Addiction Crisis

<p></p><p>Hear firsthand from individuals struggling with addiction and follow the cutting-edge work of doctors and scientists as they investigate why addiction is not a moral failing, but a chronic, treatable medical condition. Easy access to drugs like heroin, fentanyl, and even prescription medications like OxyContin has fueled an epidemic of addiction—the deadliest in U.S. history. Now, science is revealing how addiction affects the brain, and top experts are gathering evidence about how we should address our drug problem, from embracing evidence-based treatments, to rethinking public policies. (Premiered October 17, 2018)</p><p></p>

<p>Discover how opioid addiction affects the brain and how evidence-based treatments are saving lives.</p>

Addiction

swings-opioid-buffalo

<p>In Western New York, public health officials have organized a task force that’s giving people who suffer from opiate use disorder a new beginning.</p>

Restoring Hope: Fighting the Opioid Crisis in Buffalo

Could Cadaver Organs Save Your Life? Hero

<p>As the number of people who need organs goes up, the number of donors has plateaued, meaning we need to find new solutions. Dr. Doris Taylor and her team’s answer: custom-building organs from cadavers.</p>

<p>Custom-built lungs, livers, kidneys and hearts could someday save thousands of lives.</p>

Could Cadaver Organs Save Your Life?

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Body & Brain

Koch Foundation

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      <div class="rich-text"><p>At the start of his latest clinical trial in 2018, National Institutes of Health researcher <a href="https://www.niddk.nih.gov/about-niddk/staff-directory/biography/hall-kevin">Kevin Hall</a> was sure he wouldn’t see a difference.</p><p>His study, intended to monitor caloric intake and weight gain, offered its participants one of two nearly identical menus. Both contained the same number of calories, and comparable amounts of carbohydrates, fats, and proteins. Even the diets’ fiber, sugar, and sodium contents were matched. Nutrient-wise, they were about as similar as two meal plans could get.</p><p>But as the days ticked by, Hall quickly began to see how wrong his initial hunch had been. Despite the superficial similarities, one group was eating much more of the food they were offered. And by the end of two weeks, the members of that same group had gained an average of two pounds, while their counterparts had <i>lost</i> two pounds.</p></div>
  

