Chapter 5. Hormones and the Brain
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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
Laura Sanders Taking a pregnancy hormone staves off multiple sclerosis relapses, a small clinical trial suggests. The results hint at a potential therapy for women who suffer from MS, a debilitating disease in which the body’s immune system attacks the insulation that wraps around nerve cell fibers. A curious observation kicked off this line of research: Pregnancy offers a temporary reprieve for women with MS. Since that discovery, in the 1990s, scientists have been testing whether certain pregnancy hormones might combat MS in women who aren’t pregnant. In addition to a standard MS drug, 164 women with MS received either a placebo or estriol, an estrogen made by the placenta that peaks toward the end of pregnancy. After two years, women who received estriol had an average of 0.25 relapses a year, while women who received the placebo had 0.37 relapses a year, UCLA neurologist Rhonda Voskuhl and colleagues write online November 24 in Lancet Neurology. Researchers don’t know whether estriol would have similar effects in men with MS. The results warrant a larger clinical trial, the authors say. An accompanying commentary in the same issue of Lancet Neurology questions the results, though. MS specialist Annette Langer-Gould of Kaiser Permanente in Pasadena, Calif., raises methodological issues and writes that pregnancy comes with a host of changes that could be responsible for protection from MS. © Society for Science & the Public 2000 - 2015.
By Hanae Armitage CHICAGO, ILLINOIS—When prairie voles choose a mate, there’s no turning back—the “love chemical” oxytocin increases in their brains and they devote themselves to only each other. Although scientists have observed the behavioral and chemical side of prairie vole love, the neural networks behind commitment are still a mystery. Now, a group of scientists are working toward clearing up the neuronal backdrop of long-term love, and yesterday, presented their findings here at the annual meeting of the Society for Neuroscience. Studies have long suggested the nucleus accumbens, a part of the brain involved in reward processing, plays a crucial role in this type of devotion. To get a better look at the neuronal activity of this region, the scientists mounted a small-scale microscope that monitors calcium flux on top of a male prairie vole’s head (the more calcium into the neuron, the more neuronal activity). They saw that when male prairie voles interacted with their special lady vole, neuronal activity in the nucleus accumbens jumped 20% compared with when they interacted with a random female. Upon closer inspection, scientists saw that specific neurons that fired when the voles interacted with their mates stayed silent when they interacting with a different female. The result, though preliminary, indicates that mates stimulate the brain’s reward center in ways that nonmates cannot. © 2015 American Association for the Advancement of Science.
Sara Reardon Naked mole rats are among the ugliest creatures in the animal kingdom, and they engage in acts that seem repulsive — such as eating one another’s, and their own, faeces. Now researchers have found one biological motivation for this behaviour. When a queen mole rat’s subordinates feed on her hormone-filled faeces, the resulting oestrogen boost causes the beta rats to take care of the queen’s pups, according to results presented on 18 October at the Society for Neuroscience meeting in Chicago, Illinois. Like bees, naked mole rats live in eusocial colonies, with only one queen rat and a few males that can reproduce. The rest of the colony consists of dozens of infertile subordinates that help with tasks such as foraging and defending the nest. The subordinate rats also take care of the queen’s pups as though the babies were their own: they build the nests, lick the pups and keep them warm with their body heat. Because they have no mature sex organs, subordinate rats cannot produce the hormones that would usually drive parenting behaviour. To look at what generates the rats’ caring ways, animal biologist Akiyuki Watarai and behavioural scientist Takefumi Kikusui at Azabu University in Japan played recordings of crying mole-rat pups to subordinate rats. Animals whose queens had just given birth paid more attention to the crying than those from other groups, suggesting that the pregnancy itself triggered subordinates’ maternal instincts. © 2015 Nature Publishing Group
