Chapter 5. Hormones and the Brain
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By William Kenower My youngest son, Sawyer, used to spend far more time relating to his imagination than he did to the world around him. He would run back and forth humming, flapping his hands and thumping on his chest. By the time he was in first grade, attempts to draw him out of his pretend world to join his classmates or do some class work led to explosions and timeouts. At 7 he was given a diagnosis of being on the autism spectrum. That was when my wife, Jen, learned about the practice called joining. The idea behind it, which she discovered in Barry Neil Kaufman’s book “Son-Rise,” is brilliant in its simplicity. We wanted Sawyer to be with us. We did not want him to live in this bubble of his own creation. And so, instead of telling him to stop pretending and join us, we started pretending and joined him. The first time Jen joined him, the first time she ran beside him humming and thumping her chest, he stopped running, stopped thumping, stopped humming and, without a single word from us, turned to her and said, “What are you doing?” We took turns joining him every day, and a week later we got an email from his special education teacher telling us to keep doing whatever we were doing. He’d gone from five timeouts a day to one in a week. The classroom was the same, the work was the same – all that was different was that we had found a way to say to him in a language he could understand, “You’re not wrong.” Emboldened by our success, we set about becoming more fluent in this language. For the next couple of years we taught ourselves to join him constantly. This meant that whatever we were doing had to stop whenever we heard him running back and forth and humming. But we could not join him simply to get him to stop running and thumping and humming. We had to join him without any judgment or impatience. That was the trickiest part. The desire to fix him was great. I had come to believe that there were broken people in need of fixing. Sometimes, I looked like one of those people. I was a 40-year-old unpublished writer working as a waiter. My life reeked of failure. Many days I looked in the mirror and asked, “What is wrong with me?” © 2016 The New York Times Company
Link ID: 22451 - Posted: 07.16.2016
By Rebecca Brewer, Jennifer Murphy, There is a persistent stereotype that people with autism are individuals who lack empathy and cannot understand emotion. It’s true that many people with autism don’t show emotion in ways that people without the condition would recognize. But the notion that people with autism generally lack empathy and cannot recognize feelings is wrong. Holding such a view can distort our perception of these individuals and possibly delay effective treatments. We became skeptical of this notion several years ago. In the course of our studies of social and emotional skills, some of our research volunteers with autism and their families mentioned to us that people with autism do display empathy. Many of these individuals said they experience typical, or even excessive, empathy at times. One of our volunteers, for example, described in detail his intense empathic reaction to his sister’s distress at a family funeral. Yet some of our volunteers with autism agreed that emotions and empathy are difficult for them. We were not willing to brush off this discrepancy with the ever-ready explanation that people with autism differ from one another. We wanted to explain the difference, rather than just recognize it. So we looked into the overlap between autism and alexithymia, a condition defined by a difficulty understanding and identifying one’s own emotions. People with high levels of alexithymia (which we assess with questionnaires) might suspect they are experiencing an emotion, but are unsure which emotion it is. They could be sad, angry, anxious or maybe just overheated. About 10 percent of the population at large — and about 50 percent of people with autism — has alexithymia. © 2016 Scientific American