  
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      <div class="rich-text"><p>The only explanation was the one factor Hall had thought would have no effect at all: While one menu was made up mostly of whole, unprocessed foods, the other—the one tied to weight gain—was composed almost entirely of ultra-processed foods.</p><p>Compared to unprocessed foods like fresh fruits and nuts, ultra-processed foods like cookies and chips tend to have more calories, sugar, fat, and salt, all of which have been linked to putting on weight. But the <a href="https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30248-7">findings</a> from Hall’s team, published today in the journal <i>Cell Metabolism</i>, are the first to show there’s something inherent to ultra-processed foods<i>,</i> independent of nutritional makeup, that seems to encourage overeating.</p><p>“This is really important work,” says <a href="https://medicine.yale.edu/psychiatry/people/dana_small.profile">Dana Small</a>, a psychologist and neuroscientist studying food choice at Yale University who was not involved in the study. “This study produces a definitive answer to a question we did not have a definitive answer to.”</p><p>Though it’s not yet clear why ultra-processed foods have this effect, the results underscore the importance of an issue that goes beyond effective dieting. With their cheapness, convenience, and long shelf life, ultra-processed foods now make up <a href="https://bmjopen.bmj.com/content/6/3/e009892">more than half the calories</a> Americans eat. These numbers tick even further upwards for <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5855172/">underrepresented minorities, as well as in lower income populations</a>.</p><p>“This is not about willpower—we’re living in a manipulated food environment,” says <a href="https://lsa.umich.edu/psych/people/faculty/agearhar.html">Ashley Gearhardt</a>, a psychologist studying food addiction at the University of Michigan who was not involved in the study. “Ultra-processed foods are unique in ways that we are only just starting to understand.”</p>
            <figure class="richtext-image full-width"><img alt="Breakfast 4.jpg" class="richtext-image full-width" height="317" width="800"
            src="/wgbh/nova/media/images/Breakfast_4.width-800.jpg"/><figcaption><p>The unprocessed and ultra-processed breakfasts (respectively) offered to study participants on Day 4. Left: A spinach, onion, and tomato omelet made with fresh eggs and olive oil, sweet potato hash, and skim milk. Right: Scrambled eggs prepared from liquid, pork sausage, honey buns, and orange juice infused with fiber. Image Credit: Courtesy of Kevin Hall, National Institutes of Health, Hall et al. 2019</p><div class="credit"><p></p></div></figcaption>
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            <p>Technically, any food that’s been mechanically or chemically altered from its original state can be considered “processed.” That label applies to milk, tofu, frozen spinach, and countless other foods that appear in our diets, and doesn’t automatically designate a product as unhealthy.</p><p><i>Ultra-</i>processed foods, on the other hand, take things one step further by including ingredients that provide cheap, “industrial” sources of dietary energy and nutrients—like added sugars, fats, and chemical preservatives—that enhance an item’s flavor, texture, or shelf life. Some offenders in the ultra-processed arena are familiar, like candy and chicken nuggets; others, like sweetened yogurts, reduced-fat salad dressing (or reduced-fat anything, for that matter), and packaged soup, might be a little more surprising.</p><p>For years, scientists have been linking ultra-processed foods to a variety of poor health outcomes, including <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5811844/">cancer</a>, <a href="https://academic.oup.com/ajcn/article/104/5/1433/4564389">obesity</a>, and even <a href="https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2723626">an increased risk of death</a>. Most of these studies, however, have been limited to questionnaires and diet records that rely on people to accurately report what they’ve eaten, and can’t establish direct cause and effect.</p><p>So Hall and his team decided to do what no other group had done before: Round up 20 people, house them at the National Institutes of Health Clinical Center, and prepare, serve, and track every single morsel of food they ate for a month. Each person was randomly assigned to either an ultra-processed or unprocessed menu for the first two weeks, then switched. Both diets consisted of three meals and a glut of snacks, providing almost 4,000 calories each day, and participants were told to eat as much or as little as they wanted.</p>
            <figure class="richtext-image full-width"><img alt="Lunch 6.jpg" class="richtext-image full-width" height="290" width="800"
            src="/wgbh/nova/media/images/Lunch_6.width-800.jpg"/><figcaption><p>The unprocessed and ultra-processed lunches (respectively) offered to study participants on Day 6. Left: Salmon, green beans with olive oil, baked sweet potato, and plain Greek yogurt with frozen strawberries. Right: Burgers with American cheese, fries, ketchup, and diet lemonade infused with fiber. Image Credit: Courtesy of Kevin Hall, National Institutes of Health, Hall et al. 2019</p><div class="credit"><p></p></div></figcaption>
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            <p>In terms of their nutritional composition, the two diets were equivalent on almost every front, down to the average number of calories per gram of food. But while ultra-processed foods had no part in the unprocessed menu, they contributed more than 80 percent of the calories in the ultra-processed diet.</p><p>It took some serious finagling to get the menus to match, while keeping the ratio of carbohydrate to fat to protein within a healthy range, Hall says. The team also had to take great pains to keep the study’s results mum as they unfolded, even outfitting participants in loose-fitting clothing to mask any weight gain or loss.</p><p>But the work paid off. In the end, the only real difference between the groups was the proportion of ultra-processed foods in their diets.</p><p>“I can’t think of another study that has been this well controlled for so long,” Gearhardt says. “That allows us to make much more confident interpretations of what these foods are really doing.” If Hall and his team saw clear differences in outcome, there would be a pretty clear culprit.</p></div>
  

