Chapter 16. None

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By Sarah Kaplan You probably wouldn't be surprised if a scientist told you that your genes influence when you hit puberty, how tall you are, what your BMI will be and whether you're likely to develop male pattern baldness. But what if he said that the same gene could hold sway over all four things? That finding comes from a study published Monday in the journal Nature Genetics. Using data from dozens of genome-wide association studies (big scans of complete sets of DNA from many thousands of people), researchers at the New York Genome Center and the genetic analysis company 23andMe found examples of single "multitasking" genes that influence diverse and sometimes seemingly disparate traits. The scientists say that the links they uncovered could help researchers understand how certain genes work, and figure out better ways of treating some of the health problems they might control. "Most studies tend to go one disease at a time," said Joseph Pickrell, a professor at Columbia University and the New York Genome Center's lead investigator on the project. "But if we can try to make these sorts of connections between what you might think of as unrelated traits ... that gives us another angle of attack to understand the connections between these different diseases." To start, Pickrell and his team sought out genome-wide association studies (GWAS) identifying particular genetic variants associated with 42 different traits. Many had to do with diseases (for example, studies that linked certain genes to the risk of developing Alzheimer's or type 2 diabetes) and other personal health traits (body mass index, blood type, cholesterol levels).

Keyword: Genes & Behavior
Link ID: 22225 - Posted: 05.18.2016

A bionic body is closer than you think By Dwayne Godwin, Jorge Cham Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2016 Scientific American

Keyword: Robotics
Link ID: 22222 - Posted: 05.17.2016

By JONATHAN BALCOMBE Washington — IN March, two marine biologists published a study of giant manta rays responding to their reflections in a large mirror installed in their aquarium in the Bahamas. The two captive rays circled in front of the mirror, blew bubbles and performed unusual body movements as if checking their reflection. They made no obvious attempt to interact socially with their reflections, suggesting that they did not mistake what they saw as other rays. The scientists concluded that the mantas seemed to be recognizing their reflections as themselves. Mirror self-recognition is a big deal. It indicates self-awareness, a mental attribute previously known only among creatures of noted intelligence like great apes, dolphins, elephants and magpies. We don’t usually think of fishes as smart, let alone self-aware. As a biologist who specializes in animal behavior and emotions, I’ve spent the past four years exploring the science on the inner lives of fishes. What I’ve uncovered indicates that we grossly underestimate these fabulously diverse marine vertebrates. The accumulating evidence leads to an inescapable conclusion: Fishes think and feel. Because fishes inhabit vast, obscure habitats, science has only begun to explore below the surface of their private lives. They are not instinct-driven or machinelike. Their minds respond flexibly to different situations. They are not just things; they are sentient beings with lives that matter to them. A fish has a biography, not just a biology. Those giant manta rays have the largest brains of any fish, and their relative brain-to-body size is comparable to that of some mammals. So, an exception? Then you haven’t met the frillfin goby. © 2016 The New York Times Company

Keyword: Intelligence; Evolution
Link ID: 22221 - Posted: 05.16.2016

Dara Mohammadi As the small motorboat chugs to a halt, three travellers, wind-beaten from the three-hour journey along the Atrato river, step on to the muddy banks of Bellavista, an otherwise inaccessible town in the heart of the heavily forested north-west of Colombia. They swing their hessian bags – stuffed with bedsheets, dried beans and cuddly toys – to their shoulders and clamber up a dusty path. Tucked inside the bag of one of the travellers, neuropsychologist Sonia Moreno, is the reason they are here: a wad of unfinished, hand-drawn charts of family trees. The people whose names are circled on the charts have Huntington’s disease, an incurable genetic brain disorder that usually starts between the ages of 35 and 45 years. It begins with personality changes that can make them aggressive, violent, uninhibited, anxious and depressed. The disease progresses slowly, robbing them first of the control of their body, which jerks and twists seemingly of its own will, and then their ability to walk, talk and think until, about 20 years after the symptoms first begin, they die. Their children, each of whom has a 50% chance of inheriting the disease, watch and wait to see if it will happen to them. It is in this way that the disease strangles families. With Moreno is Ignacio Muñoz-Sanjuan, vice president of translational biology at CHDI Foundation, a US nonprofit research organisation that aims to find ways to prevent or slow down the progression of the disease. The foundation spent $140m–$150m (£97m-£104m) on research last year, but Muñoz-Sanjuan is not here on official business. He’s here for Factor-H, an initiative he founded four years ago to help with the other end of the problem – poor families with Huntington’s struggling in Latin America. © 2016 Guardian News and Media Limited o