By Tara Parker-Pope Hoping to alert parents to “red flags” that might signal autism, two advocacy groups yesterday launched a Web site, the ASD Video Glossary, that provides online glimpses of kids with autism to worried parents. But some experts fear the site, though well intentioned, also may cause anxiety among parents whose children are perfectly fine. The site contains videos that show subtle differences in how kids with autism speak, react, play and express themselves. The organizations behind it, Autism Speaks and First Signs, hope that parents who see resemblances in their own kids will be emboldened to seek early diagnosis and treatment, which many experts believe can improve outcomes for kids with autism. Visitors to the new site must register in order to watch the videos, and in the first two hours of its release, more than 10,000 people did so. Yet some researchers fear the video glossary is certain to be troubling for the parents of children without autism, too, because the behavior of kids without the condition can resemble that depicted in the videos. “Just as there’s a spectrum in autism…there’s a spectrum in normal development,” Dr. Michael Wasserman, a pediatrician at Ochsner Medical Center in New Orleans told the Associated Press. “Children don’t necessarily develop in a straight line.” But Amy Wetherby, a professor of communications disorders at Florida State University who helped create the site, said the videos would embolden parents to persist when doctors don’t listen to legitimate concerns about a child’s behavior. As she told the Associated Press, sometimes “parents are the first to be concerned, and the doctors aren’t necessarily worried,” she said. “This will help give them terms to take to the doctor and say, ‘I’m worried about it.”’ © 2016 The New York Times Company
Link ID: 22432 - Posted: 07.13.2016
By David Dobbs It’s difficult to tell what Gina Pace wants unless you already know what she wants. But sometimes that’s easy, and this is one of those times: Gina wants pizza. “I-buh!” she says repeatedly—her version of “I want.” We all do. We are sitting at Abate’s in New Haven, Connecticut, a town famous for—among other things—pizza and science. Gina and her father, Bernardo, who live on Staten Island in New York City, have made the two-hour drive here for both. The pizza is in the oven. The science is already at the table, represented by Abha Gupta, a developmental pediatrician at Yale’s renowned Child Study Center. Gupta is one of the few scientific experts on a condition that Bernardo and Gina know through hard experience. Gina, now 24, was diagnosed 20 years ago with childhood disintegrative disorder, or CDD. CDD is the strangest and most unsettling developmental condition you have probably never heard of. Also known as Heller’s syndrome, for the Austrian special educator who first described it in 1908, it is a late-blooming, viciously regressive form of autism. It’s rare, striking about 1 or 2 in every 100,000 children. After developing typically for two to 10 years (the average is three or four), a child with CDD will suffer deep, sharp reversals along multiple lines of development, which may include language, social skills, play skills, motor skills, cognition, and bladder or bowel control. The speed and character of this reversal varies, but it often occurs in a horrifyingly short period—as short as a couple of months, says Gupta. In about 75 percent of cases, this loss of skills is preceded by days or weeks in which the child experiences intense anxiety and even terror: nightmares and waking nightmares and bouts of confused, jumpy disturbance that resemble psychosis.
By David Shultz Making eye contact for an appropriate length of time is a delicate social balancing act: too short, and we look shifty and untrustworthy; too long, and we seem awkward and overly intimate. To make this Goldilocks-like dilemma even trickier, it turns out that different people prefer to lock eyes for different amounts of time. So what’s too long or too short for one person might be just right for another. In a new study, published today in Royal Society Open Science, researchers asked a group of 498 volunteers to watch a video of an actor staring out from a screen and press a button if their gazes met for an uncomfortably long or short amount of time (above). During the test, the movement of their eyes and the size of their pupils were recorded with eye-tracking technology. On average, participants had a “preferred gaze duration” of 3.3 seconds, give or take 0.7 seconds. That’s a pretty narrow band for someone on their first date! Making things even harder, individual preferences can also be measured: Researchers found that how quickly people’s pupils dilated—an automatic reflex whenever someone looks into the eyes of another—was a good indicator of how long they wanted to gaze. The longer their preferred gaze, the faster their pupils expanded. The differences are so subtle, though, that they can only be seen with the eye-tracking software—making any attempts to game the system is likely to end up awkward rather than informative. © 2016 American Association for the Advancement of Science.
