By Edith Sheffer Millions of people are identified with Asperger’s syndrome, as a diagnosis, an identity and even an adjective. Asperger’s name has permeated our culture—yet I believe we should no longer invoke it. Naming medical diagnoses after individuals is an honor, meant to recognize those who discover conditions and to commend their work. While there is a move toward descriptive diagnostic labels in medicine, certain eponyms have entered our everyday language and will likely endure. Alzheimer’s and Parkinson’s diseases, for example. Hans Asperger, however, neither described Asperger syndrome as we understand it today nor merits commendation. I have spent seven years researching his past in Nazi Vienna, uncovering his complicity in the Nazi regime and its “euthanasia” program that murdered children considered to be disabled. Contrary to Asperger’s reputation as a resister in the Third Reich, he approved the transfer of dozens of children to Vienna's killing center, Spiegelgrund, where they perished. He publicly spoke—and published—about the need to send the most “difficult cases” to Spiegelgrund. He was also close colleagues with top euthanasia figures in Vienna, including Erwin Jekelius, the director of Spiegelgrund, who was engaged to Hitler’s sister. Nazi ideology shaped Asperger’s research. Children in the Third Reich were to display community spirit, being enthusiastic participants in collective activities such as the Hitler youth. In Germany in the 1930s, Nazi psychiatrists identified children whom they believed lacked social feeling, unable to join the national community. Asperger, in his early 30s, warned against classifying children, arguing that they should be regarded as individuals. But right after the Third Reich annexed Austria in 1938—and the purge of his Jewish and liberal associates from the University of Vienna—Asperger followed his senior colleagues in Nazi child psychiatry and introduced his own diagnosis of social detachment: “autistic psychopathy.” © 2018 Scientific American,

Keyword: Autism
Link ID: 24937 - Posted: 05.03.2018

By Kerry Grens Neena Schwartz, a reproductive biologist at Northwestern University who discovered the hormone inhibin and its role in the regulation of reproductive cycles, died this month (April 15). She was 91. “She was a tremendous scientist, a pioneer for women in the sciences, and a leader in our discipline of endocrinology,” Teresa Woodruff and Kelly Mayo, both of Northwestern University, write in a memorial in Endocrine News. Among numerous leadership roles throughout her career, Schwartz founded the American Women in Science (AWIS) in 1971 and was a president of the Endocrine Society in the early 1980s. Schwartz was born in Baltimore, earned her undergraduate degree from Goucher College, and received her doctorate from Northwestern University in 1953. After a faculty position at the University of Illinois College of Medicine, she joined Northwestern in 1973 and remained as a professor there until her retirement in 1999. Her early work focused on rats’ hormonal cycles, and the insight she derived from her studies contributed to a basic understanding of the so-called HPG axis, the hypothalamic-pituitary-gonadal crosstalk of hormones that controls reproduction. Schwartz later discovered a peptide-based feedback system controlling hormone levels in the ovaries, and described the hormone inhibin, which blocks follicle stimulating hormone (FSH). The presence of inhibin had been proposed decades earlier, but nobody had searched for it in the follicle fluid of ovaries—until Schwartz and her colleague at the University of Maryland, Cornelia Channing took up the cause. Channing had sent Schwartz the fluid, and Schwartz found that it made FSH levels drop. © 1986-2018 The Scientist

Keyword: Hormones & Behavior
Link ID: 24925 - Posted: 05.01.2018

By CEYLAN YEGINSU LONDON — The anti-vaccine movement has come for the pets. A spreading fear of pet vaccines’ side effects has prompted the British Veterinary Association to issue a startling statement this week: Dogs cannot develop autism. The implicit message was that dog owners should keep vaccinating their pets against diseases like distemper and canine hepatitis because any concerns that the animals would develop autism after the injections were unfounded. The warning has a long tail. It grew out of an anti-vaccine theory that rippled across the United States and Europe as networks known as “anti-vaxxers” claimed that childhood vaccinations could cause autism. The belief, promoted by some celebrities like the television personality Jenny McCarthy, who says her son has autism, spurred many parents to begin boycotting traditional vaccines. The theory gained prominence in 1998, after a study published in the medical journal The Lancet purported to show a link between autism and the measles-mumps-rubella vaccination. It caused a firestorm in health circles and among parents, resulting in a significant drop in vaccination rates for children in Britain. But the study has since been thoroughly discredited. It was formally retracted by the medical magazine and its lead author, Andrew Wakefield, who at the time was a doctor at the Royal Free Hospital in London, was subsequently struck off the British medical register over ethical lapses. The theory, however, has jumped species. It is increasingly being applied to pets in the United States and is gaining momentum in Britain — raising concerns that the already low vaccination rates in this country could fall further. © 2018 The New York Times Company