Keyword: Huntingtons; Movement Disorders
Link ID: 22220 - Posted: 05.16.2016

By Julia Shaw You see a crime take place. You are interviewed about it. You give a statement about what you saw. Do you think that at a later date you would be able to detect whether someone had tampered with your statement? Or re-written parts of it? This is currently a hot topic in the UK, where a very recently published inquiry into the so-called Hillsborough disaster, in which 96 people were crushed to death during a soccer match in 1989, found that testimonies had been deliberately altered by police. Research published earlier this year by the false memory dream team at the University of California, looked directly into the implications of such police (mis)conduct. They found that it is possible that changed statements can go unnoticed by the person who gave the original testimony, and may even develop into a false memory that accommodates the false account. To describe this effect, the researchers came up with the term "memory blindness"—the phenomenon of failing to recognize our own memories. The term was intended to mirror the ‘choice blindness’ literature. Choice blindness is forgetting choices that we have made. The researchers wanted to know “Can choice blindness have lasting effects on eyewitness memory?” To examine this, PhD Student Kevin Cochran and his colleagues conducted two experiments. © 2016 Scientific American

Keyword: Learning & Memory
Link ID: 22218 - Posted: 05.16.2016

By John Horgan Speakers at the 2016 Tucson consciousness conference suggested that “temporal nonlocality” or other quantum effects in the brain could account for free will. But what happens when the brain is immersed in a hot tub? This is the second of four posts on “The Science of Consciousness” in Tucson, Arizona, which lasted from April 26 to April 30. (See Further Reading for links to other posts.) Once again, I’m trying to answer the question: What is it like to be a skeptical journalist at a consciousness conference? -- John Horgan DAY 2, THURSDAY, APRIL 28. HOT TUBS AND QUANTUM INCOHERENCE Breakfast on the patio with Stuart Kauffman, who has training in… almost everything. Philosophy, medicine, science. We’ve bumped heads in the past, but we’re friendly now. In his mid-70s, Stu is still obsessed with--and hacking away at--the biggest mysteries. We talk about… almost everything. Quantum mechanics, the origin of life, materialism, free will, God, the birth and death of his daughter, the death of his wife, his re-marriage, predictability versus possibility. As Stu speaks, his magnificent, weathered face looks happy/sad, arrogant/anxious. Superposition of emotions. He tells me about his brand-new book, Humanity in a Creative Universe, in which he outlines a perspective that can help lift us out of our spiritual crisis. Who saves the savior? I scoot to a morning session, “Consciousness and Free Will.” I hope it will supply me with ammo for my defenses of free will. I can do without God, but not free will. © 2016 Scientific American, a Division of Nature America, Inc.

Keyword: Consciousness
Link ID: 22216 - Posted: 05.16.2016

By Adam Gopnik On a bitter, soul-shivering, damp, biting gray February day in Cleveland—that is to say, on a February day in Cleveland—a handless man is handling a nonexistent ball. Igor Spetic lost his right hand when his forearm was pulped in an industrial accident six years ago and had to be amputated. In an operation four years ago, a team of surgeons implanted a set of small translucent “interfaces” into the neural circuits of his upper arm. This afternoon, in a basement lab at a Veterans Administration hospital, the wires are hooked up directly to a prosthetic hand—plastic, flesh-colored, five-fingered, and articulated—that is affixed to what remains of his arm. The hand has more than a dozen pressure sensors within it, and their signals can be transformed by a computer into electric waves like those natural to the nervous system. The sensors in the prosthetic hand feed information from the world into the wires in Spetic’s arm. Since, from the brain’s point of view, his hand is still there, it needs only to be recalled to life. Now it is. With the “stimulation” turned on—the electronic feed coursing from the sensors—Spetic feels nineteen distinct sensations in his artificial hand. Above all, he can feel pressure as he would with a living hand. “We don’t appreciate how much of our behavior is governed by our intense sensitivity to pressure,” Dustin Tyler, the fresh-faced principal investigator on the Cleveland project, says, observing Spetic closely. “We think of hot and cold, or of textures, silk and cotton. But some of the most important sensing we do with our fingers is to register incredibly minute differences in pressure, of the kinds that are necessary to perform tasks, which we grasp in a microsecond from the feel of the outer shell of the thing. We know instantly, just by touching, whether to gently squeeze the toothpaste or crush the can.”

