Patti Neighmond Having trouble getting to sleep these days? You're not alone. For people with a history of insomnia, sleep problems are magnified right now. And many who never struggled before are suddenly experiencing interruptions in their nightly rest or difficulty falling asleep. It's pretty typical that in moments of anxiety, sleep suffers, but the situation we're all living through today means the anxiety never stops, says neurologist and sleep specialist Dr. Douglas Kirsch, past president of the American Academy of Sleep Medicine. For occasional insomnia, the problems go away when the specific trigger is resolved. But now, he says, there's no resolution or relief from "the constant inflow of anxiety-provoking news." And that spells trouble for sleep. Family doctors and sleep specialists say many people who are feeling grief, frustration and anxiety, whether about the pandemic, financial worries or racial inequalities and unrest in the U.S., are finding themselves unable to sleep. And it's not just the worry. It's the interrupted schedules and isolation of the pandemic too. Here's why it's not all in your head and what they say you can do about it. We're suffering "collective social anxiety" — tame it to sleep better Before the pandemic, Arlene Rentas, a busy currency trader in Charlotte, N.C., kept a regular schedule and slept like clockwork. She would awaken at 5:30 in the morning and be out the door by 7 a.m., home by 8 p.m. and, after a quick run, in bed around 10 p.m. © 2020 npr

Keyword: Sleep; Stress
Link ID: 27276 - Posted: 06.03.2020

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 Laura Sanders The heart has its own “brain.” Now, scientists have drawn a detailed map of this little brain, called the intracardiac nervous system, in rat hearts. The heart’s big boss is the brain, but nerve cells in the heart have a say, too. These neurons are thought to play a crucial role in heart health, helping to fine-tune heart rhythms and perhaps protecting people against certain kinds of heart disease. But so far, this local control system hasn’t been mapped in great detail. To make their map, systems biologist James Schwaber at Thomas Jefferson University in Philadelphia and colleagues imaged male and female rat hearts with a method called knife-edge scanning microscopy, creating detailed pictures of heart anatomy. Those images could then be built into a 3-D model of the heart. The scientists also plucked out individual neurons and measured the amount of gene activity within each cell. These measurements helped sort the heart’s neurons into discrete groups. Most of these neuron clusters dot the top of the heart, where blood vessels come in and out. Some of these clusters spread down the back of the heart, and were particularly abundant on the left side. With this new view of the individual clusters, scientists can begin to study whether these groups have distinct jobs. The comprehensive, 3-D map of the heart’s little brain could ultimately lead to targeted therapies that could treat or prevent heart diseases, the authors write online May 26 in iScience. © Society for Science & the Public 2000–2020.

Keyword: Development of the Brain
Link ID: 27274 - Posted: 06.03.2020

by Emily Anthes The overproduction of proteins in brain cells called microglia causes social impairments, cognitive deficits and repetitive behavior in male mice, a new study has found.1 These behavioral differences are not present in female mice, or in mice that produce excess protein in other brain cells, including neurons or star-shaped support cells known as astrocytes. Microglia help eliminate excess synapses — connections between brain cells — that form early in life; this pruning process is crucial to healthy brain development. But male mice that have been engineered to overproduce proteins in these cells have enlarged microglia. That, in turn, lowers the cells’ mobility and may prevent them from migrating to synapses that need eliminating. In support of that idea, the mice have too many synapses, the researchers found — a result that mirrors evidence that certain brain regions may be overconnected in people with autism. “Increased protein synthesis in microglia is sufficient to cause autism phenotypes in mice,” says lead investigator Baoji Xu, professor of neuroscience at the Scripps Research Institute in Jupiter, Florida. “Problems in microglia could be an important pathological mechanism for autism.” Malfunctioning microglia: The researchers studied mice that produce excess levels of EIF4E, a protein that facilitates the synthesis of other proteins. Mutations in several genes linked to autism — including TSC1, TSC2, PTEN and FMR1 — are associated with elevated levels of an active form of EIF4E and, as a result, many other proteins in the brain. Mice that overproduce EIF4E also display autism-like behavior, researchers have previously found. © 2020 Simons Foundation