Keyword: Autism
Link ID: 24914 - Posted: 04.28.2018

By Matt Warren There is no one gene that, when mutated, causes autism. But over the past decade, researchers have identified hundreds of gene variations that seem to affect brain development in ways that increase the risk of autism. However, these scientists mainly searched for variants in the DNA that directly encodes the building blocks of proteins. Now, a new study probing so-called noncoding DNA has found that alterations in regions that regulate gene activity may also contribute to autism. And surprisingly, these variations tended to be inherited from fathers who aren’t autistic. “This is a really good article—it’s somewhat provocative and it makes us think about [autism genetics in a] different way,” says Lucia Peixoto, a neuroscientist and computational biologist at Washington State University in Spokane, who was not involved in the research. “I think it’s a great contribution to the field.” Research into the genetic risk for autism has mainly focused on how mutations that arise spontaneously in an individual’s genome—rather than being inherited from a parent—disrupt protein-coding regions and lead to the condition. That’s because these sporadic mutations have relatively large effects and studies have shown that such mutations, although individually rare, together contribute to about 25% to 30% of cases, says Jonathan Sebat, a geneticist at the University of California, San Diego. But only about 2% of the genome consists of protein-coding areas. Sebat says the large noncoding portion of our DNA—often previously referred to as “junk DNA”—has so far been ignored in autism research. © 2018 American Association for the Advancement of Science

Keyword: Autism; Epigenetics
Link ID: 24886 - Posted: 04.21.2018

By CEYLAN YEGINSU A new study has shed more light on the revelations that Hans Asperger, the Austrian pediatrician for whom a form of autism is named, had collaborated with the Nazis and actively assisted in the killing of disabled children. Published on Wednesday in the journal Molecular Autism by the medical historian Herwig Czech, the report relies on eight years of research that included the examination of previously unseen Nazi-era documents. The study concludes that though Dr. Asperger was not a member of the Nazi Party, he had participated in the Third Reich’s child-euthanasia program, which aimed to establish a “pure” society by eliminating those deemed a “burden.” Dr. Asperger referred disabled children to the notorious Am Spiegelgrund clinic in Vienna, where hundreds were either drugged or gassed to death from 1940 to 1945. “The picture that emerges is that of a man who managed to further his career under the Nazi regime, despite his apparent political and ideological distance from it,” Mr. Czech, of the University of Vienna, wrote in his study. Asperger syndrome is a lifelong developmental disability associated with autism that affects perception and social interaction. About one in 68 children in the United States have been identified with Autism Spectrum Disorder. © 2018 The New York Times Company

Keyword: Autism
Link ID: 24885 - Posted: 04.21.2018

By Edith Sheffer PALO ALTO, Calif. — My son’s school, David Starr Jordan Middle School, is being renamed. A seventh grader exposed the honoree, Stanford University’s first president, as a prominent eugenicist of the early 20th century who championed sterilization of the “unfit.” This sort of debate is happening all over the country, as communities fight over whether to tear down Confederate monuments and whether Andrew Jackson deserves to remain on the $20 bill. How do we decide whom to honor and whom to disavow? There are some straightforward cases: Hitler Squares were renamed after World War II; Lenin statues were hauled away after the collapse of the Soviet Union. But other, less famous monsters of the past continue to define our landscape and language. I have spent the past seven years researching the Nazi past of Dr. Hans Asperger. Asperger is credited with shaping our ideas of autism and Asperger syndrome, diagnoses given to people believed to have limited social skills and narrow interests. The official diagnosis of Asperger disorder has recently been dropped from the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders because clinicians largely agreed it wasn’t a separate condition from autism. But Asperger syndrome is still included in the World Health Organization’s International Classification of Diseases, which is used around the globe. Moreover, the name remains in common usage. It is an archetype in popular culture, a term we apply to loved ones and an identity many people with autism adopt for themselves. Most of us never think about the man behind the name. But we should. © 2018 The New York Times Company

