By Clare Wilson Just one in 10 babies exposed to the Zika virus during pregnancy get the brain damage that causes microcephaly – abnormally small heads. Now there’s a first clue about what stops this from happening in the rest – their gene activity. Blood samples were taken from three pairs of non-identical twins in Brazil. In each of these pairs, one baby had brain damage and the other didn’t. Stem cells were then made from their blood cells, and matured into brain cells, allowing researchers to see how the brain cells naturally differ between the twins. They found that, in the babies that developed microcephaly, the brain cells seem to innately make less of three particular proteins. The genes that encode these proteins are all known to be involved in normal neural development. When the team exposed these brain cells to Zika virus, they were also more susceptible to infection than ones made from the blood of their twins. Spreading to the US It may be possible to use this finding to develop a test for pregnant women that will tell them if their fetuses are particularly susceptible to Zika infection and microcephaly, says Mayana Zatz of the University of São Paulo in Brazil. Zika began causing an epidemic of brain damage in South America after it spread to the continent from Asia in 2013. But cases in Brazil dropped sharply last year, perhaps because most people there are now immune. © Copyright New Scientist Ltd.

Keyword: Development of the Brain
Link ID: 24603 - Posted: 02.02.2018

By C. CLAIBORNE RAY Q. Does an octopus have a brain? Where is it? And just how smart is an octopus? A. In a sense, an octopus has several brains, collections of neurons that control each arm. A famous 2001 study in the journal Science described how the commands that control one arm’s movement continue even when connections to the walnut-sized central processing system in the head are severed. Since then, more has been found about why the octopus is so much smarter than the average seafood. Even the relatively small central brain of an octopus is the largest among all invertebrates — proportionally, that is. A review article in 2015 in the journal Current Opinion in Neurobiology summarized the complexity of learning processes in the octopus and its remarkable adaptability. Some studies have examined the cephalopod’s ability to discern objects of different sizes, shapes, colors, brightnesses and textures; and its problem-solving, including the ability to navigate mazes and open jars. The creature also displays both short-term and long-term memory and recall over periods of weeks and even months. A possible explanation of the advanced abilities of the octopus lies in its very large genome, decoded in 2015 in a study in the journal Nature. The researchers surmised that the vast expansion of certain gene families in the octopus, and the network of linkages among the genes, could account for the development of its neurological complexity. © 2018 The New York Times Company

Keyword: Evolution; Learning & Memory
Link ID: 24602 - Posted: 02.02.2018

Jon Hamilton Scientists have found specialized brain cells in mice that appear to control anxiety levels. The finding, reported Wednesday in the journal Neuron, could eventually lead to better treatments for anxiety disorders, which affect nearly 1 in 5 adults in the U.S. "The therapies we have now have significant drawbacks," says Mazen Kheirbek, an assistant professor at the University of California, San Francisco and an author of the study. "This is another target that we can try to move the field forward for finding new therapies." But the research is at an early stage and lab findings in animals don't always pan out in humans. The discovery of anxiety cells is just the latest example of the "tremendous progress" scientists have made toward understanding how anxiety works in the brain, says Joshua Gordon, director of the National Institute of Mental Health, which helped fund the research. "If we can learn enough, we can develop the tools to turn on and off the key players that regulate anxiety in people," Gordon says. Anxiety disorders involve excessive worry that doesn't go away. These disorders include generalized anxiety disorder, panic disorder and social anxiety disorder. Kheirbek and a team including several researchers from Columbia University discovered the cells in the hippocampus, an area of the brain known to be involved in anxiety as well as navigation and memory. © 2018 npr

