Chapter 7. Life-Span Development of the Brain and Behavior
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By PAM BELLUCK The risk of developing dementia is decreasing for people with at least a high school education, according to an important new study that suggests that changes in lifestyle and improvements in physical health can help prevent or delay cognitive decline. The study, published Wednesday in The New England Journal of Medicine, provides the strongest evidence to date that a more educated population and better cardiovascular health are contributing to a decline in new dementia cases over time, or at least helping more people stave off dementia for longer. The findings have implications for health policy and research funding, and they suggest that the long-term cost of dementia care may not be as devastatingly expensive as policy makers had predicted, because more people will be able to live independently longer. There are wild cards that could dampen some of the optimism. The study participants were largely white and suburban, so results may not apply to all races and ethnicities. Still, a recent study showed a similar trend among African-Americans in Indianapolis, finding that new cases of dementia declined from 1992 to 2001. The 2001 participants had more education, and although they had more cardiovascular problems than the 1992 participants, those problems were receiving more medical treatment. Another question mark is whether obesity and diabetes, which increase dementia risk, will cause a surge in dementia cases when the large number of overweight or diabetic 40- and 50-year-olds become old enough to develop dementia. © 2016 The New York Times Company
By CARL ZIMMER The Zika virus has quickly gained Ebola-level notoriety as it has spread through the Western Hemisphere in recent months. Researchers in Brazil, where it was first detected in May, have linked infections in pregnant women to a condition known as microcephaly: infants born with undersize heads. Where birth defects are concerned, however, the Zika virus is far from unique. A number of other viruses, such as rubella and cytomegalovirus, pose a serious risk during pregnancy. Researchers have uncovered some important clues about how those pathogens injure fetuses — findings that are now helping to guide research into the potential link between Zika and microcephaly. “I think we’ll discover a lot of parallels,” said Dr. Mark R. Schleiss, the director of pediatric infectious diseases and immunology at the University of Minnesota Medical School. The risk that viruses pose during pregnancy came to light in the mid-1900s, when outbreaks of rubella, or German measles, led to waves of birth defects, including microcephaly, cataracts and deformed hearts and livers. The number of infants affected was staggering. In an epidemic in Philadelphia in 1965, 1 percent of all babies were born with congenital rubella syndrome, which can also cause deafness, developmental disability, low birth weight and seizures. Because of vaccinations, such devastation is now rare in the United States and a number of other countries. “I’m 52, and I’ve seen one case of congenital rubella syndrome,” said Dr. David W. Kimberlin, a professor of pediatrics at the University of Alabama at Birmingham. But the virus is still a grave threat in developing countries. Worldwide, more than 100,000 children are born each year with congenital rubella syndrome. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 21883 - Posted: 02.10.2016
By Nicholas Bakalar Eating seafood is linked to a reduced risk of dementia-associated brain changes in people who carry the ApoE4 gene variation, which increases the risk for Alzheimer’s disease. Eating seafood was not linked to similar changes in those who carried other forms of the ApoE gene. The study, published in JAMA, looked at 286 autopsied brains and also found that eating seafood was linked to increased mercury in the brain, but that mercury levels were not linked to brain abnormalities. After controlling for age, sex, education and other factors, the researchers found that compared with those who ate less seafood, ApoE4 carriers who had one seafood meal or more a week had lower densities of the amyloid plaques and neurofibrillary tangles typical of Alzheimer’s disease. Over all, they had a 47 percent lower likelihood of having a post-mortem diagnosis of Alzheimer’s. Consumption of fish oil supplements was not correlated with pathological brain changes. The lead author, Martha Clare Morris, a professor of epidemiology at Rush University, said that mercury from fish appears to pose little risk for aging people. But, she said, there are studies that show that mercury consumption in pregnancy can cause cognitive problems in babies. “Most studies in dementia have found that one seafood meal a week is beneficial,” she said, though “they haven’t found that the more you eat, the lower the risk.” © 2016 The New York Times Company
Link ID: 21879 - Posted: 02.10.2016