Keyword: Autism
Link ID: 24840 - Posted: 04.09.2018

by Nicholette Zeliadt Folic acid, a B vitamin, may lower autism risk and ease features of the condition, according to findings from five unrelated studies published over the past few months. Three of the studies suggest that prenatal supplements of folic acid offset autism risk associated with in utero exposure to epilepsy drugs or toxic chemicals. The supplements are also known to prevent birth defects. Another study found that people with autism and their immediate family members are more likely than those in a control group to carry immune molecules that could block folate’s passage into the brain. “These studies are particularly of interest because they suggest that people could potentially modify their risk of having a child with autism, even in the face of certain adverse exposures or conditions,” says Kristen Lyall, an assistant professor in the Modifiable Risk Factors Program at the A.J. Drexel Autism Institute in Philadelphia, who was not involved in any of the studies. A fifth study reported results from a small clinical trial suggesting that folinic acid — a form of folic acid — can ease language and communication difficulties in people with autism. “It isn’t enough to say that kids with [autism] should be taking folinic acid, necessarily, but it is enough to motivate a larger study,” says Jeremy Veenstra-VanderWeele, a professor of psychiatry at Columbia University, who was not involved in the trial. © 1996-2018 The Washington Post

Keyword: Autism; Development of the Brain
Link ID: 24813 - Posted: 04.03.2018

A new report says an estimated one in every 66 Canadian children and youth aged five to 17 has autism spectrum disorder. The report by the Public Health Agency of Canada, released on Thursday, is the first detailing the national prevalence of the neurodevelopmental disorder and is in line with estimates in the United States. Autism spectrum disorder is typically detected in early childhood and causes impairments in communication skills and social interactions, often combined with repetitive behaviours and restricted interests or activities. Boys are four to five times more likely to be diagnosed with autism spectrum disorder, or ASD, than girls. "Understanding trends and patterns in ASD diagnosis is essential to developing meaningful programs and services to support people living with ASD and their families," said Dr. Theresa Tam, chief public health officer, noting that the estimates establish a baseline that will help researchers determine if prevalence rates are changing over time. The report includes data from six provinces and one territory and found prevalence ranged from a high of one in 57 children in Newfoundland and Labrador, to one in 126 in Yukon. Newfoundland and Labrador, Nova Scotia, Prince Edward Island, New Brunswick, Quebec, British Columbia and Yukon all contributed data to the report, a spokesperson for the Public Health Agency of Canada said. ©2018 CBC/Radio-Canada.

Keyword: Autism
Link ID: 24801 - Posted: 03.30.2018

By RANDI HUTTER EPSTEIN Getting a high testosterone reading offers bragging rights for some men of a certain age — and may explain in part the lure of testosterone supplements. But once you are within a normal range, does your level of testosterone, the male hormone touted to build energy, libido and confidence, really tell you that much? Probably not, experts say. Normal testosterone levels in men range from about 300 to 1,000 nanograms per deciliter of blood. Going from one number within the normal zone to another one may not pack much of a punch. “You don’t see the big improvement once men are within the normal range,” said Dr. Shalender Bhasin, an endocrinologist and professor of medicine at Harvard Medical School. The largest differences in terms of energy and sex drive are when men go from below-normal to normal levels. A 2015 study in JAMA found that sex drive improved among men who went from about 230, considered low, to 500, around the middle of what’s considered normal. There was no difference among men who moved within the normal range from 300 to 500. Testosterone does influence muscle size. The more testosterone a man takes, the larger the muscle — regardless of starting level, one reason the hormone is popular with young bodybuilders. But testosterone supplements do not seem to help frail older men walk farther or get out of chairs more easily, goals that doctors typically look for in aiding older patients. Beginning at age 30, testosterone levels drop, on average, about 1 percent a year. About 5 percent of men between the ages of 50 and 59 have low levels of testosterone along with symptoms like loss of libido and sluggishness, according to a few small studies. © 2018 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 24792 - Posted: 03.28.2018