Susan Milius Bachelor prairie voles can’t tell females of their species apart. Yet the clueless fellows can change, forming pair-bonds for life with the opposite sex and even distinguishing between two female strangers. Bachelors aren’t blind or stupid; they recognize individual males among their fellow short-tailed Microtus ochrogaster rodents scurrying through old fields in the center of North America. And males are certainly interested in the interchangeable females. In lab tests, bachelors claw and bite at cage dividers between the sexes, says Alexander Ophir of Cornell University. Conquering the divide and mating with a female after just six hours of her company can form a lifelong pair-bond between voles. Only about 5 percent of mammal species live this socially monogamous lifestyle, and the voles have played starring roles in studies of the neurobiology of bonding. (Social monogamists, including both voles and some Homo sapiens, don’t entirely forgo extra-pair encounters.) A pair-bonded couple can crowd three litters of young into their roughly six to nine months of life in the wild, Ophir says. One aid to speeding through family life: Females can get pregnant as soon as they give birth. “You sometimes see pups being delivered as males are trying to copulate with the female,” he says. Pair-bonding requires recognizing at least one female. “It’s all well and good to fall in love, but if you don’t know who you fell in love with, it’s worthless,” Ophir says. And paired-up voles can go further. Tests show they notice the difference between two females they have never mated with, Ophir and former student Tomica Blocker report in the October Animal Behaviour. © Society for Science & the Public 2000 - 2015
By Puneet Kollipara The list of health problems that scientists can confidently link to exposure to hormone-disrupting chemicals has grown to include diabetes, cardiovascular disease, and obesity, a new scientific statement suggests. The statement, released today by the Endocrine Society, also adds support to the somewhat controversial idea that even minute doses of these chemicals can interfere with the activity of natural hormones, which play a major role in regulating physiology and behavior. But the report—which updates a similar statement released in 2009—is drawing sharp criticism from the chemical industry. An executive summary of the new statement, which synthesizes 1300 studies on endocrine disrupters, posits that scientists are more confident than ever before in linking these substances to a host of known health issues, including reproductive and developmental problems, thyroid impairment, certain reproductive cancers, and neurodevelopmental problems such as decreased IQ. But studies suggest those links can now be extended to heart and weight problems, and diabetes, says the executive summary's first author, Andrea C. Gore, a professor of pharmacology and toxicology at the University of Texas, Austin. Six years ago, scientists couldn’t make such a strong case for those links, Gore says, because there weren’t enough good studies. “But this has really been an emerging field where there is much stronger evidence now,” Gore told reporters today on a conference call. Still, some toxicologists and industry groups have long disputed the assertion that endocrine disrupters can trigger effects at minimal doses; this idea can be tough to test in lab animals, which are usually exposed to high doses in toxicology studies. © 2015 American Association for the Advancement of Science
Nancy Shute There have been suggestions that low levels of vitamin D might be a factor in cognitive decline and Alzheimer's disease, but there's no proof that the lack of D is actually causing the problems. A study published Monday doesn't prove that link, but it does find that people with low levels of vitamin D lost key thinking skills more quickly than people with enough. The study is notable because of the diversity of the participants: 62 percent were women, 30 percent were African-American, 25 percent Hispanic and 41 percent white. Most earlier studies looking at cognitive decline and vitamin D were in white people. The participants lived in California's Sacramento Valley and were mostly in their 70s when they entered the study. The researchers followed up with them for about five years, having them take annual neurological exams and neuropsychological testing at the University of California, Davis, Alzheimer's Disease Center. Most of the 382 people in the study were low on vitamin D, tested by measuring 25-hydroxyvitamin D in the blood. One-quarter of the participants were deficient in vitamin D, and 35 percent had levels deemed insufficient. That's not a surprise — most older people are below the "adequate" level of 20 to less than 50 ng/ml, often because they're not outside much. And most of the people in the study weren't getting the recommended three servings of dairy foods daily that could help. © 2015 NPR