Laura Sanders A preliminary report from scientists at the biotech company Amgen Inc. questions a cancer drug’s ability to fight Alzheimer’s disease. In experiments described February 4 in F1000Research, bexarotene, a drug approved by the FDA to treat lymphoma, didn’t reduce levels of the Alzheimer’s-related amyloid-beta protein. In the original work, described in Science in 2012 (SN: 3/10/12, p. 5), neuroscientist Gary Landreth of Case Western Reserve University in Cleveland and colleagues showed that bexarotene swiftly clears A-beta from the brains of mice, reducing both the sticky plaques and smaller forms of the protein that circulate in the brain. The mice also showed signs of improved learning and memory. A year after that work appeared, four reports, also in Science, disputed some of those findings. In tests on rats, the Amgen scientists found that bexarotene didn’t drop levels of plaques or smaller forms of A-beta. The new study didn’t describe behavioral tests. Landreth points out that this study, and previous experiments that failed to find a benefit, used a formulation of the drug that wouldn’t persist at high enough levels in the brain to be useful. “The controversy with the preclinical data is going to go away in the face of solid clinical trials,” Landreth says. A small clinical trial published online January 29 in Alzheimer’s Research & Therapy found that bexarotene reduced A-beta in the brains of people, but only people without a particular version of the ApoE gene, a known risk factor for Alzheimer’s. © Society for Science & the Public 2000 - 2016
Link ID: 21871 - Posted: 02.09.2016
By Jesse Singal On paper, Dr. Kenneth Zucker isn’t the sort of person who gets suddenly and unceremoniously fired. For decades, the 65-year-old psychologist had led the Child Youth and Family Gender Identity Clinic (GIC), in Toronto, one of the most well-known clinics in the world for children and adolescents with gender dysphoria — that is, the feeling that the body they were born with doesn’t fit their true gender identity. Zucker had built up quite a CV during his time leading the clinic: In addition to being one of the most frequently cited names in the research literature on gender dysphoria and gender-identity development, and the editor of the prestigious journal Archives of Sexual Behavior, he took a leading role helping devise diagnostic and treatment guidelines for gender dysphoric and transgender individuals. He headed the group which developed the DSM-5’s criteria for its “gender dysphoria” entry, for example, and also helped write the most recent “standards of care” guidelines for the World Professional Association for Transgender Health — one of the bibles for clinicians who treat transgender and gender-dysphoric patients. An impressive career, yes, but it’s doubtful any of this gave him much comfort on December 15. That was when he was called in from vacation for an 8:30 a.m. meeting with his employer, the Centre for Addiction and Mental Health (CAMH), one of the largest mental health and addiction research hospitals in Canada. Given the long-brewing investigation of his clinic by the hospital, it’s unlikely Zucker was feeling optimistic about what awaited him in downtown Toronto. The GIC, which operates out of CAMH, pronounced “Cam-H,” had been standing firm against a changing tide in the world of psychological treatment for children with gender dysphoria. The “gender-affirmative” approach, which focuses on identifying young transgender children and helping them socially transition — that is, express their gender to others through their everyday clothes, name changes, or other means — has been on the rise in recent years, and has become the favored protocol of many activists and clinicians. GIC clinicians, who saw clients between ages 3 and 18, had a much more cautious stance on social transitioning for their younger clients — they believed that in many cases, it was preferable to first “help children feel comfortable in their own bodies,” as they often put it, since in the GIC’s view gender is quite malleable at a young age and gender dysphoria will likely resolve itself with time. © 2016, New York Media LLC
By Jonathan Leo Last week, according to many media accounts, scientists from Harvard Medical School, Boston Children’s Hospital, and the Broad Institute discovered the genetic basis of schizophrenia. The researchers reported in Nature that people with schizophrenia were more likely to have the overactive forms of a gene called complement component 4, or C4, which is involved in pruning synapses during adolescence. However, suggesting a biologic mechanism for a small subset of those diagnosed with schizophrenia is not the same as confirming the genetic theory of schizophrenia. Benedict Carey, science reporter for the New York Times, delved into the details and reported the all-important fact that having the C4 variant would increase a person’s risk by about 25 percent over the 1-percent base rate of schizophrenia—that is, to 1.25 percent. Genes for schizophrenia and depression have been discovered before, and in those cases, the subsequent enthusiastic headlines were shortly followed by retractions and more sober thinking. There are so many open questions (for instance, why do many people with the problematic variant not develop schizophrenia, and why do many people who don’t have the variant develop schizophrenia?) that the same may occur with the C4 discovery. The idea that mental illness is the result of a genetic predisposition is the foundation for modern-day psychiatry and has been the driving force for how research money is allocated, how patients are treated, and how society views people diagnosed with conditions identified in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Schizophrenia holds a unique spot in the annals of mental health research because of its perceived anatomical underpinnings and is often cited as evidence in favor of a genetic predisposition to other conditions.