By Nicola Davis Your book is all about reproductive hormones, and their impact on our behaviour. It only focuses on female hormones. Why not look at men’s too? Two reasons. One is that the focus of research in my lab is to look at women’s hormones. The other is that I think there are problems with how people have viewed hormones and women, and I really want to debunk those myths, then pursue some of the implications for further exploring links between women’s hormones and their behaviour. I think they are really important for women’s wellbeing. You say that some people, including women, have pushed back against discussing the influence of hormones. Why is that? I get a strong sense that if you ascribe a woman’s behaviour to biology, people will automatically think that women are automatons, driven by their hormones and unable to regulate their own behaviour. That is false. There is a female stereotype, whereby any time a woman does something a little bit difficult to understand, then it is hormones that make women “irrational”. But nobody says that about men. For that reason, those who are concerned about women achieving equality with men worry that if we talk about women and hormones, then people will say such things as women shouldn’t hold higher office and so on. That’s silly, because men have hormones, too. Are you surprised by how recently we have begun investigating the impact of hormones on women? One reason is that scientists were content for many decades with studying the male as the default sex, and that was in part because women had cycles that made them messy. If you are doing a scientific experiment, you don’t want noise, you don’t want variation, you want everything to be strictly controlled. © 2018 Guardian News and Media Limited

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 24746 - Posted: 03.13.2018

By George Musser, Satsuki Ayaya remembers finding it hard to play with other children when she was young, as if a screen separated her from them. Sometimes she felt numb, sometimes too sensitive; sometimes sounds were muted, sometimes too sharp. As a teenager, desperate to understand herself, she began keeping a journal. “I started to write my ideas in my notebooks, like: What’s happened to me? Or: What’s wrong with me? Or: Who am I?” she says, “I wrote, wrote, wrote. I filled maybe 40 notebooks.” Today, at 43, Ayaya has a better sense of who she is: She was diagnosed with autism when she was in her early 30s. As a Ph.D. student in the history and philosophy of science at the University of Tokyo, she is using the narratives from her teen years and after to generate hypotheses and suggest experiments about autism — a form of self-analysis called Tojisha-Kenkyu, introduced nearly 20 years ago by the disability-rights movement in Japan. In Ayaya’s telling, her autism involves a host of perceptual disconnects. For example, she feels in exquisite detail all the sensations that typical people readily identify as hunger, but she can’t piece them together. “It’s very hard for me to conclude I’m hungry,” she says. “I feel irritated, or I feel sad, or I feel something [is] wrong. This information is separated, not connected.” It takes her so long to realize she is hungry that she often feels faint and gets something to eat only after someone suggests it to her. © 2018 American Association for the Advancement of Science

Keyword: Autism
Link ID: 24736 - Posted: 03.10.2018

By Shawna Williams In recent years, US society has seen a sea change in the perception of transgender people, with celebrities such as Caitlyn Jenner and Laverne Cox becoming the recognizable faces of a marginalized population. Transgender rights have also become a mainstream political issue, and the idea that people should be referred to by the names and pronouns they find most fitting—whether or not these designations match those on their birth certificates, or align with the categories of male and female—is gaining acceptance. Yet a biological understanding of the contrast between the natal sex and the gender identity of transgender people remains elusive. In recent years, techniques such as functional magnetic resonance imaging (fMRI) have begun to yield clues to possible biological underpinnings of the condition known as gender dysphoria. In particular, researchers are identifying similarities and differences between aspects of the structure and function of the brains of trans- and cisgender individuals that could help explain the conviction that one’s gender and natal sex don’t match. The results may not have much effect on how gender dysphoria is diagnosed and treated, notes Baudewijntje Kreukels, who studies gender incongruence at VU University Medical Center in Amsterdam. “It’s really important that it will not be seen as, ‘When you see [gender dysphoria] in the brain, then it’s true.’” But the insights from such research could go a long way toward satisfying the desire of some transgender people to understand the roots of their condition, she adds. “In that way, it is good to find out if these differences between them and their sex assigned at birth are reflected by measures in the brain.” © 1986-2018 The Scientist