  
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      <div class="rich-text"><p>But even Hall was surprised to discover how quickly changes in eating behavior unfolded. When put on the ultra-processed diet, participants started eating an average of 500 extra calories a day, resulting in several people gaining weight and body fat over the two-week stint. The difference had nothing to do with the amount of food they’d been offered, or even how good it tasted (when asked, participants reported the two menus were equally appetizing and satisfying). But the inclusion of ultra-processed food had triggered a subtle, and likely subconscious, shift in behavior.</p><p>The study was brief, and there’s no telling if these results will hold true on a longer time scale, says <a href="https://www.hsph.harvard.edu/vasanti-malik/">Vasanti Malik</a>, a nutrition researcher at the Harvard School of Public Health who was not involved in the study. To that point, the difference in the number of calories consumed on each diet actually decreased slightly as time went on. But that doesn’t make the upshot any less concerning: Something in this ultra-processed diet was making people eat more, and it didn’t take long to see the effects.</p><p>What exactly that something was, though, is still an open question. Finding the answer will require a lot more research, but Hall has a few theories.</p><p>Although both diets were similar in energy density, or the number of calories per gram, these calculations also counted drinks, including juices and lemonade that acted as vehicles for fiber supplements in the ultra-processed diet. But beverages might not make people feel full in the same way that solid food does—and when the researchers took liquids out of the equation, the solid foods on the ultra-processed menu packed in more calories per bite. This might have made it easy for people on this diet to scarf down a lot of calories, Hall says.</p><p>People also ate much faster when put on the ultra-processed diet, consuming 17 more calories per minute compared to the unprocessed diet. It takes a while for our brains to register the feeling of fullness, and this lag gives our mouths plenty of time to overeat—an easy thing to do with ultra-processed foods, which are often softer and easier to chew and swallow, Hall says.</p><p>The researchers are currently gearing up for a repeat study that might put these theories to the test. One critical change will involve revamping the ultra-processed diet to include more stews and gumbos. Hopefully, Hall says, this swap will both dilute the energy density of the solid food portion of the meal and encourage people to eat more slowly.</p>
            <figure class="richtext-image full-width"><img alt="iStock-1077073380.jpg" class="richtext-image full-width" height="533" width="800"
            src="/wgbh/nova/media/images/iStock-1077073380.width-800.jpg"/><figcaption><p>Plain yogurt is technically a &quot;processed&quot; food, but still healthful. The addition of flavors and sweeteners, however, transforms plain yogurt into an ultra-processed product. Image Credit: alexialex, iStock</p><div class="credit"><p></p></div></figcaption>
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            <p>There’s plenty to grapple with, but one needn’t see directly into the belly of the beast to know to avoid its bite. The study’s results are a resounding confirmation of years of nutritional counsel—and if anything, the problem is only getting worse.</p><p>As food production becomes increasingly industrialized, ultra-processed foods have taken over the diets of modern Americans. Even when put on diets at two extremes of a spectrum, study participants experienced a bigger change in their hormone levels when shifting to the <i>unprocessed</i> menu, suggesting that their baseline was more aligned with an ultra-processed diet.</p><p>That’s not terribly surprising, given that these products tend to be rich in fat and sugars, which set off the brain’s pleasure system, Gearhardt says. Over time, our bodies get used to the reward, and crave it in even higher quantities. This vicious cycle of addiction makes ultra-processed foods a tough habit to break.</p><p>But weaning ourselves off ultra-processed foods entirely isn’t a practical goal. The fact remains that ultra-processed foods require less time, money, and effort to purchase and consume—and they’re effectively marketed as such. In the study, the ingredients that went into the unprocessed meal plan cost nearly 50 percent more than those for the ultra-processed menu. Tacking on the hours, skills, equipment, and energy invested in the storage and preparation of perishable whole foods, it’s no wonder ultra-processed foods have become a mealtime fixture over the past 30 years, Hall says.</p>
            <figure class="richtext-image full-width"><img alt="iStock-941132318.jpg" class="richtext-image full-width" height="534" width="800"
            src="/wgbh/nova/media/images/iStock-941132318.width-800.jpg"/><figcaption><p>Whole foods, while healthful, carry a bigger price tag than ultra-processed foods—even before taking into account the added expenses of storing, preparing, and serving them. Image Credit: Vera_Petrunina, iStock</p><div class="credit"><p></p></div></figcaption>
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            <p>What’s more, because cost is such a big incentive, the burden of ultra-processed foods is <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5855172/">disproportionately shouldered</a> by people who make less money—those with the fewest means to avoid them. This trend threatens to exacerbate existing health disparities between socioeconomic brackets.</p><p>There’s no quick fix to this problem. But the path forward is with studies like these, Small says. By pinpointing the mystery factor in ultra-processed foods—whatever it is that’s causing us to eat more and gain weight—researchers might be able to partner with the food industry to cook up cheap, convenient foods that can still confer some health benefits.</p><p>In the end, “just giving people nutrition advice won’t be enough,” Gearhardt says. “We need to advocate for policy initiatives and support people’s needs. This is a social justice issue. And we’re living it right now.”</p></div>
  