Keyword: Pain & Touch
Link ID: 22215 - Posted: 05.14.2016

By JONAH BROMWICH It’s relatively easy to determine when someone is too drunk to drive. If a driver’s blood-alcohol level is 0.08 percent or higher, that person is considered legally impaired. But a study says that measuring the effects of marijuana on drivers is far trickier, and that blood tests are an unreliable indication of impairment by cannabis. As more states consider legalizing the substance, that presents a challenge to legislators seeking to create laws on driving while impaired by marijuana. The study, commissioned by the AAA Foundation for Traffic Safety, found that laws in six states that legally assess impairment by measuring how much THC (the active ingredient in marijuana) is in a person’s blood are not supported by science. “There is no concentration of the drug that allows us to reliably predict that someone is impaired behind the wheel in the way that we can with alcohol,” said Jake Nelson, AAA’s director of traffic safety advocacy and research. Lawmakers in those states looked to policies on drunken driving for cues on how to legislate against driving while high. But the body absorbs alcohol and cannabis in different ways, the study said. While drunkenness directly correlates to alcohol in the bloodstream, cannabis impairment takes place only when THC makes its way into the fatty tissue of the brain. Regular marijuana users, including those who take the drug medicinally, often show no signs of impairment after using, according to Jolene Forman, a staff lawyer for the Drug Policy Alliance, a drug-reform advocacy group. She also said that marijuana can stay in the blood for hours, days and even weeks after its effects wear off. © 2016 The New York Times Company

Keyword: Drug Abuse
Link ID: 22214 - Posted: 05.14.2016

By Hazem Zohny Here is a picture of the nine-dot problem. The task seems simple enough: connect all nine dots with four straight lines, but, do so without lifting the pen from the paper or retracing any line. If you don’t already know the solution, give it a try – although your chances of figuring it out within a few minutes hover around 0 percent. In fact, even if I were to give you a hint like “think outside of the box,” you are unlikely to crack this deceptively (and annoyingly!) simple puzzle. And yet, if we were to pass a weak electric current through your brain (specifically your anterior temporal lobe, which sits somewhere between the top of your ear and temple), your chances of solving it may increase substantially. That, at least, was the finding from a study where 40 percent of people who couldn’t initially solve this problem managed to crack it after 10 minutes of transcranial direct current stimulation (tDCS) – a technique for delivering a painlessly weak electric current to the brain through electrodes on the scalp. How to explain this? It is an instance of the alleged power of tDCS and similar neurostimulation techniques. These are increasingly touted as methods that can “overclock” the brain in order to boost cognition, improve our moods, make us stronger, and even alter our moral dispositions. The claims are not completely unfounded: there is evidence that some people become slightly better at holding and manipulating information in their minds after a bout of tDCS. It also appears to reduce some people’s likelihood of formulating false memories, and seems to have a lasting improvement on some people’s ability to work with numbers. It can even appear to boost creativity, enhancing the ability of some to make abstract connections between words to come up with creative analogies. But it goes further, with some evidence that it can help people control their urges as well improve their mood. And beyond these psychological effects, tDCS of the part of the brain responsible for movement seems to improve muscular endurance and reduce fatigue. © 2016 Scientific American

Keyword: Learning & Memory
Link ID: 22205 - Posted: 05.11.2016

By PAM BELLUCK BALTIMORE — Leave it to the youngest person in the lab to think of the Big Idea. Xuyu Qian, 23, a third-year graduate student at Johns Hopkins, was chatting in late January with Hongjun Song, a neurologist. Dr. Song was wondering how to test their three-dimensional model of a brain — well, not a brain, exactly, but an “organoid,” essentially a tiny ball of brain cells, grown from stem cells and mimicking early brain development. “We need a disease,” Dr. Song said. Mr. Qian tossed out something he’d seen in the headlines: “Why don’t we check out this Zika virus?” Within a few weeks — a nanosecond compared with typical scientific research time — that suggestion led to one of the most significant findings in efforts to answer a central question: How does the Zika virus cause brain damage, including the abnormally small heads in babies born to infected mothers? The answer could spur discoveries to prevent such devastating neurological problems. And time is of the essence. One year after the virus was first confirmed in Latin America, with the raging crisis likely to reach the United States this summer, no treatment or vaccine exists. “We can’t wait,” said Dr. Song, at the university’s Institute for Cell Engineering, where he and his wife and research partner, Dr. Guo-Li Ming, provided a pipette-and-petri-dish-level tour. “To translate our work for the clinic, to the public, normally it takes years. This is a case where we can make a difference right away.” The laboratory’s initial breakthrough, published in March with researchers at two other universities, showed that the Zika virus attacked and killed so-called neural progenitor cells, which form early in fetal development and generate neurons in the brain. © 2016 The New York Times Company

