Chapter 5. Hormones and the Brain
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
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
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