Keyword: Autism; Glia
Link ID: 27273 - Posted: 06.01.2020

Ruth Williams With their tiny brains and renowned ability to memorize nectar locations, honeybees are a favorite model organism for studying learning and memory. Such research has indicated that to form long-term memories—ones that last a day or more—the insects need to repeat a training experience at least three times. By contrast, short- and mid-term memories that last seconds to minutes and minutes to hours, respectively, need only a single learning experience. Exceptions to this rule have been observed, however. For example, in some studies, bees formed long-lasting memories after a single learning event. Such results are often regarded as circumstantial anomalies, and the memories formed are not thought to require protein synthesis, a molecular feature of long-term memories encoded by repeated training, says Martin Giurfa of the University of Toulouse. But the anomalous findings, together with research showing that fruit flies and ants can form long-term memories after single experiences, piqued Giurfa’s curiosity. Was it possible that honeybees could reliably do the same, and if so, what molecular mechanisms were required? Giurfa reasoned that the ability to form robust memories might depend on the particular type of bee and the experience. Within a honeybee colony, there are nurses, who clean the hive and feed the young; guards, who patrol and protect the hive; and foragers, who search for nectar. Whereas previous studies have tested bees en masse, Giurfa and his colleagues focused on foragers, tasking them with remembering an experience relevant to their role: an odor associated with a sugary reward. © 1986–2020 The Scientist.

Keyword: Learning & Memory; Evolution
Link ID: 27272 - Posted: 06.01.2020

By Tina Hesman Saey A genetic variant that raises one’s risk of developing Alzheimer’s disease may also make people more susceptible to COVID-19. People with two copies of a version of the APOE gene called APOE4 are 14 times as likely to develop Alzheimer’s disease as people with two copies of the APOE3 version of the gene (SN: 9/22/17). Those people were also more than twice as likely to test positive for the coronavirus than people with two copies of the APOE3 version, researchers report May 26 in the Journals of Gerontology: Series A. The results come from a study of more than 600 people in England diagnosed with COVID-19 from March 16 to April 26. Two previous studies showed that people with dementia were more likely to have severe cases or to die of COVID-19. This new study found that even people with no signs of dementia or other diseases associated with having APOE4 were still more susceptible to COVID-19 than people with the APOE3 version. Among nearly 400,000 participants in the large genetic database called the UK Biobank, only 3 percent have two copies of APOE4, while 69 percent have two copies of APOE3. The remainder have one of each version. But the APOE4 version was more common than expected among people diagnosed with COVID-19, the study found. Of 622 people who tested positive for the coronavirus, 37 had two copies of APOE4. On a population scale, that means about 410 of every 100,000 people with two copies of that version of the gene would test positive, the researchers calculate. That compares with 179 of every 100,000 people with two copies of APOE3 testing positive. © Society for Science & the Public 2000–2020.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27271 - Posted: 06.01.2020

by Laura Dattaro Correcting a mutation in the autism gene SHANK3 in fetal mice lessens some autism-like behaviors after birth, according to a new study1. The work adds to evidence that gene therapy may help some people with SHANK3 mutations. In people, mutations in SHANK3 can lead to Phelan-McDermid syndrome, a condition that causes developmental delays and often autism. Up to 2 percent of people with autism have a mutation in SHANK32. “Our findings imply that early genetic correction of SHANK3 has the potential to provide therapeutic benefit for patients,” lead investigator Craig Powell, professor of neurobiology at the University of Alabama at Birmingham, wrote in an email. A 2016 study showed that correcting mutations in SHANK3 in both young and adult mice can decrease excessive grooming, which is thought to correspond to repetitive behaviors in people with autism. Last year, Powell and his team also showed that correcting SHANK3 mutations in adult mice eliminates some autism-like behaviors3. But the results were difficult to interpret. The team reversed the mutation using an enzyme called Cre-recombinase that could edit SHANK3 if the animals were given a drug called tamoxifen. Control mice in that study that did not receive tamoxifen but had the gene for Cre still showed behavior changes, raising the possibility that the enzyme affected their brains. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27270 - Posted: 05.29.2020