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 24724 - Posted: 03.06.2018

By Dina Fine Maron Suspicions of a link between prenatal ultrasound scans and autism spectrum disorder are nothing new. The technology has exploded in recent decades, giving expectant parents more detailed images of their developing offspring than ever before. And as ultrasound use has sharply increased, so too have diagnoses of autism—prompting questions about a potential relationship. A rigorous new study examining the association between ultrasounds during the first or second trimester of pregnancy and later development of autism spectrum disorder, however, delivers some good news. The study, which analyzed the medical records and ultrasound details of more than 400 kids who were born at Boston Medical Center, found there was no increase in the number of prenatal scans or duration of ultrasound exposure in children with autism compared with kids with typical development or separate developmental delays. In fact, the group with autism had less average exposure time during its first and second trimesters of development than individuals without autism did. The finding adds weight to earlier studies that suggested such scans—which use high-frequency sound waves to create an image of the fetus, placenta and surrounding maternal organs—are not a powerful enough environmental risk to cause autism on their own. But the new study, published Monday in JAMA Pediatrics, did leave one question unanswered: Does the depth of the actual ultrasound scan make a difference? The work found the children with autism were exposed to prenatal ultrasounds with greater penetration than the control group: During the first trimester, the group with autism had scans with an average depth of 12.5 centimeters compared with 11.6 centimeters for the control group. And during the second trimester the group with autism had scan depths of 12.9 centimeters compared with 12.5 centimeters for the typical development control group. Ultrasounds may not be uniform for reasons including the position of the fetus in the womb. © 2018 Scientific American

Keyword: Autism
Link ID: 24655 - Posted: 02.13.2018

Lee Burdette Williams The call came from a former colleague who coaches college students on the autism spectrum. “We’ve got someone who’s in trouble, and we could use some advice. It’s one of those Title IX things.” She told me the story. The student loves punk music and wanted to start a band. He put up fliers on the campus, which in itself was an issue because he violated the institutional posting policy. But even in today’s climate, I thought, that doesn’t usually rise to a Title IX complaint. She continued. “He wrote something in Morse code on the flyer, a message directed to women, because he was trying to recruit some to join the band. It was a little ‘stalky-creepy’ -- OK, pretty creepy -- but this guy is totally harmless and clueless and just doesn’t know how to meet women.” My first reaction was to smile. Morse code? How many college students even know what it is? But it didn’t surprise me to learn this about a student with Asperger’s syndrome, the commonly used term for those with high-functioning autism. Indeed, this kind of situation, I have come to realize, exemplifies a disastrous nexus of two trends on college campuses: the increased awareness of Title IX’s expectations for student behavior and institutional response, and the growing number of students with a diagnosis (or simply just characteristics) of autism who are attending college. I imagined the student had learned Morse code at the age of 5 and was no doubt still fluent in it. In his mind, a wondrous place created by the distinct neural connections common among those with this diagnosis, the use of Morse code to signal his interest in meeting women made perfect sense. To those who know him, it is one of many quirky characteristics -- some of them sweet, some of them annoying -- that require a bit of translation for him and about him as he moves within the world of higher education. © 2018