By Susana Martinez-Conde Take a look at the red chips on the two Rubik cubes below. They are actually orange on the left and purple on the right, if you look at them in isolation. They only appear more or less equally red across the images because your brain is interpreting them as red chips lit by either yellow or blue light. This kind of misperception is an example of perceptual constancy, the mechanism that allows you to recognize an object as being the same in different environments, and under very diverse lighting conditions. Constancy illusions are adaptive: consider what would have happened if your ancestors thought a friend became a foe whenever a cloud hid the sun, or if they lost track of their belongings–and even their own children—every time they stepped out of the cave and into the sunlight. Why, they might have even eaten their own kids! You are here because the perceptual systems of your predecessors were resistant to annoying changes in the physical reality–as is your own (adult) perception. There are many indications that constancy effects must have helped us survive (and continue to do so). One such clue is that we are not born with perceptual constancy, but develop it many months after birth. So at first we see all differences, and then we learn to ignore certain types of differences so that we can recognize the same object as unchanging in many varied scenarios. When perceptual constancy arises, we lose the ability to detect multiple contradictions that are nevertheless highly noticeable to young babies. © 2016 Scientific American
Mo Costandi The human brain is immediately recognizable by its cortex (meaning bark in Latin), the prominent outer layer of tissue, with its characteristic pattern of ridges and furrows, which sits atop the deep structures. The cortex is just several millimetres thick, but has a surface area of about two-and-a-half square feet, and is therefore heavily convoluted so it can be packed into the skull. This fleshy landscape begins to form during the second trimester of pregnancy, and continues into the first year of life. It is often assumed to be the result of genetics, like most other aspects of brain development. Forty years ago, however, Harvard researchers put forward the controversial idea that the brain folds up because of physical forces, and a new study now provides the first evidence this. According to this old model, the brain’s folds form as a result of differential growth which causes the cortex to grow in size far more quickly than other brain structures, leading it to buckle and fold as its surface area increases, due to the constraints of the skull. To test this, Tuomos Tallinen of the University of Jyväskylä in Finland and his colleagues used magnetic resonance images to create a 3D-printed cast of an unfolded 22-week-old human brain. This was made with a technique called layer-by-layer drop casting, and consisted of a soft polymer core coated with a thin sheet of an absorbent elastomer gel representing the cortex. © 2016 Guardian News and Media Limited
Keyword: Development of the Brain
Link ID: 21857 - Posted: 02.04.2016
By Jonathan Webb Science reporter, BBC News Scientists have reproduced the wrinkled shape of a human brain using a simple gel model with two layers. They made a solid replica of a foetal brain, still smooth and unfolded, and coated it with a second layer which expanded when dunked into a solvent. That expansion produced a network of furrows that was remarkably similar to the pattern seen in a real human brain. This suggests that brain folds are caused by physics: the outer part grows faster than the rest, and crumples. Such straightforward, mechanical buckling is one of several proposed explanations for the distinctive twists and turns of the brain's outermost blanket of cells, called the "cortex". Alternatively, researchers have suggested that biochemical signals might trigger expansion and contraction in particular parts of the sheet, or that the folds arise because of stronger connections between specific areas. "There have been several hypotheses, but the challenge has been that they are difficult to test experimentally," said Tuomas Tallinen, a soft matter physicist at the University of Jyväskylä in Finland and a co-author of the study, which appears in Nature Physics. "I think it's very significant... that we can actually recreate the folding process using this quite simple, physical model." Humans are one of just a few animals - among them whales, pigs and some other primates - that possess these iconic undulations. In other creatures, and early in development, the cortex is smooth. The replica in the study was based on an MRI brain scan from a 22-week-old foetus - the stage just before folds usually appear. © 2016 BBC.