Keyword: Development of the Brain; Neurogenesis
Link ID: 22203 - Posted: 05.11.2016

By Maia Szalavitz Both the FDA and the CDC have recently taken steps to address an epidemic of opioid overdose and addiction, which is now killing some 29,000 Americans each year. But these regulatory efforts will fail unless we acknowledge that the problem is actually driven by illicit—not medical—drug use. You’ve probably read that 80 percent of heroin users started with prescription medications—and you may have seen billboards that compare giving pain medication to children to giving them heroin. You have probably also heard and seen media stories of people with addiction who blame their problem on medical use. But the simple reality is this: According to the large, annually repeated and representative National Survey on Drug Use and Health, 75 percent of all opioid misuse starts with people using medication that wasn’t prescribed for them—obtained from a friend, family member or dealer. And 90 percent of all addictions—no matter what the drug—start in the adolescent and young adult years. Typically, young people who misuse prescription opioids are heavy users of alcohol and other drugs. This type of drug use, not medical treatment with opioids, is by far the greatest risk factor for opioid addiction, according to a study by Richard Miech of the University of Michigan and his colleagues. For this research, the authors analyzed data from the nationally representative Monitoring the Future survey, which includes thousands of students. While medical use of opioids among students who were strongly opposed to alcohol and other drugs did raise later risk for misuse, the overall risk for this group remained small and their actual misuse occurred less than five times a year. In other words, it wasn’t actually addiction. Given that these teens had generally rejected experimenting with drugs, an increased risk of misuse associated with medical care makes sense since they’d otherwise have no source of exposure. © 2016 Scientific American

Keyword: Drug Abuse
Link ID: 22202 - Posted: 05.11.2016

Aaron E. Carroll People get hooked on cigarettes, and enjoy them for that matter, because of the nicotine buzz. The nicotine doesn’t give them cancer and lung disease, though. It’s the tar and other chemicals that do the real harm. A robust debate is going on among public health officials over whether electronic cigarettes, or e-cigarettes, can alleviate the harms of smoking tobacco, or whether they should be treated as negatively as conventional cigarettes. In other countries, such as Britain, officials are more in favor of e-cigarettes, encouraging smokers to switch from conventional to electronic. Last week, the Food and Drug Administration issued new rules on e-cigarettes, banning their sale to anyone under 18 and requiring that adults under the age of 26 show a photo identification to buy them. Electronic cigarettes carry the promise of delivering the nicotine without the dangerous additives. The use of e-cigarettes by youth has increased sharply in recent years. In 2011, about 1.5 percent of high school students reported using them in the last month. In 2014, more than 12 percent of students did. That means that nearly 2.5 million American middle and high school students used them in the past month. The problem is that nicotine is generally considered less safe for children and adolescents than for adults. Poisoning is possible. It’s thought that nicotine may interfere with brain development. Most worrisome, it’s believed that becoming addicted to nicotine in any form makes smoking more likely later in life. E-cigarettes are perceived to be less harmful than conventional cigarettes, and they are thought to be useful aids to quitting. These perceptions, however, are not always fully grounded in evidence. © 2016 The New York Times Company

Keyword: Drug Abuse
Link ID: 22201 - Posted: 05.11.2016

Nancy Shute A body mass index under 25 is deemed normal and healthy, and a higher BMI that's "overweight" or "obese" is not. But that might be changing, at least when it comes to risk of death. The body mass index, or BMI, associated with the lowest risk of death has increased since the 1970s, a study finds, from 23.7, in the "normal" weight category, to 27, which is deemed "overweight." That means a person who is 5-foot-8 could weigh 180 pounds and be in that epidemiological sweet spot, according to the NIH's online BMI calculator. The results were published Tuesday in JAMA, the journal of the American Medical Association. The researchers came to that conclusion by looking at data from three studies of people in Copenhagen, one from the 1970s, one from the 1990s and one from 2003-2013. More than 100,000 people were involved. Because Denmark has an excellent national health registry, they were able to pinpoint the cause of death for every single one of those people. The risk of death for people who are obese, with a BMI of 30 or greater, also declined, to the point that it was on a par with some people of so-called "normal" weight. So being fatter, at least a bit, may be healthier. "I was surprised as a scientist to see how clear the result was," Borge Nordestgaard, a clinical professor and chief physician at Copenhagen University Hospital and senior author of the study, told Shots. So he and his colleagues sliced and diced the data to see what could account for the shift. They looked at age, sex, smoking, cancer and heart disease. The most relevant was the decline in smoking since the 1970s. But when they looked at the mortality rates in nonsmokers who had never had cancer or heart disease, it also became associated with a higher BMI over time. © 2016 npr