Keyword: Emotions; Stress
Link ID: 24601 - Posted: 02.01.2018

By Bret Stetka For the most part, clinical trials in Alzheimer’s disease have been woefully disappointing—failed drug after failed drug. Even colossal drugmaker Pfizer announced earlier this month that it will stop pursuing treatments for the disorder out of scientific and financial frustration. Yet a Japanese study published Jan. 31 in Nature reports on a screening test that could improve the success of Alzheimer’s drug research. The new findings suggest a simple blood test can accurately predict levels of a protein called amyloid beta in the brain that begins appearing early in the course of the disease before symptoms appear. Amyloid buildup is a key pathological feature of Alzheimer’s, and determining the degree to which someone’s brain is riddled with the molecule is essential for designing effective clinical trials. At the moment the only way to accurately measure amyloid in a living person is either via costly positron emission tomography imaging (PET scan) or by sampling cerebrospinal fluid (CSF) with a lumbar puncture, or spinal tap. A blood test would offer a cheaper, far less invasive means of determining a patient’s amyloid status. This could encourage more patients to enter clinical trials. It could also help researchers distinguish people with brewing Alzheimer’s from those with other forms of dementia. Senior study author Katsuhiko Yanagisawa, director general of the National Center for Geriatrics and Gerontology in Japan, is convinced that enough amyloid penetrates the blood–brain barrier to make its way into the bloodstream to be a useful measure of cognitive function. “We think amyloid blood tests could replace costly, invasive amyloid tests, especially when it comes to detecting preclinical Alzheimer’s,” he says. “We hope our biomarker better facilitates clinical trials for [Alzheimer’s] by improving enrollment of participants.” © 2018 Scientific American

Keyword: Alzheimers
Link ID: 24600 - Posted: 02.01.2018

Carl Zimmer In September 1944, trains in the Netherlands ground to a halt. Dutch railway workers were hoping that a strike could stop the transport of Nazi troops, helping the advancing Allied forces. But the Allied campaign failed, and the Nazis punished the Netherlands by blocking food supplies, plunging much of the country into famine. By the time the Netherlands was liberated in May 1945, more than 20,000 people had died of starvation. The Dutch Hunger Winter has proved unique in unexpected ways. Because it started and ended so abruptly, it has served as an unplanned experiment in human health. Pregnant women, it turns out, were uniquely vulnerable, and the children they gave birth to have been influenced by famine throughout their lives. When they became adults, they ended up a few pounds heavier than average. In middle age, they had higher levels of triglycerides and LDL cholesterol. They also experienced higher rates of such conditions as obesity, diabetes and schizophrenia. By the time they reached old age, those risks had taken a measurable toll, according to the research of L.H. Lumey, an epidemiologist at Columbia University. In 2013, he and his colleagues reviewed death records of hundreds of thousands of Dutch people born in the mid-1940s. They found that the people who had been in utero during the famine — known as the Dutch Winter Hunger cohort — died at a higher rate than people born before or afterward. “We found a 10 percent increase in mortality after 68 years,” said Dr. Lumey. The patterns that Dr. Lumey and his colleagues documented are not disputed, but scientists still are struggling to understand how they come about. “How on earth can your body remember the environment it was exposed to in the womb — and remember that decades later?” wondered Bas Heijmans, a geneticist at Leiden University Medical Center in the Netherlands. © 2018 The New York Times Company

Keyword: Epigenetics; Development of the Brain
Link ID: 24599 - Posted: 02.01.2018

Sara Reardon The research chimpanzees owned or supported by the US National Institutes of Health (NIH) are ready to retire — but nearly 300 are still stuck in 3 US research facilities, awaiting spots at the country’s only federally funded sanctuary. Moving has proved too much for some of the chimps that have already been relocated, most of which were elderly or had chronic diseases. And in the wake of multiple deaths of sanctuary newcomers between 2015 and 2016, the agency is now rethinking how it assesses the primates’ fitness for travel. The NIH will form a working group to develop recommendations for veterinarians to consider when determining whether or not to move a chimpanzee, said James Anderson, director of the NIH’s Division of Program Coordination, Planning, and Strategic Initiatives, at an advisory-council meeting on 26 January in Bethesda, Maryland. “We will move every chimp that is possible while respecting its welfare,” Anderson told the group. The announcement suggests that the NIH might be reassessing its chimp-retirement plans, which have been criticized by scientists who want to continue using the animals in non-invasive research, and by groups who think that the agency is moving too slowly on relocation. Only 78 have been transferred to the sanctuary since 2015. Under US law, the government’s retired chimps can be moved only to a federally funded sanctuary, and just one such facility exists: Chimp Haven in Keithville, Louisiana. According to the NIH’s retirement plans, all of its chimps would be relocated to the sanctuary by 2026 (see ‘Research chimpanzees’). © 2018 Macmillan Publishers Limited,

