but “it does not alone put to rest the idea of using intranasal oxytocin as an autism treatment.” © 2021 Simons Foundation

Keyword: Autism; Hormones & Behavior
Link ID: 28036 - Posted: 10.16.2021

Sophie Fessl The hormone irisin is necessary for the cognitive benefits of exercise in healthy mice and can rescue cognitive decline associated with Alzheimer’s disease, according to a study published August 20 in Nature Metabolism. According to the authors, these results support the hypothesis that irisin undergirds the cognitive benefits of exercise—a link that has been long debated. In addition, this study has “paved the way for thinking whether irisin could be a therapeutic agent against Alzheimer’s disease,” says biologist Steffen Maak with the Leibniz Institute for Farm Animal Biology in Germany, who has been critical of the methods used to study irisin in the past and was not involved in the study. Many studies have found that exercise is good for the brain, but the molecular mechanisms responsible for the cognitive boost have remained elusive. During her postdoctoral studies, neuroscientist Christiane Wrann found that the gene that codes for irisin becomes highly expressed in the brain during exercise—one of the first studies linking irisin with the brain. See “Irisin Skepticism Goes Way Back” When she joined the faculties at Massachusetts General Hospital and Harvard Medical School, she decided to investigate the hormone further. Wrann, who holds a patent related to irisin and is academic cofounder and consultant for Aevum Therapeutics, a company developing drugs that harness the protective molecular mechanisms of exercise to treat neurodegenerative and neuromuscular disorders, began to investigate whether irisin mediates the positive effects of exercise on the brain. © 1986–2021 The Scientist.

Keyword: Learning & Memory; Hormones & Behavior
Link ID: 27985 - Posted: 09.13.2021

By Lisa Sanders, M.D. The young woman was awakened by the screams of her 39-year-old husband. “Please make it stop!” he shouted, leaping from the bed. “It hurts!” He paced back and forth across the room, arms crossed over his chest as if to protect himself. Two days earlier, he had inhaled a breath mint when his wife startled him. He felt it move slowly down his throat as he swallowed repeatedly. His chest had hurt ever since. But not like this. The man squirmed miserably throughout the short drive to the emergency room at Westerly Hospital, near the Rhode Island and Connecticut border. No position was comfortable. Everything hurt. Even breathing was hard. Although the doctors in the E.R. immediately determined that the young man wasn’t having a heart attack, it was clear something was very wrong. His blood pressure was so low that it was hard to measure. A normal blood pressure may be 120/80. On arrival, his was 63/32. With a pressure this low, blood couldn’t get everywhere it was needed — a condition known as shock. His lips, hands and feet had a dusky hue from this lack of well-​oxygenated blood. He was given intravenous fluids to bring up his pressure, and when that didn’t work, he was started on medications for it. Three hours later, he was on two of these medicines and his fourth liter of fluid. Despite that, his pressure remained in the 70s. He had to be put on a breathing machine to help him keep up with his body’s demand for more oxygen. The most common cause of shock is infection. But this man, as sick as he was, had no signs of infection. The medical team started him on antibiotics anyway. Could the painful mint have torn his esophagus? Up to 50 percent of patients with that injury will die. A CT scan showed no evidence of perforation or of fluid in his chest. What else could this be? There was no sign of a clot keeping blood from entering the lungs, another cause of deadly low blood pressure. An ultrasound of the heart showed that he had some fluid in the sac called the pericardium, which contains and protects the heart, but not enough to interfere with how well it was beating. He was tested for Covid and for recreational drugs — both negative. © 2021 The New York Times Company

Keyword: Hormones & Behavior; Neuroimmunology
Link ID: 27981 - Posted: 09.08.2021

by Angie Voyles Askham Male mice exposed to atypically low levels of a placental hormone in the womb have altered brain development and asocial behaviors, according to a new study. The findings may help explain why preterm birth — which coincides with a deficiency in hormones made by the placenta — is linked to an increased likelihood of having autism. The hormone, called allopregnanolone, crosses the blood-brain barrier, binds to receptors for the chemical messenger gamma-aminobutyric acid (GABA) and helps regulate aspects of neurodevelopment, including the growth of new neurons. Its levels typically peak in the fetus during the second half of gestation. In the new study, researchers engineered a mouse model to have low fetal levels of allopregnanolone, mimicking the hormone’s loss due to preterm birth or placental dysfunction. The male mice in particular have structural changes in the cerebellum, a brain region known for balance and motor control, and exhibit more pronounced autism-like traits than control mice or female model mice. The new model “has a good translational potential for understanding the underlying mechanisms of sex differences in neurodevelopmental conditions such as autism,” says Amanda Kentner, professor of psychology at the Massachusetts College of Pharmacy and Health Sciences in Boston, who was not involved in the work. Injecting a pregnant mouse with allopregnanolone partway through gestation decreased the likelihood that its offspring would have autism-like traits, the researchers found. © 2021 Simons Foundation