By Elizabeth Pennisi Cave fish have long fascinated biologists because of their missing eyes and pale skin. Now, one researcher is studying them for another reason: Their behavior may provide clues to the genetic basis of some human psychiatric disorders. Last week at the 23rd International Conference on Subterranean Biology in Fayetteville, Arkansas, he demonstrated how drugs that help people with schizophrenia and autism similarly affect the fish. “I think there is a lot of potential” for these fish to teach us about mental disorders, says David Culver, an evolutionary biologist at American University in Washington, D.C., who was not involved in the study. Culver adds that—like other work on the cause of cave fish blindness—the new research may also have implications for human disease. A decade ago, the lead author on the new study, Masato Yoshizawa, wanted to understand brain evolution by investigating the effects of natural selection on behavior. The Mexican tetra (Astyanax mexicanus), a cave fish with very close surface relatives, seemed an excellent prospect for that work. Because the two populations can interbreed, it’s easier to pin down genes that might be related to the neural defects underlying behavioral differences. Such breeding studies are not possible in humans. The blind cave fish differ from their surface relatives in several notable ways. They don’t have a social structure and they don’t school. Instead, they lead solitary lives—a behavior that makes sense given their lack of natural predators. They also almost never sleep. They are hyperactive, and—unlike other fish—they are attracted to certain vibrations in the water. Finally, they tend to do the same behavior over and over again and seem to have higher anxiety than their surface relatives. © 2016 American Association for the Advancement of Science.
By Ruth Williams The offspring of certain mice fed a high-fat diet have altered gut microbiomes and may be prone to autism-like behaviors including social deficits, according to a study published today (June 16) in Cell. But treating these offspring with a specific microbial species they lack can rectify the animals’ social behavior. “There’s growing evidence that the microbiome, particularly early in life, can have long-term effects on brain development and behavior,” said anatomist and neuroscientist John Cryan of University College Cork in Ireland who was not involved in the study. “What this paper does is take advantage of the fact that we get our microbiome from our mums, and looks at what happens if the mum disturbs her microbiome during pregnancy.” According to the US Centers for Disease Control and Prevention, one in 68 U.S. children have autism spectrum disorder (ASD). Recent evidence suggests that the risk of ASD is increased for the offspring of mothers with obesity. In both humans and non-human primates, the offspring of obese mothers have also been shown to have abnormal microbiomes. And some people with ASD have imbalanced gut microbes, or dysbiosis. Baylor College of Medicine’s Mauro Costa-Mattioli and colleagues sought to better understand how maternal obesity, the microbiome, and ASD are interconnected. The team turned to mice for answers. The researchers gave female animals high-fat diets before setting up matings, later finding that a “large proportion” of the offspring exhibited ASD-like behaviors, including reduced social interaction, repetitive behaviors, and anxiety. The team analyzed the microbiomes of these offspring, finding that they differed from those of control animals. © 1986-2016 The Scientist
Link ID: 22336 - Posted: 06.18.2016
By Teal Burrell Sociability may be skin deep. The social impairments and high anxiety seen in people with autism or related disorders may be partly due to a disruption in the nerves of the skin that sense touch, a new study in mice suggests. Autism spectrum disorders are primarily thought of as disorders of the brain, generally characterized by repetitive behaviors and deficits in communication skills and social interaction. But a majority of people with autism spectrum disorders also have an altered tactile sense; they are often hypersensitive to light touch and can be overwhelmed by certain textures. “They tend to be very wary of social touch [like a hug or handshake], or if they go outside and feel a gust of wind, it can be very unnerving,” says neuroscientist Lauren Orefice from Harvard Medical School in Boston. An appreciation for this sensory aspect of autism has grown in recent years. The newest version of psychiatry’s bible, the Diagnostic and Statistical Manual of Mental Disorders, includes the sensory abnormalities of autism as core features of the disease. “That was a big nod and a recognition that this is a really important aspect of autism,” says Kevin Pelphrey, a cognitive neuroscientist at The George Washington University in Washington, D.C., who was not involved in the work. The sensation of touch starts in the peripheral nervous system—in receptors at the surface of the skin—and travels along nerves that connect into the central nervous system. Whereas many autism researchers focus on the end of the pathway—the brain—Orefice and colleagues wondered about the first leg of the trip. So the group introduced mutations that silenced genes associated with autism spectrum disorders in mice, adding them in a way that restricted the effects to peripheral nerve cells, they report today in Cell. The team singled out the gene Mecp2, which encodes a protein that regulates the expression of genes that help forge connections between nerve cells. © 2016 American Association for the Advancement of Science