Keyword: Development of the Brain
Link ID: 21848 - Posted: 02.02.2016
By CATHERINE SAINT LOUIS The images pouring out of Brazil are haunting: struggling newborns with misshapen heads, cradled by mothers who desperately want to know whether their babies will ever walk or talk. There are thousands of these children in Brazil, and scientists fear thousands more might come as the Zika virus leaps across Latin America and the Caribbean. But the striking deformity at the center of the epidemic, microcephaly, is not new: It has pained families across the globe and mystified experts for decades. For parents, having a child with microcephaly can mean a life of uncertainty. The diagnosis usually comes halfway through pregnancy, if at all; the cause may never be determined — Zika virus is only suspected in the Brazilian cases, while many other factors are well documented. And no one can say what the future might hold for a particular child with microcephaly. For doctors, the diagnosis means an ailment with no treatment, no cure and no clear prognosis. If the condition surges, it will significantly burden a generation of new parents for decades. Dr. Hannah M. Tully, a neurologist at Seattle Children’s Hospital, sees the pain regularly, particularly among expectant parents who have just been told that an ultrasound showed their child to be microcephalic: “a terrible situation with which to be confronted in a pregnancy,” she said. An estimated 25,000 babies receive a microcephaly diagnosis each year in the United States. Microcephaly simply means that the baby’s head is abnormally small — sometimes just because the parents themselves have unusually small heads. “By itself, it doesn’t necessarily mean you have a neurological problem,” said Dr. Marc C. Patterson, a pediatric neurologist at the Mayo Clinic Children’s Center in Rochester, Minn. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 21844 - Posted: 02.01.2016
By Lisa Rapaport Mothers who are obese during pregnancy have almost twice the odds of having a child with autism as women who weigh less, a U.S. study suggests. When women are both obese and have diabetes, the autism risk for their child is at least quadrupled, researchers reported online January 29 in Pediatrics. "In terms of absolute risk, compared to common pediatric diseases such as obesity and asthma, the rate of autism spectrum disorder (ASD) in the U.S. population is relatively low, however, the personal, family and societal impact of ASD is enormous," said senior study author Dr. Xiaobin Wang, a public health and pediatrics researcher at Johns Hopkins University in Baltimore. About one in 68 children have ASD, according to the U.S. Centers for Disease Control and Prevention, or about 1.5 percent of U.S. children. The study findings suggest the risk rises closer to about 3 percent of babies born to women who are obese or have diabetes, and approaches 5 percent to 6 percent when mothers have the combination of obesity and diabetes. Wang and colleagues analyzed data on 2,734 mother-child pairs followed at Boston Medical Center between 1998 and 2014. Most of the children, 64 percent, weren't diagnosed with any other development disorders, but there were 102 kids who did receive an ASD diagnosis. © 2016 Scientific American
By Mitch Leslie Identical twins may be alike in everything from their eye color to their favorite foods, but they can diverge in one important characteristic: their weight. A new study uncovers a molecular mechanism for obesity that might explain why one twin can be extremely overweight even while the other is thin. Heredity influences whether we become obese, but the genes researchers have linked to the condition don’t explain many of the differences in weight among people. Identical twins with nonidentical weights are a prime example. So what accounts for the variation? Changes in the intestinal microbiome—the collection of bacteria living in the gut—are one possibility. Another is epigenetic changes, or alterations in gene activity. These changes occur when molecules latch on to DNA or the proteins it wraps around, turning sets of genes “on” or “off.” Triggered by factors in the environment, epigenetic modifications can be passed down from one generation to the next. This type of transmission happened during the Hunger Winter, a famine that occurred when the Germans cut off food supplies to parts of the Netherlands in the final months of World War II. Mothers who were pregnant during the famine gave birth to children who were prone to obesity decades later, suggesting that the mothers’ diets had a lasting impact on their kids’ metabolism. However, which epigenetic changes in people promote obesity remains unclear. © 2016 American Association for the Advancement of Science