Diana Kwon What if you could boost your brain’s processing capabilities simply by sticking electrodes onto your head and flipping a switch? Berkeley, California–based neurotechnology company Humm has developed a device that it claims serves that purpose. Their “bioelectric memory patch” is designed to enhance working memory—the type of short-term memory required to temporarily hold and process information—by noninvasively stimulating the brain. In recent years, neurotechnology companies have unveiled direct-to-consumer (DTC) brain stimulation devices that promise a range of benefits, including enhancing athletic performance, increasing concentration, and reducing depression. Humm’s memory patch, which resembles a large, rectangular Band-Aid, is one such product. Users can stick the device to their forehead and toggle a switch to activate it. Electrodes within the patch generate transcranial alternating current stimulation (tACS), a method of noninvasively zapping the brain with oscillating waves of electricity. The company recommends 15 minutes of stimulation to give users up to “90 minutes of boosted learning” immediately after using the device. The product is set for public release in 2021. Over the last year or so, Humm has generated much excitement among investors, consumers, and some members of the scientific community. In addition to raising several million dollars in venture capital funding, the company has drawn interest both from academic research labs and from the United States military. According to Humm cofounder and CEO Iain McIntyre, the US Air Force has ordered approximately 1,000 patches to use in a study at their training academy that is set to start later this year. © 1986–2020 The Scientist

Keyword: Learning & Memory
Link ID: 27269 - Posted: 05.29.2020

A team of researchers has generated a developmental map of a key sound-sensing structure in the mouse inner ear. Scientists at the National Institute on Deafness and Other Communication Disorders (NIDCD), part of the National Institutes of Health, and their collaborators analyzed data from 30,000 cells from mouse cochlea, the snail-shaped structure of the inner ear. The results provide insights into the genetic programs that drive the formation of cells important for detecting sounds. The study also sheds light specifically on the underlying cause of hearing loss linked to Ehlers-Danlos syndrome and Loeys-Dietz syndrome. The study data is shared on a unique platform open to any researcher, creating an unprecedented resource that could catalyze future research on hearing loss. Led by Matthew W. Kelley, Ph.D., chief of the Section on Developmental Neuroscience at the NIDCD, the study appeared online in Nature Communications(link is external). The research team includes investigators at the University of Maryland School of Medicine, Baltimore; Decibel Therapeutics, Boston; and King’s College London. “Unlike many other types of cells in the body, the sensory cells that enable us to hear do not have the capacity to regenerate when they become damaged or diseased,” said NIDCD Director Debara L. Tucci, M.D., who is also an otolaryngology-head and neck surgeon. “By clarifying our understanding of how these cells are formed in the developing inner ear, this work is an important asset for scientists working on stem cell-based therapeutics that may treat or reverse some forms of inner ear hearing loss.”

Keyword: Hearing; Development of the Brain
Link ID: 27268 - Posted: 05.29.2020

Jef Akst The APOE ε4 gene variant that puts people at a greater risk of developing Alzheimer’s disease also has a link to COVID-19. According to a study published today (May 26) in The Journals of Gerontology, Series A, carrying two copies of the variant, often called APOE4, makes people twice as likely to develop a severe form of the disease, which is caused by the SARS-CoV-2 coronavirus currently spreading around the world. David Melzer of Exeter University and colleagues used genetic and health data on volunteers in the UK Biobank to look at the role of the APOE4 variant, which affects cholesterol transport and inflammation. Of some 383,000 people of European descent included in the study, more than 9,000 carried two copies. The researchers cross-referenced this list with people who tested positive for COVID-19 between March 16 and April 26—the assumption being that most such cases were severe because testing at the time was largely limited to hospital settings. The analysis suggested that the APOE4 homozygous genotype was linked to a doubled risk of severe disease, compared with people who had two copies of another variant called ε3. The result isn’t due to nursing home settings or to a greater likelihood of having a diagnosis of dementia, which none of the 37 people with two copies of APOE4 who tested positive for COVID-19 had. “It is pretty bulletproof—whatever associated disease we remove, the association is still there,” Melzer tells The Guardian. “So it looks as if it is the gene variant that is doing it.” © 1986–2020 The Scientist.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27267 - Posted: 05.29.2020