Keyword: Autism
Link ID: 24644 - Posted: 02.12.2018

By RONI CARYN RABIN Most dieters know the hard truth: Sticking to a weight loss regimen gets more difficult as the day wears on. But while those who give in to food cravings and binge at night may blame flagging willpower, a new study suggests the problem could lie in the complex orchestra of hormones that drive hunger and signal feelings of satiety, or fullness. The small study of 32 obese men and women, half of whom had a habit of binge eating, suggests that satiety hormones may be lower during the evening hours, while hunger hormones rise toward nightfall and may be stoked even higher by stressful situations. Overweight binge eaters may be particularly susceptible to the influence of fluctuations in these appetite-regulating hormones, the researchers found. “There’s more opportunity to eat in the evening, but this study is showing that hormonal responses are setting them up to do this,” said Susan Carnell, an assistant professor of psychiatry and behavioral sciences at Johns Hopkins University School of Medicine who was a first author of the study along with Charlotte Grillot of Florida State University. It’s not clear whether these hormonal patterns precede and cause the binge eating behaviors or are conditioned by an individual’s eating habits, Dr. Carnell said. But either way, “you can get stuck in the cycle.” The study is an important reminder that myriad factors contribute to weight gain, and that shaming and blaming people for their weight problems is inappropriate, said Kelly Costello Allison, director of the Center for Weight and Eating Disorders at the University of Pennsylvania, who was not involved in the new research. © 2018 The New York Times Company

Keyword: Obesity; Hormones & Behavior
Link ID: 24591 - Posted: 01.31.2018

By Jessica Wright Nearly 20 years ago, a new strain of mice debuted in a California laboratory. The mice were missing a gene called SCN2A that helps neurons transmit electrical currents. And the study announcing their genesis was the last word on the matter for many years. About a decade later, the mouse’s creator, Maurice Montal, sacrificed the few animals left from the colony. He had sent some of his mice to other researchers, and some ended up with a team in Houston, Texas. But they, too, eventually stopped working with the strain. Perhaps the only one who continued to work with the mice was a postdoctoral researcher named Edward Glasscock, who brought the mice from Houston to the University of Louisiana when he launched his own lab. After years of work, Glasscock found that a mutation in SCN2A can muffle the effect of another mutation that triggers sudden death in people with epilepsy. That turned out to be only the beginning of the mice’s comeback. In June 2016, Kevin Bender, an autism researcher, sent Glasscock an urgent request asking for the mice. Requests from two other autism researchers quickly followed. Soon the mice were populating labs in San Francisco, Baltimore, and France. “I was surprised that there would be such a rush to get them,” says Glasscock, assistant professor of cellular biology and anatomy at Louisiana State University. “Back when I first started working with the mice, it would never have been on my radar that they would have been an important gene for autism.” © 1986-2018 The Scientist

Keyword: Autism
Link ID: 24586 - Posted: 01.30.2018

By Jessica Wright, The prevalence of autism in the United States remained relatively stable from 2014 to 2016, according to a new analysis. The results were published January 2 in the Journal of the American Medical Association. The researchers report the frequency of autism in the U.S. as 2.24 percent in 2014, 2.41 percent in 2015 and 2.76 percent in 2016, respectively. The new data come from the National Health Interview Survey—a yearly interview in which trained census workers ask tens of thousands of parents about the health of their children. These questions include whether a healthcare professional has ever told them that their child has autism. The new figures, released by the U.S. Centers for Disease Control and Prevention (CDC), represent the highest autism prevalence in the U.S. reported by the agency to date. “We cannot consider autism as rare a condition as people previously thought,” says lead researcher Wei Bao, assistant professor of epidemiology at the University of Iowa. The peak is likely to result from the fact that the data are based on parent reports. These reports may capture children with relatively mild autism features better than do approaches that rely on medical records, Bao says. Autism’s reported prevalence in the U.S. has climbed steadily in the past few decades. Researchers attribute most of this increase to changes in how the prevalence is measured, increased awareness of the condition and shifts in the criteria for diagnosing autism. © 2018 Scientific American,