Keyword: Obesity
Link ID: 22200 - Posted: 05.11.2016

By Dan Kiefer I’m on the heavy bag, throwing left jabs, ignoring the relentless blare of Kanye’s “Drive Slow, Homie” played at a volume that would raise the dead. I punch to a one-two count: left jab, right cross. I’m working as hard as I’ve ever worked, and even in this unheated gym I sweat as if it’s a sauna. Finally, the bell rings. It feels as if I’ve been at it for an hour; actually, three minutes have passed. The ensuing one-minute break seems to last four seconds. Let’s be clear: Boxing, even when the opponent is only a heavy bag, is a brutal sport. But brutality is needed, even welcome, when you’re facing a progressive, incurable neurological disease. I have Parkinson’s disease, and it causes my body to just freeze up. Weirdly enough, boxing helps me get unstuck. All 12 of us in this class bear the unmistakable signs of Parkinson’s disease. I spot a dapper, cheerful white-haired fellow shaking like a leaf (tremor). Next, a balding, heavyset guy stumbling forward awkwardly on his toes (dystonia, or muscle cramping). Then I see myself in a mirror: a man in a white T-shirt, khaki shorts and Nike running shoes, standing still, seemingly paralyzed. I’m in the midst of a Parkinson’s freeze (an extreme form of bradykinesia, or slow movement). Although Parkinson’s is generally thought of as an old-person’s disease, I was diagnosed with a young-onset version 18 years ago, at age 35. Since then, I’ve taken every sort of medication known to science. I’ve had brain surgery — two tiny electrodes were implanted deep in my brain to stimulate an area affected by Parkinson’s — which unquestionably have helped treat some of my symptoms. But medicine and surgery have not cured my freezing and falling, my gait and balance issues that worsen as my disease progresses: When walking across a busy street, I may suddenly, inexplicably come to a full stop as the light is about to change. Even the slightest downhill slope of a path causes me to fall forward.

Keyword: Parkinsons
Link ID: 22198 - Posted: 05.10.2016

Chris Woolston A story about epigenetics in the 2 May issue of The New Yorker has been sharply criticized for inaccurately describing how genes are regulated. The article by Siddhartha Mukherjee — a physician, cancer researcher and award-winning author at Columbia University in New York — examines how environmental factors can change the activity of genes without altering the DNA sequence. Jerry Coyne, an evolutionary ecologist at the University of Chicago in Illinois, posted two widely discussed blog posts calling the piece “superficial and misleading”, largely because it ignored key aspects of gene regulation. Other researchers quoted in the blog posts called the piece “horribly damaging” and “a truly painful read”. Mukherjee responded by publishing a point-by-point rebuttal online. Speaking to Nature, he says he now realizes that he erred by omitting key areas of the science, but that he didn’t mean to mislead. “I sincerely thought that I had done it justice,” he says. Mukherjee’s article, ‘Same But Different’, takes a personal view of epigenetics — a term whose definition is highly contentious in the field. The story features his mother and aunt, identical twins who have distinct personalities. Mukherjee, who won a Pulitzer Prize in 2011 for his best-selling book The Emperor of All Maladies: A Biography of Cancer (Scribner, 2010), writes that identical twins differ because: “Chance events — injuries, infections, infatuations; the haunting trill of that particular nocturne — impinge on one twin and not on the other. Genes are turned on and off in response to these events, as epigenetic marks are gradually layered above genes, etching the genome with its own scars, calluses, and freckles.” The article is drawn from a book by Mukherjee that is due out later this month, called The Gene: An Intimate History (Scribner, 2016). © 2016 Nature Publishing Group