Keyword: Animal Rights
Link ID: 24598 - Posted: 02.01.2018

By NICHOLAS BAKALAR Having migraine headaches increases the risk for cardiovascular diseases, a new study has found. Using the Danish National Patient Registry, researchers matched 51,032 people with migraines, 71 percent of them women, with 510,320 people in the general population without migraines. The subjects were, on average, age 35 at the start of the study, and researchers followed them for 19 years. The absolute risk for cardiovascular disease was small, unsurprising in a group this young. Nevertheless, after adjustment for other variables, over the course of the study people with migraines had a 49 percent increased chance of heart attack, and roughly double the risk of stroke. They also had a 59 percent increased risk of a blood clot in their veins. These risks were even higher in the first year after a migraine diagnosis. The observational study, in BMJ, found no association of migraine with peripheral artery disease or heart failure. “We now have accumulating evidence that migraine is a risk factor for cardiovascular disease. It’s important to take it into consideration,” said the lead author, Dr. Kasper Adelborg, a postdoctoral researcher at Aarhus University. “And it’s important to find out if the agents that prevent migraine could also reduce the burden of cardiovascular disease.” © 2018 The New York Times Company

Keyword: Stroke; Pain & Touch
Link ID: 24597 - Posted: 02.01.2018

Susan Milius Ready for sketch comedy she’s not. But a 14-year-old killer whale named Wikie has shown promise in mimicking strange sounds, such as a human “hello” — plus some rude noises. Scientists recorded Wikie at her home in Marineland Aquarium in Antibes, France, imitating another killer whale’s loud “raspberry” sounds, as well as a trumpeting elephant and humans saying such words as “one, two, three.” The orca’s efforts were overall “recognizable” as attempted copies, comparative psychologist José Zamorano Abramson of Complutense University of Madrid and colleagues report January 31 in Proceedings of the Royal Society B. Just how close Wikie’s imitations come to the originals depends on whether you’re emphasizing the rhythm or other aspects of sound, Abramson says. Six people judged Wikie’s mimicry ability, and a computer program also rated her skills. She did better at some sounds, like blowing raspberries and saying “hello-hello,” than others, including saying “bye-bye.” Imitating human speech is especially challenging for killer whales. Instead of vocalizing by passing air through their throats, they sound off by forcing air through passageways in the upper parts of their heads. It’s “like speaking with the nose,” Abramson says. The research supports the idea that imitation plays a role in how killer whales develop their elaborate dialects of bleating pulses. Cetaceans are rare among mammals in that, like humans, they learn how to make the sounds their species uses to communicate. © Society for Science & the Public 2000 - 2017

Keyword: Animal Communication; Language
Link ID: 24596 - Posted: 01.31.2018

By GRETCHEN REYNOLDS When a teenager is hit in the head, his brain can begin to show signs, within days, of the kind of damage associated with degenerative brain disease, according to an unsettling new study of young men and head injuries. The findings, which also involve tests with animals, indicate that this damage can occur even if the hit does not result in a full-blown concussion. With the Super Bowl taking place on Sunday, the issue of head impacts is on many of our minds. It is well known, of course, that some deceased football players’ brains have shown tissue damage and spreading clumps of a protein called tau that can strangle and kill brain cells. This brain condition, called chronic traumatic encephalopathy, or C.T.E., is thought to be caused by blows to the head, including the kind of impacts that occur frequently during tackle football and other contact sports. These impacts often lead to a concussion, a brain injury characterized by a multitude of symptoms, such as headaches, dizziness, wobbly balance and changes in attention and memory. For many of us who watch, play or are the parents of young athletes in contact sports, concussions are a great and growing concern. But surprisingly little is conclusively known about the relationships between head impacts, concussions and C.T.E., or about how quickly or slowly a head injury might begin to shade into early signs of disease. Those precise questions have gripped a large and distinguished group of scientists at Boston University School of Medicine and many other institutions around the world. These researchers were among the first to identify C.T.E. in the brains of football players and later in soldiers who had experienced blast injuries to their heads. Their work has established strong links between such hits to the head and later C.T.E. But for the small new study, which was published recently in Brain, they hoped to learn more about how and how quickly such injuries might contribute to the disease. © 2018 The New York Times Company

Keyword: Brain Injury/Concussion; Development of the Brain
Link ID: 24595 - Posted: 01.31.2018