By Laura Sanders I’m on deadline, but instead of focusing, my mind buzzes with unrelated tidbits. My first-grader’s tablet needs an update before her online school session tomorrow. Heartbreaking deaths from COVID-19 in New York City make me tear up again. Was that a kid’s scream from upstairs? Do I need to run up there, or will my husband take care of it? These hornets of thoughts drive out the clear thinking my job demands. Try as I might to conjure up a coherent story, the relevant wisps float away. I’m scattered, worried and tired. And even though we’re all socially isolated, I’m not alone. The pandemic — and its social and economic upheavals — has left people around the world feeling like they can’t string two thoughts together. Stress has really done a number on us. That’s no surprise to scientists who study stress. Our brains are not built to do complex thinking, planning and remembering in times of massive upheaval. Feeling impaired is “a natural biological response,” says Amy Arnsten, a neuroscientist at Yale School of Medicine. “This is how our brains are wired.” Decades of research have chronicled the ways stress can disrupt business as usual in our brains. Recent studies have made even more clear how stress saps our ability to plan ahead and have pointed to one way that stress changes how certain brain cells operate. Scientists recognize the pandemic as an opportunity for a massive, real-time experiment on stress. COVID-19 foisted on us a heavy mix of health, economic and social stressors. And the end date is nowhere in sight. Scientists have begun collecting data to answer a range of questions. But one thing is clear: This pandemic has thrown all of us into uncharted territory. © Society for Science & the Public 2000–2020

Keyword: Stress
Link ID: 27266 - Posted: 05.28.2020

By Maria Cramer Quarantinis. Zoom happy hours. Easy front-door liquor delivery. The boredom of staying home and the intense anxiety produced by the pandemic have given rise to Twitter jokes about drinking before noon as alcohol sales have spiked. But addiction experts say they are worried it could also trigger more serious drinking problems and even create new ones for people who have never struggled with alcohol dependency before. “I expect we’re going to see pretty significant increases in what I call unhealthy alcohol use, which means drinking above recommended limits,” said Dr. Sarah Wakeman, an addiction medicine doctor at Massachusetts General Hospital in Boston. “It will be pretty unlikely for someone who has never tried alcohol before to start drinking for the first time and immediately develop an alcohol use disorder,” Dr. Wakeman said. “I would see this as a risk more in people who are already drinking and then their alcohol use escalates.” Before the pandemic, Mhairi McFarlane, a 44-year-old novelist in Nottingham, England, had been thinking of cutting back. But the first weekend she was in quarantine, she said, she was “cheerfully” having three or four drinks a night, usually gin and tonics or “very cold bottles of cava.” “It was very much not my style of drinking,” she said. “I’ve always associated drink with going out and being social. I was never really one for opening a bottle of wine in front of the television.” Drinking alone worried her. Then she woke up one Thursday with a headache and a sense that her body was unhappy with what she was doing. She decided to give herself a two-night break from drinking. To her surprise, she wanted to keep going. It has been two months since she had a drink. © 2020 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 27265 - Posted: 05.28.2020