By Sarah DeWeerdt, Spectrum Brains from people with autism show patterns of gene expression similar to those from people with schizophrenia, according to a new analysis. The findings, published May 24 in Translational Psychiatry, deepen the connections between the two conditions, says study leader Dan Arking, associate professor of genetic medicine at Johns Hopkins University in Baltimore, Maryland. People who have either autism or schizophrenia share features such as language problems and difficulty understanding other people’s thoughts and feelings. They also have genetic risk factors in common. “And now I think we can show that they share overlap in gene expression,” Arking says. The study builds on previous work, in which Arking’s team characterized gene expression in postmortem brain tissue from 32 individuals with autism and 40 controls. In the new analysis, the researchers made use of that dataset as well as one from the Stanley Medical Research Institute that looked at 31 people with schizophrenia, 25 with bipolar disorder and 26 controls3. They found 106 genes expressed at lower levels in autism and schizophrenia brains than in controls. These genes are involved in the development of neurons, especially the formation of the long projections that carry nerve signals and the development of the junctions, or synapses, between one cell and the next. The results are consistent with those from previous studies indicating a role for genes involved in brain development in both conditions. “On the one hand, it’s exciting because it tells us that there’s a lot of overlap,” says Jeremy Willsey, assistant professor of psychiatry at the University of California, San Francisco, who was not involved in the work. “On the other hand, these are fairly general things that are overlapping.” © 2016 Scientific American
By Ann Griswold, Women who develop infections during pregnancy run an increased risk of having a child with autism. Most data indicate that an overactive maternal immune response underlies the risk. But a new analysis runs contrary to this view: It ties high levels of an inflammatory protein in pregnant women to a low risk of autism in their children, suggesting that a strong immune response is protective. Researchers looked at 1,315 mother-child pairs, including 500 children with autism and 235 with developmental delay. They found that healthy pregnant women with high levels of C-reactive protein (CRP), a marker of inflammation, are less likely to have a child with autism than are women with typical levels of the protein. The findings contradict a 2013 report from a large Finnish cohort that tied high CRP levels during pregnancy to an increased risk of having a child with autism. “It was the opposite of what we expected to find,” says senior researcher Lisa Croen, director of the Autism Research Program at Kaiser Permanente in Oakland, California. The work appeared in April in Translational Psychiatry. The results suggest that the strength of a woman’s immune system, rather than its response to infection, is the important factor in determining autism risk. Moderate or low baseline levels of CRP might indicate a relatively weak ability to fight off infection. And a less vigorous immune response might boost the risk in some women, the researchers say. © 2016 Scientific American,
By Simon Oxenham The “cuddle chemical”. The “moral molecule”. Oxytocin has quite a reputation – but much of what we thought about the so-called “love hormone” may be wrong. Oxytocin is made by the hypothalamus and acts on the brain, playing a role in bonding, sex and pregnancy. But findings that a sniff of the hormone is enough to make people trust each other more are being called into question after a string of studies failed to replicate classic experiments. Paul Zak at the Centre for Neuroeconomic Studies in Claremont, California, made his moral molecule hypothesis famous in 2011 when he memorably squirted a syringe of the hormone into the air while delivering a TED talk. When people sniff oxytocin before playing a money-lending game, it increases how much they trust each other, he explained. But several teams have been unable to replicate his finding. Last November, Gideon Nave at the California Institute of Technology in Pasadena and his colleagues reviewed studies of oxytocin, and concluded that the effect of nasal squirts of the hormone on trust are not reliably different from zero. Nave’s team aren’t the only ones calling the moral molecule hypothesis into question. In 2012, Moïra Mikolajczak at the Catholic University of Louvain (UCL) in Belgium and her colleagues published their own seminal findings backing a link between trust and oxytocin. They found that when people filled out an anonymous questionnaire about their sex lives and fantasies, they were less likely to seal the envelopes they returned them in if given a nasal dose of oxytocin beforehand. © Copyright Reed Business Information Ltd.