By Elizabeth Landau Ask a physician what the hormone vasopressin is good for, and she will explain that it regulates the volume of water in your body and also affects blood pressure. But since the 1990s, vasopressin has been a hot topic in a very different field: social behavior. And recently it has emerged as a possible target for treating autism spectrum disorders (ASD), which are characterized by social, behavioral and communication impairments. The research is still in early stages, however, and has yielded more questions than answers. Given that one out of 68 children in the U.S. has an autism spectrum disorder, researchers are scrambling to figure out what in the brain might be related to the symptoms, and how they might design an effective treatment. Vasopressin may be a key player in the disorder. But scientists do not yet know whether too much or too little of the hormone—or perhaps some combination of both—is tied to autism. New clinical trials may yield insights. “I think that the work is exciting and important” says Suma Jacob, who leads an autism research laboratory at the University of Minnesota. “I also think we still have a lot more work to do in this field as a whole.” Previous research has shown that vasopressin, like the hormone oxytocin, is associated with parenting behavior and social bonding, including falling in love. In fact, the two hormones are structurally very similar, and there are receptors in the brain that interact with both of them. But high levels of vasopressin are also associated with anxiety and aggression. Intriguingly, some animal studies have found that higher levels of vasopressin increased aggression specifically in males. © 2015 Scientific American
By Melinda Wenner Moyer As many as four out of every five pregnant women say that they suffer from “pregnancy brain”—deficits in memory and cognitive ability that arise during pregnancy, making women more forgetful and slow-witted. Yet studies on the phenomenon have generally not supported these claims: although some have found evidence of problems on certain types of tasks, others, including a recent paper published by researchers in Utah, have found no signs of cognitive problems at all. Some experts believe that pregnancy brain and its postnatal cousin, “baby brain,” could largely be a product of confirmation bias: pregnant women and new moms expect to experience brain fog and therefore believe they are actually affected. Others argue that the mental symptoms might simply be too difficult to confirm in a laboratory setting. In the most recent study, researchers at Brigham Young University gave cognitive and neuropsychological tests to 21 women in their third trimester of pregnancy and then tested them again six months after they gave birth. They administered the same tests at similar intervals to 21 women who had never been pregnant. They found no differences between the groups no matter when they were tested, including before and after giving birth. These findings mesh with those from a 2003 study, which found that pregnant women did not score differently from nonpregnant women on tests of verbal memory, divided attention and focused attention. “There is variety in the results, but overall most studies suggest there are few to no memory impairments associated with pregnancy,” says Michael Larson, a psychologist at Brigham Young and a co-author of the recent paper. He thinks the reason the myth persists may be that women selectively look for evidence that supports the cultural expectation. © 2015 Scientific American
A placebo can make you feel a little better – and now we know how to boost the effect. Drugs based on hormones that make us more cooperative seem to enhance the placebo effect. The finding could lead to changes in the way some trials are performed. Sometimes a sugar pill can be all you need, even when you know it doesn’t contain any medicine. We’re still not entirely sure why. The brain’s natural painkillers, such as dopamine and opioids, seem to be involved, but other factors may be at work too. Evidence that a compassionate, trustworthy carer can speed recovery suggests that there is also a social dimension to the placebo effect. “This interaction between the patient and care provider seems to be based on a more complex system,” says Luana Colloca at the University of Maryland in Baltimore. Hormones that modulate our social behaviour might play a role. Last year, a team led by Ulrike Bingel of the University Duisburg-Essen in Germany, found that oxytocin – the so-called “cuddle chemical” that is thought to help us trust, bond and form relationships – seems to boost the placebo effect, at least in men. In the study, Bingel’s team applied an inert ointment to the arms of male volunteers. Half of them were told that the cream would reduce the degree of pain caused by the painfully hot stimulus subsequently applied. Men who were told that they were receiving pain relief said that the heat was less painful than those who knew that the cream was inert. When oxytocin was squirted up volunteers’ noses, the men reported being in even less pain. The team didn’t test oxytocin in women. © Copyright Reed Business Information Ltd.