By Micah Johnson Charles Whitman lived a fairly unremarkable life until August 1, 1966, when he murdered 16 people including his wife and mother. What transformed this 25-year-old Eagle Scout and Marine into one of modern America’s first and deadliest school shooters? His autopsy suggests one troubling explanation: Charles Whitman had a brain tumor pressing on his amygdala, a region of the brain crucial for emotion and behavioral control. Can murder really be a symptom of brain disease? And if our brains can be hijacked so easily, do we really have free will? Neuroscientists are shedding new light on these questions by uncovering how brain lesions can lead to criminal behavior. A recent study contains the first systematic review of 17 known cases where criminal behavior was preceded by the onset of a brain lesion. Is there one brain region consistently involved in cases of criminal behavior? No—the researchers found that the lesions were widely distributed throughout different brain regions. However, all the lesions were part of the same functional network, located on different parts of a single circuit that normally allows neurons throughout the brain to cooperate with each other on specific cognitive tasks. In an era of increasing excitement about mapping the brain’s “connectome,” this finding fits with our growing understanding of complex brain functions as residing not in discrete brain regions, but in densely connected networks of neurons spread throughout different parts of the brain. © 2018 Scientific American

Keyword: Aggression; Brain Injury/Concussion
Link ID: 24594 - Posted: 01.31.2018

By Clare Wilson Two thin wires implanted in the brain may help treat Alzheimer’s disease by delivering electrical current. In the first test of this technique in people, two out of the three people who received the treatment showed less of a decline in their mental abilities than people at a similar stage of the disease who didn’t have the surgery. However, a larger randomised control trial is needed to know if the treatment really does work. The technique used is called deep brain stimulation, and is already used to treat the tremors and movement problems of some people with severe Parkinson’s disease. As well as having wires surgically inserted into the brain, recipients also get a power supply for the wires implanted under the skin near their collar bones. Depending on the current, the wires can either boost activity in nearby brain cells or reduce it. In Parkinson’s disease, they are used to turn down the excessive firing of discrete clusters of nerve cells that control movement. Alzheimer’s disease, however, is a less obvious target for such a treatment, because what causes this form of dementia is unknown. There has already been a small trial of brain stimulation using wires inserted into the brain’s memory centres, but this failed to help people with the condition. © Copyright New Scientist Ltd.

Keyword: Alzheimers
Link ID: 24593 - Posted: 01.31.2018

Robert D. Martin This may be surprising to some: A woman's age is not alone in affecting pregnancy and birth, despite the impression often given. Reviewing Paul Raeburn's book Do Fathers Matter?, Tabitha Powledge wrote: "Everybody knows that older mothers run higher risks of a baby with birth defects — Down syndrome being the most common and best-known. By comparison, hardly anybody knows that the older Dad gets, the riskier it is for him to conceive a child." Partners age together, so a fetus or baby with an older mother will mostly have an older father, too. Logic demands exploration of age effects in both sexes. Though few and far between, such studies do indeed reveal that both men and women contribute. With Down syndrome, age effects for fathers and mothers are roughly balanced. But new data clearly show that, when it comes to inherited defects, fathers actually carry greater risks than mothers. Random changes in DNA — mutations — accumulate four times faster in sperms than in eggs. Charles Darwin and Alfred Russel Wallace realized that variety is not just the spice of life; it is the very essence. Inherited differences between individuals are the raw material for natural selection. And the prime source of natural variation in genes is new mutations. These have been studied intensively, notably regarding rates of change. Yet mutation also has a dark side because it can produce adverse effects along with variety. Hence, the mutation rate has fundamental implications for medical genetics as well as for evolutionary biology. © 2018 npr