Laura Glynn, Pregnancy brain typically refers to lapses in attention and memory. About 80 percent of new mothers report difficulties remembering things that once came naturally, and although not all studies support this, the weight of the evidence shows that during pregnancy, women exhibit measurable declines in important cognitive skills. But it's not all bad news. The maternal brain also features important enhancements. Mother rats score higher in tests of attention, foraging and planning than peers who have never given birth. These gains most likely render them better able to defend and provide for their pups. The benefits for human moms are less clear, but data are emerging that suggest human pregnancies initiate neural restructuring. A 2010 study found that in the first few months after giving birth, human females show changes in several key brain regions. Specifically, they often exhibit increased volume in the hypothalamus, striatum and amygdala—areas essential for emotional regulation and parental motivation—as well as in regions governing decision making and protective instincts. We can glean further evidence from behavioral changes during pregnancy. Many women exhibit blunted physiological and psychological responses to stress, which may afford mother and fetus protection from the potentially adverse effects of taxing situations. And in the postpartum period, the hormones that sustain breast-feeding maintain these dampened stress responses. © 2016 Scientific American
By Jordana Cepelewicz Everyone is familiar with the complaints of a hungry stomach. For years, scientists attributed the gnawing increase in appetite before a meal to ghrelin, a hormone which is secreted in the gut and circulates in the blood, playing a role in food intake and storage. Researchers have found that levels of ghrelin, dubbed the “hunger hormone,” peak before meals and recede after eating. Given its association with appetite, ghrelin is a tempting drug target for potential obesity treatments—but findings thus far have not lived up to expectations. Experiments that knock out the genes coding for ghrelin and its single receptor, GHSR (growth hormone secretagogue receptor), have been inconclusive: Remove the hormone or receptor, and rodents used in the experiments do not necessarily lose their drive to eat. Now a team of researchers at the French Institute of Health and Medical Research (INSERM) in Paris believe that scientists have had it wrong all along. In a study published this week in Science Signaling, they report that ghrelin does not enhance appetite in rats but rather increases weight gain and fat buildup. Unlike in earlier work, in the new study the researchers used a novel genetic method that kept the ghrelin receptor functional but modified it to have greater signaling in response to ghrelin—in other words, the receptor would enhance the hormone’s effects. The team then performed a series of experiments, first in isolated cells and then in rats. As expected, exposing ghrelin to modified receptors prompted a more potent response compared with the unaltered GHSR. © 2016 Scientific American
By Lisa Sanders, M.D. On Thursday we challenged Well readers to take on the case of a 59-year-old woman who had not been able to stop gaining weight. I presented the case as it was presented to the doctor who made the diagnosis and asked for the final piece of data provided by the patient as well as the correct cause of her symptoms. I thought the tough part of this case was something that few of my readers would have to contend with – that her complaints and past medical history were quite ordinary. Like many of us, she was overweight and she came to the doctor because she had difficulty losing weight. In the background she also had high blood pressure, obstructive sleep apnea and low back pain, knee pain and leg swelling. These are some of the most common reasons patients seek medical attention. Although her problems were run of the mill, the cause was not. And many of you had no difficulty spotting this zebra. The correct diagnosis was… Acromegaly The last piece of data, provided by the patient, was a photograph taken several years before. It was only by seeing the changes in the patient’s face that had occurred over the past few years that the doctor recognized that this patient’s problem was unusual. The first person to make this diagnosis was Dr. Clare O’Connor, a physician in the second year of her training in internal medicine. She plans to subspecialize in endocrinology. She says it was the swollen legs that didn’t compress that gave her the first clue. Well done. Acromegaly is a rare disease caused by an excess of growth hormone, usually due to a tumor in the pituitary gland of the brain. The disease’s name, from the Greek, serves as a fitting description of the most obvious symptoms: great (mega) extremity (akron). The tumor secretes a protein called growth hormone that signals the liver to produce a substance called insulin-like growth factor 1, or IGF 1, which in turn tells cells throughout the body to start proliferating. © 2016 The New York Times Company