Keyword: Autism
Link ID: 24522 - Posted: 01.12.2018

Aimee Cunningham Internist Gail Povar has many female patients making their way through menopause, some having a tougher time than others. Several women with similar stories stand out in her mind. Each came to Povar’s Silver Spring, Md., office within a year or two of stopping her period, complaining of frequent hot flashes and poor sleep at night. “They just felt exhausted all the time,” Povar says. “The joy had kind of gone out.” And all of them “were just absolutely certain that they were not going to take hormone replacement,” she says. But the women had no risk factors that would rule out treating their symptoms with hormones. So Povar suggested the women try hormone therapy for a few months. “If you feel really better and it makes a big difference in your life, then you and I can decide how long we continue it,” Povar told them. “And if it doesn’t make any difference to you, stop it.” At the follow-up appointments, all of these women reacted the same way, Povar recalls. “They walked in beaming, absolutely beaming, saying, ‘I can’t believe I didn’t do this a year ago. My life! I’ve got my life back.’ ” That doesn’t mean, Povar says, that she’s pushing hormone replacement on patients. “But it should be on the table,” she says. “It should be part of the discussion.” Hormone replacement therapy toppled off the table for many menopausal women and their doctors in 2002. That’s when a women’s health study, stopped early after a data review, published results linking a common hormone therapy to an increased risk of breast cancer, heart disease, stroke and blood clots. The trial, part of a multifaceted project called the Women’s Health Initiative, or WHI, was meant to examine hormone therapy’s effectiveness in lowering the risk of heart disease and other conditions in women ages 50 to 79. It wasn’t a study of hormone therapy for treating menopausal symptoms. |© Society for Science & the Public 2000 - 2018.

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 24512 - Posted: 01.10.2018

By Sarah DeWeerdt Older men and women are more likely than young ones to have a child with autism, according to multiple studies published in the past decade. Especially regarding fathers, this effect is one of the most consistent findings in the epidemiology of autism. The link between a mother’s age and autism is more complex: Women seem to be at an increased risk both when they are much older and much younger than average, according to some studies. Nailing down why either parent’s age influences autism risk has proved difficult, however. How do we know that older men are at elevated risk of fathering a child with autism? Epidemiologists have gathered data on large numbers of families and calculated how often men of different ages have a child with autism. The first rigorous study of this type, published in 2006, drew on medical records of 132,000 Israeli adolescents. It showed that men in their 30s were 1.6 times as likely to have a child with autism as men younger than 30. Men in their 40s had a sixfold increase in risk. Since then, scientists have conducted similar analyses of data on children born in California, Denmark and Sweden, as well as of an international data set on 5.7 million children. Nearly all of this research has shown an increased prevalence of autism among the children of older fathers. At what age does the risk increase for men? No one knows. The age ranges and ages of the men differ across studies, making results hard to compare. Overall, the findings indicate that the risk increases steadily over time rather than suddenly rising after a certain age. © 1996-2017 The Washington Post

Keyword: Autism; Epigenetics
Link ID: 24436 - Posted: 12.18.2017

By Mitch Leslie Scientists once had high hopes that inhibiting a hormone named ghrelin would be the key to preventing obesity. Ghrelin didn’t turn out to be a weight loss panacea. But now, the discovery of the first molecule naturally made by the body that blocks ghrelin’s effects may open up new avenues for treating other conditions, including diabetes and anorexia. The finding may also explain some of the benefits of bariatric surgery, which shrinks or reroutes the stomach to control weight. “It’s a very impressive piece of research,” says bariatric physician Carel le Roux of University College Dublin, who wasn’t connected to the study. “I think it will have significant clinical impact.” When researchers discovered ghrelin about 20 years ago, they dubbed it the “hunger hormone” because early results suggested it ramped up our appetite. But studies soon found that thwarting the molecule didn’t curtail food consumption or promote weight loss in mice. Still, the hormone induces a variety of other positive changes in our metabolism. For example, ghrelin may bolster muscle strength, spurring scientists to test whether drugs that mimic the hormone can counteract the muscle deterioration and weakness often suffered by cancer patients. The new study didn’t start as a hunt for ghrelin-blocking compounds. Instead, a team headed by researchers at NGM Biopharmaceuticals in South San Francisco, California, was investigating how bariatric surgery overhauls metabolism. The scientists operated on obese mice, performing a type of bariatric surgery called vertical sleeve gastrectomy that involves removing most of the stomach. They then examined which genes became more or less active after the procedure. As they report online today in Cell Metabolism, the rodents’ downsized stomachs produced 52 times more of a protein named LEAP2 than normal. © 2017 American Association for the Advancement of Science

Keyword: Obesity; Hormones & Behavior
Link ID: 24407 - Posted: 12.08.2017