R. Douglas Fields Discoveries that transcend boundaries are among the greatest delights of scientific research, but such leaps are often overlooked because they outstrip conventional thinking. Take, for example, a new discovery for treating dementia that defies received wisdom by combining two formerly unrelated areas of research: brain waves and the brain’s immune cells, called microglia. It’s an important finding, but it still requires the buy-in and understanding of researchers to achieve its true potential. The history of brain waves shows why. In 1887, Richard Caton announced his discovery of brain waves at a scientific meeting. “Read my paper on the electrical currents of the brain,” he wrote in his personal diary. “It was well received but not understood by most of the audience.” Even though Caton’s observations of brain waves were correct, his thinking was too unorthodox for others to take seriously. Faced with such a lack of interest, he abandoned his research and the discovery was forgotten for decades. Flash forward to October 2019. At a gathering of scientists that I helped organize at the annual meeting of the Society for Neuroscience in Chicago, I asked if anyone knew of recent research by neuroscientists at the Massachusetts Institute of Technology who had found a new way to treat Alzheimer’s disease by manipulating microglia and brain waves. No one replied. I understood: Scientists must specialize to succeed. Biologists studying microglia don’t tend to read papers about brain waves, and brain wave researchers are generally unaware of glial research. A study that bridges these two traditionally separate disciplines may fail to gain traction. But this study needed attention: Incredible as it may sound, the researchers improved the brains of animals with Alzheimer’s simply by using LED lights that flashed 40 times a second. Even sound played at this charmed frequency, 40 hertz, had a similar effect. All Rights Reserved © 2020

Keyword: Alzheimers; Glia
Link ID: 27264 - Posted: 05.28.2020

By Pooja Lakshmin After going through a harrowing bout of postpartum depression with her first child, my patient, Emily, had done everything possible to prepare for the postpartum period with her second. She stayed in treatment with me, her perinatal psychiatrist, and together we made the decision for her to continue Zoloft during her pregnancy. With the combination of medication, psychotherapy and a significant amount of planning, she was feeling confident about her delivery in April. And then, the coronavirus hit. Emily, whose name has been changed for privacy reasons, called me in late-March because she was having trouble sleeping. She was up half the night ruminating about whether she’d be able to have her husband with her for delivery and how to manage taking care of a toddler and a newborn without help. The cloud that we staved off for so long was returning, and Emily felt powerless to stop it. Postpartum depression and the larger group of maternal mental health conditions called perinatal mood and anxiety disorders are caused by neurobiological factors and environmental stressors. Pregnancy and the postpartum period are already vulnerable times for women due in part to the hormonal fluctuations accompanying pregnancy and delivery, as well as the sleep deprivation of the early postpartum period. Now, fears about the health of an unborn child or an infant and the consequences of preventive measures, like social distancing, have added more stress. As a psychiatrist who specializes in taking care of pregnant and postpartum women, I’ve seen an increase in intrusive worry, obsessions, compulsions, feelings of hopelessness and insomnia in my patients during the coronavirus pandemic. And I’m not alone in my observations: Worldwide, mental health professionals are concerned. A special editorial in a Scandinavian gynecological journal called attention to the psychological distress that pregnant women and new mothers will experience in a prolonged global pandemic. A report from Zhejiang University in China detailed the case of a woman who contracted Covid-19 late in her pregnancy and developed depressive symptoms. In the United States, maternal mental health experts have also described an increase in patients with clinical anxiety. © 2020 The New York Times Company

Keyword: Depression; Stress
Link ID: 27263 - Posted: 05.28.2020

Peter Hess The relative contributions of genetic and environmental factors to autism and traits of the condition have held steady over multiple decades, according to a large twin study. Among tens of thousands of Swedish twins born over the span of 26 years, genetic factors have consistently had a larger impact on the occurrence of autism and autism traits than environmental factors have. The study suggests that genetics account for about 93 percent of the chance that a person has autism, and 61–73 percent of the odds she shows autism traits. The figures fall in line with previous work that shows genetics exert an outsized influence on autism odds. The findings also indicate that environmental factors are unlikely to explain the rise in autism prevalence. Otherwise, their contribution to autism among the twins would have also risen over time. “I think the relative consistency of the genetic and environmental factors underlying autism and autism traits is the most important aspect of this work,” says Mark Taylor, senior research specialist at the Karolinska Institutet in Stockholm, Sweden, who led the study. “Prior to our study, there had been no twin studies examining whether the genetic and environmental factors underlying autism had changed over time.” Family factors: The researchers analyzed data from two sources: 22,678 pairs of twins in the Swedish Twin Registry, who were born from 1982 to 2008; and 15,280 pairs of twins from the Child and Adolescent Twin Study in Sweden, born from 1992 to 2008. © 1986–2020 The Scientist.