Keyword: Sexual Behavior; Evolution
Link ID: 24592 - Posted: 01.31.2018

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

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

By Lauren Aguirre Just over five years ago, a man suffering from amnesia following a suspected drug overdose appeared at Lahey Hospital and Medical Center in Burlington, Massachusetts, a Boston suburb. He was 22, and had injected what he believed to be heroin. When he woke up the next morning, he was extremely confused, repeatedly asking the same questions and telling the same stories. Doctors at Lahey quickly diagnosed the man with anterograde amnesia — the inability to form new memories. “I thought it was an extremely strange [brain] scan — it was almost hard to believe.” His brain scan revealed why. “I thought it was an extremely strange scan — it was almost hard to believe,” said Jed Barash, a neurologist working at Lahey at the time. In the scan, the twin, seahorse-shaped structures of the man’s hippocampi were lit up against the dark background of the rest of the brain — a clear sign of severe injury to just that one region. “It was strange because that was all there was,” Barash said. Memory researchers have known since the late 1950s that the hippocampi are responsible for turning short-term memories into lasting ones, so the amnesia was not surprising. Just how the damage occurred, however, remained a mystery. Lack of oxygen to the brain that would have occurred during the overdose could not be the only explanation. The number of survivors in the state that year could easily have numbered in the thousands, so why was there only one patient with this seemingly unique brain damage? Along with his colleagues, Barash — now medical director at the Soldiers’ Home health care facility in Chelsea, Massachusetts — figured that the opioids must have played a role, and that hunch became only more acute as three more patients — each fitting the same pattern — appeared at Lahey over the next three years. All had the same unique destruction of the hippocampi, all had amnesia, and all were suspected to have overdosed. By that point, the doctors at Lahey faced two fundamental questions: What was causing the strange new syndrome? And precisely how rare was it? Copyright 2018 Undark

Keyword: Learning & Memory; Drug Abuse
Link ID: 24590 - Posted: 01.30.2018

LaVonne Moore has Alzheimer's disease, but her doctors hope her dementia symptoms could possibly be kept in check by a new type of treatment. Electric wires implanted deep in her brain stimulate areas involved with decision-making and problem-solving. Unlike many long-term dementia patients, LaVonne, 85, can cook meals, dress herself and organise outings. But it remains unclear whether her deep brain stimulation (DBS) therapy is responsible for her independence. DBS is already helping hundreds of thousands of patients with Parkinson's disease to overcome symptoms of tremor, but its use in Alzheimer's is still very experimental. Image copyright Ohio State University Only a small number of DBS studies have been done for Alzheimer's and they have focused on stimulating brain regions governing memory, rather than judgement. But Dr Douglas Scharre and colleagues at the Ohio State University Wexner Medical Center believe their approach, which targets the decision-making frontal lobe of the brain, might help patients keep their independence for longer. LaVonne's brain pacemaker was implanted three and a half years ago. Since then, her husband, Tom, from Delaware, Ohio, says her dementia has worsened - but more slowly than he had expected. "LaVonne has had Alzheimer's disease longer than anybody I know, and that sounds negative, but it's really a positive thing because it shows that we're doing something right." Two other patients have had the same treatment as LaVonne, but only one of them appeared to benefit significantly, according to the Journal of Alzheimer's Disease. Experts say it is too early to say if the treatment will help counteract cognitive decline. © 2018 BBC

Keyword: Alzheimers
Link ID: 24589 - Posted: 01.30.2018

By NIRAJ CHOKSHI Years of scolding from health experts about a good night’s rest may be breaking through. Americans are finally getting more sleep — about 18 minutes more per weeknight compared with 2003. It may not sound like much, but researchers say it’s a positive sign. Weeknight Sleep, in Hours Americans gained an average 1.4 minutes per year in weeknight sleep between 2003 and 2016. “If we only got more sleep, we would then see that we actually perform better and would probably be more creative and more productive during the day,” said Dr. Mathias Basner, the associate professor of sleep and chronobiology in psychiatry at the University of Pennsylvania and the lead author of the analysis of federal survey data, published this month in the journal “Sleep.” The incremental gains took place over 13 years. Dr. Basner and his colleague, Dr. David F. Dinges, found that Americans gained about 1.4 minutes of sleep per weeknight each year between 2003 and 2016. People also slept more on weekends, though the improvement was not as great — an extra 50 seconds of sleep per weekend night per year, a total gain of about 11 minutes. On average, Americans get more than eight hours of sleep on weeknights and more on weekends, according to the data. But sleep length varies widely. According to the Centers for Disease Control and Prevention, more than a third of adults get insufficient sleep, which it defines as less than seven hours. © 2018 The New York Times Company