Keyword: Epigenetics; Genes & Behavior
Link ID: 22197 - Posted: 05.10.2016

by Julia Belluz and Javier Zarracina "I'm going to make you work hard," a blonde and perfectly muscled fitness instructor screamed at me in a recent spinning class, "so you can have that second drink at happy hour!" At the end of the 45-minute workout, my body was dripping with sweat. I felt like I had worked really, really hard. And according to my bike, I had burned more than 700 calories. Surely I had earned an extra margarita. The spinning instructor was echoing a message we've been getting for years: As long as you get on that bike or treadmill, you can keep indulging — and still lose weight. It's been reinforced by fitness gurus, celebrities, food and beverage companies like PepsiCo and Coca-Cola, and even public-health officials, doctors, and the first lady of the United States. Countless gym memberships, fitness tracking devices, sports drinks, and workout videos have been sold on this promise. There's just one problem: This message is not only wrong, it's leading us astray in our fight against obesity. To find out why, I read through more than 60 studies on exercise and weight loss. I also spoke to nine leading exercise, nutrition, and obesity researchers. Here's what I learned. 1) An evolutionary clue to how our bodies burn calories When anthropologist Herman Pontzer set off from Hunter College in New York to Tanzania to study one of the few remaining hunter-gatherer tribes on the planet, he expected to find a group of calorie burning machines. Unlike Westerners, who increasingly spend their waking hours glued to chairs, the Hadza are on the move most of the time. Men typically go off and hunt — chasing and killing animals, climbing trees in search of wild honey. Women forage for plants, dig up tubers, and comb bushes for berries. "They're on the high end of physical activity for any population that's been looked at ever," Pontzer said. © 2016 Vox Media, Inc

Keyword: Obesity
Link ID: 22196 - Posted: 05.09.2016

By DAN BARRY IDIOT. Imbecile. Cretin. Feebleminded. Moron. Retarded. Offensive now but once quite acceptable, these terms figured in the research for a lengthy article I wrote in 2014 about 32 men who spent decades eviscerating turkeys in a meat-processing plant in Iowa — all for $65 a month, along with food and lodging in an ancient former schoolhouse on a hill. These were men with intellectual disability, which meant they had significant limitations in reasoning, learning and problem solving, as well as in adaptive behavior. But even though “intellectual disability” has been the preferred term for more than a decade, it gave my editors and me pause. We wondered whether readers would instantly understand what the phrase meant. What’s more, advocates and academicians were recommending that I suppress my journalistic instinct to tighten the language. I was told that it was improper to call these men “intellectually disabled,” instead of “men with intellectual disability.” Their disability does not define them; they are human beings with a disability. This linguistic preference is part of society’s long struggle to find the proper terminology for people with intellectual disability, and reflects the discomfort the subject creates among many in the so-called non-disabled world. It speaks to a continuing sense of otherness; to perceptions of what is normal, and not. “It often doesn’t matter what the word is,” said Michael Wehmeyer, the director and senior scientist at the Beach Center on Disability at the University of Kansas. “It’s that people associate that word with what their perceptions of these people are — as broken, or as defective, or as something else.” For many years, the preferred term was, simply, idiot. When Massachusetts established a commission on idiocy in the mid-1840s, it appointed Dr. Samuel G. Howe, an abolitionist and early disability rights advocate, as its chairman. The commission argued for the establishment of schools to help this segment of society, but made clear that it regarded idiocy “as an outward sign of an inward malady.” © 2016 The New York Times Company

Keyword: Development of the Brain
Link ID: 22195 - Posted: 05.09.2016

By Aleszu Bajak In its May 2 issue, The New Yorker magazine published a report titled “Same But Different,” with the subhead: “How epigenetics can blur the line between nature and nurture.” The piece was written by Siddhartha Mukherjee, a physician and author of the Pulitzer prize-winning book “The Emperor of all Maladies: A Biography of Cancer.” In his New Yorker story, Mukherjee, with deft language and colorful anecdotes, examines a topic that is very much du jour in science writing: Epigenetics. Google defines epigenetics as “the study of changes in organisms caused by modification of gene expression, rather than alteration of the genetic code itself.” Merriam Webster’s definition is similar — but not exactly the same: “The study of heritable changes in gene function that do not involve changes in DNA sequence.” The slight variation in definition is telling in itself — and it’s really that “heritable” part that has sparked intense interest not just among scientists, but in the popular mind. Steven Henikoff, a molecular biologist at the Fred Hutchinson Cancer Research Center in Seattle, called Siddhartha Mukherjee’s lyrical take on epigenetics “baloney.” It’s the idea that external factors like diet, or stress or even lifestyle choices can impact not just your own genes, but the genetic information you pass down to all of your descendants. Spend your life smoking cigarettes and eating fatty foods, the thinking goes, and you’ll not just make yourself sick, you’ll predispose your offspring — and their offspring, and their offspring — to associated diseases as well. It’s heady stuff, but much of it remains speculative and poorly supported, which is where Mukherjee may have run into trouble. The publication of his story — an excerpt from his forthcoming book “The Gene: An Intimate History” — was met with swift criticism from biologists working in epigenetics and the broader field of gene regulation. They argue that Mukherjee played fast and loose with his description of epigenetic processes and misled readers by casting aside decades of research into how genes are regulated during development. Copyright 2016 Undark