Keyword: Autism; Genes & Behavior
Link ID: 27262 - Posted: 05.28.2020

By Rachel Nuwer Humans are not the only animals that get drunk. Birds that gorge on fermented berries and sap are known to fall out of trees and crash into windows. Elk that overdo it with rotting apples get stuck in trees. Moose wasted on overripe crab apples get tangled in swing sets, hammocks and even Christmas lights. Elephants, though, are the animal kingdom’s most well-known boozers. One scientific paper describes elephant trainers rewarding animals with beer and other alcoholic beverages, with one elephant in the 18th century said to have drunk 30 bottles of port a day. In 1974, a herd of 150 elephants in West Bengal, India, became intoxicated after breaking into a brewery, then went on a rampage that destroyed buildings and killed five people. Despite these widespread reports, scientists have questioned whether animals — especially large ones such as elephants and elk — actually become inebriated. In 2006, researchers calculated that based on the amount of alcohol it takes to get a human drunk, a 6,600-pound elephant on a bender would have to quickly consume up to 27 liters of seven percent ethanol, the key ingredient in alcohol. Such a quantity of booze is unlikely to be obtained in the wild. Intoxicated wild elephants, the researchers concluded, must be a myth. As the lead author said at the time, “People just want to believe in drunken elephants.” If you are one who wanted to believe, a study published in April in Biology Letters might serve as your vindication. A team of scientists say that the earlier myth-busting researchers made a common mistake: They assumed that elephants would have to consume as much alcohol to get drunk as humans do. In fact, elephants are likely exceptional lightweights because they — and many other mammals — lack a key enzyme that quickly metabolizes ethanol. The findings highlight the need to consider species on an individual basis. © 2020 The New York Times Company

Keyword: Drug Abuse; Evolution
Link ID: 27261 - Posted: 05.21.2020

by Marcus A. Banks Brain structures differ in volume depending on a person’s social environment and socioeconomic status, and between men and women, according to a new analysis1. The findings could help explain differences seen in the brains of autistic women and men, many of whom find social communication challenging. Researchers analyzed brain scans from about 10,000 people enrolled in the UK Biobank, a large-scale initiative to understand health trends in the United Kingdom. The participants were 55 years old, on average. They completed surveys, answering questions about their income level, satisfaction with friends and family, participation in social activities and feelings of loneliness. The researchers found that associations between the survey responses and the volume of brain regions linked to social contact differ by sex. For example, women who live with two or more people have a larger amygdala — a brain region involved in decision-making and emotional responses — than do women from smaller households. By contrast, household size has little effect on the size variation of amygdalae among men. The study appeared 18 March in Science Advances. The scans also showed that men who say they lack social support from siblings and friends tend to have a larger nucleus accumbens, part of the brain’s reward circuitry, than men who reported having more social support. The researchers did not see this difference in women. Other differences between men and women appeared in networks involving multiple brain regions, such as those involved with visual processing. © 2020 Simons Foundation