By BENEDICT CAREY Scientists reported on Wednesday that they had taken a significant step toward understanding the cause of schizophrenia, in a landmark study that provides the first rigorously tested insight into the biology behind any common psychiatric disorder. More than two million Americans have a diagnosis of schizophrenia, which is characterized by delusional thinking and hallucinations. The drugs available to treat it blunt some of its symptoms but do not touch the underlying cause. The finding, published in the journal Nature, will not lead to new treatments soon, experts said, nor to widely available testing for individual risk. But the results provide researchers with their first biological handle on an ancient disorder whose cause has confounded modern science for generations. The finding also helps explain some other mysteries, including why the disorder often begins in adolescence or young adulthood. “They did a phenomenal job,” said David B. Goldstein, a professor of genetics at Columbia University who has been critical of previous large-scale projects focused on the genetics of psychiatric disorders. “This paper gives us a foothold, something we can work on, and that’s what we’ve been looking for now, for a long, long time.” The researchers pieced together the steps by which genes can increase a person’s risk of developing schizophrenia. That risk, they found, is tied to a natural process called synaptic pruning, in which the brain sheds weak or redundant connections between neurons as it matures. During adolescence and early adulthood, this activity takes place primarily in the section of the brain where thinking and planning skills are centered, known as the prefrontal cortex. People who carry genes that accelerate or intensify that pruning are at higher risk of developing schizophrenia than those who do not, the new study suggests. Some researchers had suspected that the pruning must somehow go awry in people with schizophrenia, because previous studies showed that their prefrontal areas tended to have a diminished number of neural connections, compared with those of unaffected people. © 2016 The New York Times Company
By Ellen Hendriksen This topic comes by request on the Savvy Psychologist Facebook page from listener Anita M. of Detroit. Anita works with foster kids and, too often, sees disadvantaged kids who have been on a cocktail of psychiatric medications from as early as age 6. She asks, does such early use alter a child’s brain or body? And have the effects of lifelong psychiatric medication been studied? Childhood mental illness (and resulting medication) is equally overblown and under-recognized. Approximately 21% of American kids - that’s 1 in 5 - will battle a diagnosable mental illness before they reach the age of 17, whether or not they actually get treatment. The problem is anything but simple. Some childhood illnesses - ADHD and autism, for example - often get misused as “grab-bag” diagnoses when something’s wrong but no one knows what. This leads to overdiagnosis and sometimes, overmedicating. Other illnesses, like substance abuse, get overlooked or written off as rebellion or experimentation, leading to underdiagnosis and kids slipping through the cracks. But the most common problem is inconsistent diagnosis. For example, a 2008 study found that fewer than half of individuals diagnosed with bipolar disorder actually had the illness, while 5% of those diagnosed with something completely different actually had bipolar disorder. But let’s get back to Anita’s questions: Does early psychotropic medication alter a child’s brain? The short answer is yes, but the long answer might be different than you think. © 2016 Scientific American
Ian Sample Science editor Genetically modified (GM) monkeys that develop symptoms of autism have been created to help scientists discover treatments for the condition. The macaques carry a genetic fault that causes a rare disorder in humans called MeCP2 duplication syndrome. This produces a wide range of medical conditions, some of which mirror those seen in autism, such as difficulties with social interactions. Researchers say groups of the GM monkeys could be used to identify brain circuits involved in common autistic behaviours and to test new treatments designed to alleviate the symptoms. Because the monkeys pass the genetic defects on to their offspring, scientists can breed large populations of the animals for medical research. A group of 200 monkeys has been established at the scientists’ lab in China. The research, described in the journal Nature, paves the way for more varieties of GM monkeys that develop different mental and psychiatric problems which are almost impossible to study in other animals. “The first cohort of transgenic monkeys shows very similar behaviour to human autism, including increased anxiety, but most importantly, defects in social interactions,” said Zilong Qiu who led the research at the Institute of Neuroscience in Shanghai. © 2016 Guardian News and Media Limited or it