Keyword: Epigenetics
Link ID: 22194 - Posted: 05.09.2016

By John Horgan Scientists trying to explain consciousness are entitled to be difficult, but what’s philosophers’ excuse? Don’t they have a moral duty to be comprehensible to non-specialists? I recently attended “The Science of Consciousness,” the legendary inquest held every two years in Tucson, Arizona. I reported on the first meeting in 1994 and wanted to see how it’s evolved since then. This year’s shindig lasted from April 26 to April 30 and featured hundreds of presenters, eminent and obscure. I arrived on the afternoon of April 27 and stayed through the closing “End-of-Consciousness Party.” The only event I regret missing is a chat between philosopher David Chalmers, who loosed his “hard problem of consciousness” meme here in Tucson in 1994, and Deepak Chopra, the New Age mogul and a sponsor of this year’s meeting. I feel obliged to post something fast, because conference organizer and quantum-consciousness advocate Stuart Hameroff complained that most reporters “come for free, drink our booze and don’t write anything.” Hameroff also generously allowed me to give a talk, “The Quest to Solve Consciousness: A Skeptic’s View,” even though I teased him in my 1994 article for Scientific American, calling him an “aging hipster.” What follows is a highly subjective account of my first day at the meeting. I’d call this a “stream-of-consciousness report on consciousness,” but that would be pretentious. I'm just trying to answer this question: What is it like to be a skeptical journalist at a consciousness conference? I’ll post on the rest of the meeting soon. -- John Horgan DAY 1, WEDNESDAY, APRIL 27. THE HOROR A bullet-headed former New York fireman picks me up at the Tucson airport. Driving to the Loews Ventana Canyon Resort, he argues strenuously that President Trump will make us great again. As we approach the resort, he back-peddles a bit, no doubt worried about his tip. I tip him well, to show how tolerant I am. Everyone’s entitled to an irrational belief or two. © 2016 Scientific American

Keyword: Consciousness
Link ID: 22193 - Posted: 05.09.2016

By Jane E. Brody Truth to tell, sometimes I don’t follow my own advice, and when I suffer the consequences, I rediscover why I offer it. I’ve long recommended drinking plenty of water, perhaps a glass with every meal and another glass or two between meals. If not plain water, which is best, then coffee or tea without sugar (but not alcoholic or sugary drinks) will do. I dined out recently after an especially active day that included about five miles of walking, 40 minutes of lap swimming and a 90-minute museum visit. I drank only half a glass of water and no other beverage with my meal. It did seem odd that I had no need to use the facilities afterward, not even after a long trip home. But I didn’t focus on why until the next day when, after a fitful night, I awoke exhausted, did another long walk and swim, and cycled to an appointment four miles away. I arrived parched, begging for water. After downing about 12 ounces, I was a new person. I no longer felt like a lead balloon. It seems mild dehydration was my problem, and the experience prompted me to take a closer look at the body’s need for water under a variety of circumstances. Although millions of Americans carry water bottles wherever they go and beverage companies like Coke and Pepsi would have you believe that every life can be improved by the drinks they sell, the truth is serious dehydration is not common among ordinary healthy people. But there are exceptions, and they include people like me in the Medicare generation, athletes who participate in particularly challenging events like marathons, and infants and small children with serious diarrhea. Let’s start with some facts. Water is the single most important substance we consume. You can survive for about two months without food, but you would die in about seven days without water. Water makes up about 75 percent of an infant’s weight and 55 percent of an older person’s weight. © 2016 The New York Times Company

Keyword: Miscellaneous
Link ID: 22192 - Posted: 05.09.2016