By Esther Landhuis The birth of a child leaves its mark on the brain. Most investigations of these changes have focused on mothers, but scientists have recently begun looking more closely at fathers. Neural circuits that support parental behaviors appear more robust in moms a few weeks after the baby is born, whereas in dads the growth can take several months. A study in Social Neuroscience analyzed 16 dads several weeks after their baby's birth and again a few months later. At each check, the researchers administered a multiple-choice test to check for signs of depression and used MRI to image the brain. Compared with the earlier scans, MRI at three to four months postpartum showed growth in the hypothalamus, amygdala and other regions that regulate emotion, motivation and decision making. Furthermore, dads with more growth in these brain areas were less likely to show depressive symptoms, says first author Pilyoung Kim, who directs the Family and Child Neuroscience Lab at the University of Denver. Although some physiological brain changes are similar in new moms and dads, other changes seem different and could relate to the roles of each parent, says senior author James Swain, a psychiatrist at the University of Michigan (brain diagrams below). A 2014 behavioral study of expectant fathers showed that midpregnancy ultrasound imaging was a “magic moment” in the dads' emerging connection with their baby. Yet the emotional bond was different than it is in expectant moms. Instead of thinking about cuddling or feeding the baby, dads-to-be focused on the future: they imagined saving money for a college fund or walking down the aisle at their daughter's wedding. © 2015 Scientific American
By Sarah Schwartz Researchers have developed a chemical that transforms into a powerful hormone once inside a rat — but only in the brain, not the body. A protein in rats’ brains turns a chemical nicknamed DHED into the hormone estrogen, scientists report July 22 in Science Translational Medicine. This targeted treatment could provide estrogen to the brain and avoid potentially dangerous side effects in the body, the researchers say. “This is an interesting breakthrough,” says neuroendocrinologist Bruce McEwen of the Rockefeller University in New York City. The idea of treatments that affect the brain but not the body, or the body but not the brain, could be useful in treating a number of conditions, including cancer, he says. But the implications of this study for hormone replacement therapy in women is up for debate, a number of researchers say. In menopausal women or those who have had their ovaries surgically removed, lack of estrogen in the brain can cause symptoms such as hot flashes and sleep disturbances. Taking estrogen can relieve those symptoms but can cause side effects in the rest of the body, including an increased risk of certain cancers. The chemical DHED is nearly identical to natural human estrogen, but it has an extra oxygen atom. A specialized protein found in rodents’ brains recognizes the chemical and chops off the oxygen, turning DHED into estrogen. The body’s other organs lack this protein, so they can’t turn DHED into estrogen, says study author Laszlo Prokai, a chemical biologist at the University of North Texas Health Science Center in Fort Worth. © Society for Science & the Public 2000 - 2015.
Helen Shen In April 2011, Robert Froemke and his team were reprogramming the brains of virgin mice with a single hormone injection. Before the treatment, the female mice were largely indifferent to the cries of a distressed baby, and were even known to trample over them. But after an injection of oxytocin, the mice started to respond more like mothers, picking up the mewling pup in their mouths. Froemke, a neuroscientist at New York University's Langone Medical Center in New York City, was monitoring the animals' brains to find out why that happened. At first, the mice showed an irregular smattering of neural impulses when they heard the baby's cries. Then, as the oxytocin kicked in, the signal evolved into a more orderly pattern typical of a maternal brain. The study showed in unusual detail how the hormone changed the behaviour of neurons1. “Oxytocin is helping to transform the brain, to make it respond to those pup calls,” Froemke says. Oxytocin has been of keen interest to neuroscientists since the 1970s, when studies started to show that it could drive maternal behaviour and social attachment in various species. Its involvement in a range of social behaviours2, including monogamy in voles, mother–infant bonding in sheep, and even trust between humans, has earned it a reputation as the 'hug hormone'. “People just concluded it was a bonding molecule, a cuddling hormone, and that's the pervasive view in the popular press,” says Larry Young, a neuroscientist at Emory University in Atlanta, Georgia, who has been studying the molecule since the 1990s. “What we need to start thinking about is the more fundamental role that oxytocin has in the brain.” © 2015 Nature Publishing Group,