Alison Abbott For the second time in four months, researchers have reported autopsy results that suggest Alzheimer’s disease might occasionally be transmitted to people during certain medical treatments — although scientists say that neither set of findings is conclusive. The latest autopsies, described in the Swiss Medical Weekly1 on 26 January, were conducted on the brains of seven people who died of the rare, brain-wasting Creutzfeldt–Jakob disease (CJD). Decades before their deaths, the individuals had all received surgical grafts of dura mater — the membrane that covers the brain and spinal cord. These grafts had been prepared from human cadavers and were contaminated with the prion protein that causes CJD. But in addition to the damage caused by the prions, five of the brains displayed some of the pathological signs that are associated with Alzheimer’s disease, researchers from Switzerland and Austria report. Plaques formed from amyloid-β protein were discovered in the grey matter and blood vessels. The individuals, aged between 28 and 63, were unusually young to have developed such plaques. A set of 21 controls, who had not had surgical grafts of dura mater but died of sporadic CJD at similar ages, did not have this amyloid signature. According to the authors, it is possible that the transplanted dura mater was contaminated with small ‘seeds’ of amyloid-β protein — which some scientists think could be a trigger for Alzheimer’s — along with the prion protein that gave the recipients CJD. © 2016 Nature Publishing Group,
By Esther Landhuis Amid gloomy reports of an impending epidemic of Alzheimer’s and other dementias, emerging research offers a promising twist. Recent studies in North America, the U.K. and Europe suggest that dementia risk among seniors in some high-income countries has dropped steadily over the past 25 years. If the trend is driven by midlife factors such as building “brain reserve” and maintaining heart health, as some experts suspect, this could lend credence to staying mentally engaged and taking cholesterol-lowering drugs as preventive measures. At first glance, the overall message seems somewhat confusing. Higher life expectancy and falling birth rates are driving up the global elderly population. “And if there are more 85-year-olds, it’s almost certain there will be more cases of age-related diseases,” says Ken Langa, professor of internal medicine at the University of Michigan. According to the World Alzheimer Report 2015 (pdf), 46.8 million people around the globe suffered from dementia last year, and that number is expected to double every 20 years. Looking more closely, though, new epidemiological studies reveal a surprisingly hopeful trend. Analyses conducted over the last decade in the U.S., Canada, England, the Netherlands, Sweden and Denmark suggest that “a 75- to 85-year-old has a lower risk of having Alzheimer’s today than 15 or 20 years ago,” says Langa, who discussed the research on falling dementia rates in a 2015 Alzheimer’s Research & Therapy commentary (pdf). © 2016 Scientific America
Link ID: 21821 - Posted: 01.26.2016
By David Shultz A rat navigating a maze has to rank somewhere near the top of science tropes. Now, scientists report that they’ve developed an analogous test for humans—one that involves driving through a virtual landscape in a simulated car. The advance, they say, may provide a more sensitive measure for detecting early signs of Alzheimer’s disease. “I think it’s a very well-done study,” says Keith Vossel, a translational neuroscientist at the University of California, San Francisco (UCSF), who was not involved with the work. In the rodent version of the so-called Morris Maze Test, researchers fill a large cylindrical container with water and place a platform just above the waterline. A scientist then places a rat into the tank, and the rodent must swim to the platform to avoid drowning. The experimenter then raises the water level just above the height of the platform and adds a compound to the water to make it opaque. The trial is repeated, but now the rat must find the platform without seeing it, using only its memory of where the safe zone exists relative to the tank’s walls and the surrounding environment. In subsequent trials, researchers place the rat at different starting points along the tank’s edge, but the platform stays put. In essence, the task requires the rat to move to a specific but invisible location within a circular arena from different starting points. © 2016 American Association for the Advancement of Science.