By GINA KOLATA More than a million men have smeared testosterone gels on their bodies in recent years, hoping it would rejuvenate them, energize them, and increase their libido. But until now, there has never been a rigorous study asking if there were any real benefits to testosterone therapy for healthy men with so-called low T. The first results of such research were published Wednesday in The New England Journal of Medicine. Although it found at best modest benefits, mostly in sexual functioning, it is a landmark study, said Dr. Eric S. Orwoll, a professor of medicine at Oregon Health and Science University, because it provides the first credible data on testosterone’s effects on some of the problems it is thought to resolve. Some doctors said they hoped the modest results might bring some sanity to the testosterone frenzy of recent years. “Frankly,” said Dr. Sundeep Khosla, a dean at the Mayo Clinic College of Medicine, “there is a lot of abuse.” Men lured by advertisements seek the drug, and Dr. Khosla said he had heard of doctors who prescribed it without first measuring the man’s testosterone levels to see if they were low. “What I hope is that this will bring a more conservative approach,” Dr. Orwoll said. “There is a lot of prescribing out there, and it doesn’t look like, for the average man, it will have a big effect.” The study, led by the Perelman School of Medicine at the University of Pennsylvania and funded by the National Institutes of Health and AbbVie, the maker of the testosterone gel AndroGel, involved 790 men 65 and older with low testosterone levels for their age. Testosterone levels normally fall as men age, but these men had levels on the low end — below 275 nanograms per deciliter of blood. Some of the men said they had lost their sexual drive, others said they were walking much slower than they used to, and others said they just felt blah, as if they had lost their zest for life. The men were randomly assigned to use AndroGel or a placebo for a year. © 2016 The New York Times Company
By Darryl Fears Flushed down toilets, poured down sinks and excreted in urine, a chemical component in the pill wafts into sewage systems and ends up in various waterways where it collects in fairly heavy doses. That's where fish soak it up. A recent survey by the U.S. Geological Survey found that fish exposed to a synthetic hormone called 17a-ethinylestradiol, or EE2, produced offspring that struggled to fertilize eggs. The grandchildren of the originally exposed fish suffered a 30 percent decrease in their fertilization rate. The authors mulled the impact of what they discovered and decided it wasn't good. "If those trends continued, the potential for declines in overall population numbers might be expected in future generations," said Ramji Bhandari, a University of Missouri assistant research professor and a visiting scientist at USGS. "These adverse outcomes, if shown in natural populations, could have negative impacts on fish inhabiting contaminated aquatic environments." The study, with Bhandari as lead author, also determined that the chemical BPA, used widely in plastics, had a similar effect on the small Japanese medaka fish used for the research. The medaka was chosen because it reproduces quickly so that scientists can see results of subsequent generations faster than slow reproducing species such as smallmouth bass.
By Darryl Fears For male smallmouth bass, sex change is increasingly not an option. In the chemical-laced Chesapeake Bay watershed and in rivers up through New England, it comes with the territory. Based on the latest U.S. Geological Survey on intersex fish, 85 percent of male smallmouth bass in waters in and around national wildlife refuges in the Northeast have developed "characteristics of the opposite sex." That's in addition to 90 percent of the species in some West Virginia waters and 50 percent to 100 percent in the southern stretch of the Potomac River. All of the affected fish had eggs where their testes should be, according to previous studies. Why this is happening remains a mystery, says the lead author of a new study, despite the problem being detected more than a decade ago. “It is not clear what the specific cause of intersex is in these fish,” said Luke Iwanowicz, a USGS research biologist. “This study was designed to identify locations that may warrant further investigation." The strongest suspicion focuses on what is poured down the drains of homes, businesses and farms every day. Scientists are worried that prescription drugs such as birth control and mood-control pharmaceuticals, flushed down toilets, and chemical pesticides such as atrazine, washed off farms by rain, have turned creeks, streams and rivers into chemical soups that disrupt the endocrines of marine life.