Keyword: Sexual Behavior; Brain imaging
Link ID: 27260 - Posted: 05.21.2020

Ashley Yeager It had been seven weeks since I’d touched another human being. Arms outstretched, I walked quickly toward my dad, craving his embrace. In the instant before we touched, we paused, our minds probably running quick, last-minute calculations on the risk of physical contact. But, after turning our faces away from each other and awkwardly shuffling closer, we finally connected. Wrapped in my dad’s bear hug, I momentarily forgot we were in the midst of the worst global crisis I have ever experienced. “Touch is the most powerful safety signal of togetherness,” says Steve Cole, a psychiatrist and biobehavioral scientist at the University of California, Los Angeles. Like more than 35 million other Americans, I live alone, and with the guidelines of physical distancing set by the Centers for Disease Control and Prevention, I hadn’t been getting close to anyone to avoid being infected with (or potentially spreading) SARS-CoV-2, the virus that causes COVID-19. I’d been working, thankfully, at home and staying connected with friends and family through Zoom and Skype, but those virtual interactions were no replacement for being with loved ones in person. “When we get lonely and isolated our brainstem recognizes that suddenly we are in insecure territory and flips on a bunch of fight-or-flight stress responses without us even knowing it,” Cole says. “There’s all sorts of things in our social world that lead us to calculate that we are either safe or unsafe. You can think of physical touch, supportive and affectionate touch, as the most fundamental signal that you’re with somebody who cares about you . . . a fundamental signal of safety and well-being.” © 1986–2020 The Scientist.

Keyword: Pain & Touch; Stress
Link ID: 27259 - Posted: 05.21.2020

By Benedict Carey The mental health toll of the coronavirus pandemic is only beginning to show itself, and it is too early to predict the scale of the impact. The coronavirus pandemic is an altogether different kind of cataclysm — an ongoing, wavelike, poorly understood threat that seems to be both everywhere and nowhere, a contagion nearly as psychological as it is physical. Death feels closer, even well away from the front lines of emergency rooms, and social isolation — which in pre-Covid times was often a sign of a mind turning in on itself — is the new normal for tens of millions of people around the world. The ultimate marker of the virus’s mental toll, some experts say, will show up in the nation’s suicide rate, in this and coming years. The immediate effect is not at all clear, despite President Trump’s recent claim that lockdown conditions were causing deaths. “Just look at what’s happening with drug addiction, look at what’s happening with suicides,” he said in a press briefing in the White House Rose Garden on Monday. In fact, doctors won’t know for many months if suicide is spiking in 2020; each death must be carefully investigated to determine its cause. The rolling impact of Covid-19 on these rates give scientists a sense of how extended uncertainty and repeating undercurrents of anxiety affect people’s will to live. “It’s a natural experiment, in a way,” said Matthew Nock, a psychology professor at Harvard. “There’s not only an increase in anxiety, but the more important piece is social isolation.” He added, “We’ve never had anything like this — and we know social isolation is related to suicide.” The earliest signs of whether the pandemic is driving up suicides will likely emerge among those who have had a history of managing persistent waves of self-destructive distress. Many of these people, who number in the millions worldwide, go through each day compulsively tuned to the world’s casual cruelties — its suspicious glances and rude remarks — and are prone to isolate themselves, at times contemplating a final exit plan. © 2020 The New York Times Company

Keyword: Depression
Link ID: 27258 - Posted: 05.20.2020

Dana Najjar The old riddle, “Which came first, the chicken or the egg?” is relatively easy to answer as a question about the evolution of birth in animals. Egg laying almost certainly came before live birth; the armored fish that inhabited the oceans half a billion years ago and were ancestral to all land vertebrates seem to have laid eggs. But the rest of the story is far from straightforward. Over millennia of evolution, nature has come up with only two ways for a newborn animal to come into the world. Either its mother lays it in an egg, where it can continue to grow before hatching, or it stays inside its mother until emerging as a more fully formed squirming newborn. “We have this really fundamental split,” said Camilla Whittington, a biologist at the University of Sydney. Is there some primordial reason for this strict reproductive dichotomy between egg laying (oviparity) and live birth (viviparity)? When and why did live birth evolve? These are just some of the questions that new research — including studies of a remarkable lizard that can lay eggs and bear live young at the same time — is exploring, all the while underscoring the enormous complexity and variability of sexual reproduction. Early female animals laid eggs in the sense that they released their ova into the world, often thousands at a time. Sperm released by males then fertilized some of these eggs in a hit-or-miss fashion, and the resulting embryos took their chances on surviving in the hostile world until they hatched. Many creatures, particularly small, simple ones, still reproduce this way. All Rights Reserved © 2020

Keyword: Sexual Behavior; Evolution
Link ID: 27257 - Posted: 05.20.2020