Keyword: Autism; Development of the Brain
Link ID: 27977 - Posted: 09.04.2021

By Gretchen Reynolds An intriguing new study shows how exercise may bolster brain health. The study was in mice, but it found that a hormone produced by muscles during exercise can cross into the brain and enhance the health and function of neurons, improving thinking and memory in both healthy animals and those with a rodent version of Alzheimer’s disease. Earlier research shows that people produce the same hormone during exercise, and together the findings suggest that moving could alter the trajectory of memory loss in aging and dementia. We have plenty of evidence already that exercise is good for the brain. Studies in both people and animals show that exercise prompts the creation of new neurons in the brain’s memory center and then helps those new cells survive, mature and integrate into the brain’s neural network, where they can aid in thinking and remembering. Large-scale epidemiological studies also indicate that active people tend to be far less likely to develop Alzheimer’s disease and other forms of dementia than people who rarely exercise. But how does working out affect the inner workings of our brains at a molecular level? Scientists have speculated that exercise might directly change the biochemical environment inside the brain, without involving muscles. Alternatively, the muscles and other tissues might release substances during physical activity that travel to the brain and jump-start processes there, leading to the subsequent improvements in brain health. But in that case, the substances would have to be able to pass through the protective and mostly impermeable blood-brain barrier that separates our brains from the rest of our bodies. Those tangled issues were of particular interest a decade ago to a large group of scientists at Harvard Medical School and other institutions. In 2012, some of these researchers, led by Bruce M. Spiegelman, the Stanley J. Korsmeyer Professor of Cell Biology and Medicine at the Dana-Farber Cancer Institute and Harvard Medical School, identified a previously unknown hormone produced in the muscles of lab rodents and people during exercise and then released into the bloodstream. They named the new hormone irisin, after the messenger god Iris in Greek mythology. © 2021 The New York Times Company

Keyword: Learning & Memory; Muscles
Link ID: 27961 - Posted: 08.25.2021

By Kim Tingley During menopause, which marks the end of a woman’s menstrual cycles, her ovaries stop producing the hormones estrogen and progesterone, bringing an end to her natural childbearing years. But those hormones also regulate how the brain functions, and the brain governs their release — meaning that menopause is a neurological process as well. “Many of the symptoms of menopause cannot possibly be directly produced by the ovaries, if you think about the hot flashes, the night sweats, the anxiety, the depression, the insomnia, the brain fog,” says Lisa Mosconi, an associate professor of neurology at Weill Cornell Medicine and director of its Women’s Brain Initiative. “Those are brain symptoms, and we should look at the brain as something that is impacted by menopause at least as much as your ovaries are.” In June, Mosconi and her colleagues published in the journal Scientific Reports one of the few studies to observe in detail what happens to the brain throughout the menopause transition, not just before and after. Using various neuroimaging techniques, they scanned the brains of more than 160 women between the ages of 40 and 65 who were in different stages of the transition to examine the organ’s structure, blood flow, metabolism and function; they did many of the same scans two years later. They also imaged the brains of men in the same age range. “What we found in women and not in men is that the brain changes quite a lot,” Mosconi says. “The transition of menopause really leads to a whole remodeling.” On average, women in the United States enter the menopause transition — defined as the first 12 consecutive months without a period — at around 50; once diagnosed, they are in postmenopause. But they may begin to have hormonal fluctuations in their 40s. (For some women, this happens in their 30s, and surgical removal of the ovaries causes immediate menopause, as do some cancer treatments.) Those fluctuations cause irregular periods and potentially a wide variety of symptoms, including hot flashes, insomnia, mood swings, trouble concentrating and changes in sexual arousal. During this phase, known as perimenopause, which averages four years in length (but can last from several months to a decade), Mosconi and colleagues observed that their female subjects experienced a loss of both gray matter (the brain cells that process information) and white matter (the fibers that connect those cells). Postmenopause, however, that loss stopped, and in some cases brain volume increased, though not to its premenopausal size. © 2021 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 27917 - Posted: 07.21.2021

By Gina Kolata Obesity has stalked Marleen Greenleaf, 58, all of her life. Like most people with obesity, she tried diet after diet. But the weight always came back. With that, she has suffered a lifetime of scorn and stigma. Jeering comments from strangers when she walked down the street. Family members who told her, when she trained for a half-marathon, “I don’t think it’s good for you.” Then, in 2018, Ms. Greenleaf, an administrator at a charter school in Washington, D.C., participated in a clinical trial for semaglutide, which is a new type of obesity drug, known as incretins. Over the course of the 68-week study, Ms. Greenleaf slowly lost 40 pounds. Until then, she had always believed that she could control her weight if she really tried. “I thought I just needed more motivation,” she said. But when she took semaglutide, she said that “immediately, the urge to eat just dissipated.” Incretins appear to elicit significant weight loss in most patients, enough to make a real medical and aesthetic difference. But experts hope that the drugs also do something else: change how society feels about people with obesity, and how people with obesity feel about themselves. If these new drugs allow obesity to be treated like a chronic disease — with medications that must be taken for a lifetime — the thought is that doctors, patients and the public might understand that obesity is truly a medical condition. © 2021 The New York Times Company

Keyword: Obesity; Hormones & Behavior
Link ID: 27821 - Posted: 05.15.2021

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