By Roni Caryn Rabin Melatonin has been shown to be effective in randomized clinical trials — the kind considered the gold standard in medicine — but it may work better for some sleep problems than others. “There is pretty strong evidence it’s effective for jet lag,” said D. Craig Hopp, a program director at the National Center for Complementary and Integrative Health, part of the National Institutes of Health. But “the evidence is more equivocal for chronic things like insomnia.” A 2002 Cochrane review that analyzed 10 randomized trials, most of them comparing oral melatonin to placebo, concluded that melatonin is “remarkably effective in preventing or reducing jet lag.” It not only helped people fall asleep faster and sleep more soundly, but also led to less daytime fatigue and improved general well-being. Eight of the 10 trials found that taking melatonin for several days after arriving at a destination reduced jet lag from flights crossing at least five time zones. In many of the trials, people also took melatonin on the day of the flight or for several days before the trip, usually in the late afternoon or early evening. Once at the destination, melatonin should be taken close to bedtime, aiming for the local hours between 10 p.m. and midnight. Doses of 0.5 milligrams and 5 milligrams were both effective, though people fell asleep faster and slept better with the larger dose. For others with insomnia, melatonin has more modest benefits. A 2013 analysis that looked at 19 randomized controlled trials involving 1,683 subjects determined that on average, melatonin reduced the amount of time it took to fall asleep by seven minutes when compared with placebo and increased total sleep time by eight minutes. © 2015 The New York Times Company
Love a sugar hit? Your sweet tooth may hail from an unlikely source: your liver. A hormone made by the organ appears to control how much carbohydrate and sugar we want to eat, and helps slow us down when we are overindulging. The hormone, called FGF21, has already been found to help obese mice lose weight and regain their sensitivity to insulin. A modified form is currently in clinical trials to test whether it has the same effect in people with diabetes. Our bodies break down carbohydrates into sugars such as sucrose, glucose and fructose. Recent genetic studies have suggested that people with altered levels of FGF21 consume more carbohydrates. To find out more, a team co-led by Matthew Potthoff at the University of Iowa observed the eating habits of mice with either abnormally high or low levels of the hormone. They found that mice genetically modified to lack the hormone chose to drink much higher levels of sugar-sweetened drinks than normal mice. Those given an extra dose of the hormone, on the other hand, reduced their sugar intake. The team also showed that the hormone is produced in response to high carbohydrate levels; it then enters the bloodstream, where it sends a signal to the brain to suppress our sugar intake. In people, blood levels of FGF21 triple 24 hours after a spike in blood sugar levels. When monkeys were given the synthetic version of the hormone being tested in clinical trials, they also opted for a diet low in sugar, according to a separate study by Steven Kliewer at the University of Texas Southwestern Medical Center at Dallas and colleagues. The team also found that these monkeys consumed less alcohol than those that weren’t given the compound. © Copyright Reed Business Information Ltd.
By SINDYA N. BHANOO Prairie voles are small Midwestern rodents known for monogamous behavior. But some males are also known to stray and seek out other females. A new study reports that mating preferences in the voles are linked to genetic differences, and that both monogamous and nonmonogamous males are readily found in nature. The study appears in the journal Science. Generally, animal neuroscientists believe that natural selection minimizes genetic variation. In this case, however, one mating strategy does not seem to be more successful than the other. Monogamous males stay near their nests, which ensures that female mates remain faithful. Promiscuous males have more partners, but they also lose sight of their own mates. “When you roam, your own female is free to mate with whoever she wants,” said Steven M. Phelps, a neurobiologist at the University of Texas at Austin and one of the study’s authors. The genetic differences between nonmonogramous and monogamous males affect a part of the brain important for spatial memory. Good memory may help a male keep track of his mate or keep him from returning to a hostile male’s territory. “We’ve shown for the first time that not only can brains be variable, but natural selection can keep that variability around,” Dr. Phelps said. © 2015 The New York Times Company