Link ID: 21803 - Posted: 01.20.2016
By DONALD G. McNEIL Jr. Federal health officials on Friday advised pregnant women to postpone traveling to 13 Latin American or Caribbean countries and Puerto Rico where mosquitoes are spreading the Zika virus, which has been linked to brain damage in babies. Women considering becoming pregnant were advised to consult doctors before traveling to countries with Zika cases, and all travelers were urged to avoid mosquito bites, as were residents of Puerto Rico and the United States Virgin Islands. “We believe this is a fairly serious problem,” said Dr. Lyle R. Petersen, chief of vector-borne diseases for the Centers for Disease Control and Prevention. “This virus is spreading throughout the Americas. We didn’t feel we could wait.” The C.D.C. advisory applies to 14 Western Hemisphere countries and territories: Brazil, Colombia, El Salvador, French Guiana, Guatemala, Haiti, Honduras, Martinique, Mexico, Panama, Paraguay, Suriname, Venezuela, and the Commonwealth of Puerto Rico. It applies to the entire countries “unless there is specific evidence the virus is not occurring somewhere,” Dr. Petersen said. This appears to be the first time the Centers for Disease Control and Prevention has advised pregnant women to avoid a specific region. The warning is expected to affect the travel industry and could affect the Summer Olympics, set for Brazil in August. Officials at Brazil’s Health Ministry were not available for comment Friday night. Hours earlier, Philip Wilkinson, a spokesman for the Rio 2016 organizing committee, said that Olympic venues “will be inspected on daily basis during the Rio 2016 Games to ensure there are no puddles of stagnant water and therefore minimize the risk of coming into contact with mosquitos.” Dr. Petersen said he did not want to speculate about how his agency’s warning might affect the Olympics. “This is a dynamic situation,” he said. “We’re going to wait and see how this all plays out. Viruses can spread in a population for some periods of time.” © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 21792 - Posted: 01.16.2016
Laura Beil When Elinor Sullivan was a postdoctoral fellow at Oregon Health & Science University in Portland, she set out to explore the influence of food and exercise habits on obesity. In one experiment, she and her colleagues fed a troop of macaque monkeys regular chow. Other macaques dined American-style, with a hefty 32 percent of calories from fat and ready access to peanut butter treats. Over time, the second group of monkeys grew noticeably fatter. Then they all had babies. Sullivan, now at the University of Portland, noticed odd behavior in the plump moms’ offspring. At playtime, they often slinked off by themselves. When handled by keepers, the infants tended to vocalize anxiously, and the males became aggressive. They were prone to repetitive habits, like pacing. In their carefully controlled world, the only difference between those monkeys and others at the facility was their mothers’ extra pounds and indulgent diet. The behavior was so striking that Sullivan changed the course of her research. “It made me start thinking about human children,” she says, and the twin epidemics of obesity and behavioral problems such as attention-deficit/hyperactivity disorder. Her research, published in 2010 in the Journal of Neuroscience, was one of the first studies to note that the progeny of female monkeys eating a high-fat diet were more likely to experience altered brain development and suffer anxiety. Not long after, researchers worldwide began compiling evidence linking the heaviness of human mothers to mental health in their children. One headline-grabbing study of more than 1,000 births, reported in 2012, found that autism spectrum disorders showed up more often in children of obese mothers than in normal-weight women (SN: 5/19/12, p. 16). © Society for Science & the Public 2000 - 2015.