Keyword: Sleep
Link ID: 24588 - Posted: 01.30.2018

Nearly a third of older adults don’t get solid zzz’s, according to a University of Michigan poll of 1,065 people age 65 and older. To help them sleep, 36 percent report taking a prescription drug, over-the-counter aid or a dietary supplement such as melatonin. But research suggests the benefits are modest at best. A Consumer Reports Best Buy Drugs analysis found that people taking prescription sleep medications such as Ambien (zolpidem and generic) or Lunesta (eszopiclone and generic) fell asleep only eight to 20 minutes faster than people taking a placebo. Worse, prescription sedatives and some OTC sleep aids can be risky, especially for older adults, with side effects that can include dry mouth, confusion, dizziness, next-day drowsiness, and impaired balance and coordination. Taking sleep meds may also cause dependency, increase the risk of car accidents, and more than double the risk of falls and fractures — common reasons for hospitalization and death in older adults, according to Consumer Reports’ Choosing Wisely campaign. Because of these dangers, the American Geriatrics Society includes the potent prescription sleep drugs — Ambien, Lunesta and zaleplon (Sonata) — on its list of medications that adults age 65 and older should avoid. Compounding those dangers is the tendency for many to use the medications for longer than recommended. In a 2015 Consumer Reports survey of 4,023 U.S. adults, 41 percent of people who used OTC sleep aids reported taking them for a year or longer. Most of these drugs should be taken for just a few weeks or less. That’s because mounting evidence suggests that long-term use of certain sleep meds that contain diphenhydramine, found in products including Sominex, Tylenol PM and ZzzQuil; antihistamines such as Benadryl; and some cold and cough medicines may increase the chances of dementia. © 1996-2018 The Washington Post

Keyword: Sleep; Development of the Brain
Link ID: 24587 - Posted: 01.30.2018

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

Keyword: Autism
Link ID: 24586 - Posted: 01.30.2018

By JANE E. BRODY The media love contrarian man-bites-dog stories that purport to debunk long-established beliefs and advice. Among the most popular on the health front are reports that saturated fats do not cause heart disease and that the vegetable oils we’ve been encouraged to use instead may actually promote it. But the best-established facts on dietary fats say otherwise. How well polyunsaturated vegetable oils hold up health-wise when matched against saturated fats like butter, beef fat, lard and even coconut oil depends on the quality, size and length of the studies and what foods are eaten when fewer saturated fats are consumed. So before you succumb to wishful thinking that you can eat well-marbled steaks, pork ribs and full-fat dairy products with abandon, you’d be wise to consider the findings of what is probably the most comprehensive, commercially untainted review of the dietary fat literature yet published. They are found in a 26-page advisory prepared for the American Heart Association and published last June by a team of experts led by Dr. Frank M. Sacks, professor of cardiovascular disease prevention at the Harvard T.H. Chan School of Public Health. The report helps to explain why the decades-long campaign to curb cardiovascular disease by steering the American diet away from animal fats has been less successful than it might have been and how it inadvertently promoted expanding waistlines and an epidemic of Type 2 diabetes. When people cut back on a particular nutrient, they usually replace it with something else to maintain their needed caloric input. Unfortunately, in too many cases, saturated fats — and fats in general — gave way to refined carbohydrates and sugars, the so-called SnackWell phenomenon that prompted fat-wary eaters to overindulge in high-calorie, low-nutrient foods. © 2018 The New York Times Company

Keyword: Obesity
Link ID: 24585 - Posted: 01.30.2018

Tim McDonnell Last April, Fredua Agyemang, a musician in Kumasi, Ghana, was performing onstage at a funeral, which in this country is often a festive affair with hundreds of guests. Suddenly, he began to feel dizzy, then lost consciousness and collapsed. When he woke up three days later, his bandmates broke the news: He had suffered a stroke. Immediately, he thought of another doctor visit eight years earlier, when, at the age of 34, he had been diagnosed with hypertension and prescribed medication to reduce his blood pressure. The medication had given him problems with erectile dysfunction, a common side effect, and he soon stopped taking it regularly. That decision seemed foolish, he recalls. He was having difficulty moving and speaking and knew that he wouldn't be back onstage anytime soon. "I still have weakness," he says, nine months later. "I'm not able to walk well, I can't use my left arm, I can't sing." Doctors found that Agyemang's stroke was hemorrhagic, meaning that a blood vessel in his brain burst from excessive pressure. In the U.S., this type of stroke is rare; nearly 90 percent of strokes in the U.S. are "ischemic," meaning they're caused by a clot or other blockage of a blood vessel in the brain. But according to a new study, the largest-ever of stroke patients in Africa, up to one-third of strokes in this area of the world are hemorrhagic. And while the survival rate for ischemic strokes is around 80 percent, for hemorrhagic strokes the odds of survival are only 50/50. Agyemang is lucky to be alive. © 2018 npr

Keyword: Stroke
Link ID: 24584 - Posted: 01.29.2018