  
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<p>Two groups of study participants were offered nutritionally identical diets. Those eating ultra-processed foods consumed more calories and gained weight.</p>

Ultra-Processed Foods Make Us Eat More, and It’s Not About Their Nutritional Makeup





  
      <div class="rich-text"><p>Neurons are notoriously picky. A few will fire like crazy for <a href="https://www.nature.com/articles/nature03687.epdf?referrer_access_token=SJKImQtOrPY0IWUuhZPketRgN0jAjWel9jnR3ZoTv0OT5GxW2TgiUHZmXETmpiUnUkcqRaQgND2VvyOMl2Jp7IqPMir0s4LiVdjGb0BWT8_ltEY0SUTOfl1M8IogrNEK9hFHgXZkeUizW9Sz_MMhdUfnMbAJIY-t1Had1hQ4JFH_ndU1q1DdarpSnzTYnNIH&amp;tracking_referrer=www.nature.com">Jennifer Aniston</a>, but not for Halle Berry; some pay homage to Kobe Bryant, while turning a cold shoulder to Bill Clinton.</p><p>Others still, it turns out, might prefer to party with Pokémon.</p></div>
  

  
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      <div class="rich-text"><p>According to a new <a href="https://www.nature.com/articles/s41562-019-0592-8">study</a>, people who spent their childhoods capturing, training, and battling Pokémon on a Game Boy share a region in their brains devoted solely to recognizing these nostalgic pocket monsters. The findings, published yesterday in the journal <i>Nature Human Behavior,</i> could help explain how the brain tunes into visual cues—and the ways in which information gets encoded during our early years.</p><p>Our brains are constantly being bombarded with information. To keep things straight, certain clusters of neurons will only send signals in the presence of certain triggers, like specific colors, words, objects, or faces. Not everyone reacts to the same things, but for those with common interests, these brain regions tend to be consistent across people, regardless of age, sex, or race and ethnicity. It’s not clear exactly how these pathways are set, but many seem to have their origins in childhood, when the brain is still particularly sensitive to new information.</p></div>
  

  
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      <div class="rich-text"><p>To test this idea, a team of researchers led by Jesse Gomez, a neuroscientist at Stanford University, turned to a familiar cultural juggernaut: the popular video game Pokémon, which illuminated many a Nintendo Game Boy in the 1990s. Through consistent gameplay, children worldwide had been exposed to the same set of images over and over, some for many years in a row. It was, in a sense, the perfect natural experiment.</p><p>“What was unique about Pokémon is that there are hundreds of characters, and you have to know everything about them in order to play the game successfully. The game rewards you for individuating hundreds of these little, similar‑looking characters,” <a href="https://news.stanford.edu/2019/05/06/regular-pokemon-players-pikachu-brain/">Gomez said in a statement</a>. “I figured, ‘If you don’t get a region for that, then it’s never going to happen.’’’</p><p>Gomez and his colleagues used functional magnetic resonance imaging, a technique that track blood flow, to scan the brains of 11 “experienced” and 11 “novice” Pokémon players as they gazed upon images of all 150 original Pokémon. To qualify as a Pokéveteran, the participants had to have begun playing the Nintendo game between the ages of five and eight, and played some into adulthood—criteria that Gomez himself met.</p><p>It soon became clear that Gomez’s hunch had paid off. While a specific region in the brains of experienced players consistently lit up in response to Poképics, but not to other cartoons or images, the same wasn’t true for the novice noggins. The brain region was also consistent across individuals, in a teeny, pea-sized fold located in just behind the ears, that takes in images seen with our central, rather than peripheral, vision.</p><p>That makes sense, given that most players of the Nintendo game spent their days with their eyes fixed on a tiny screen positioned roughly a foot from their face. In this way, the game provided a “unique, yet consistent, visual experience to children,” study author Kalanit Grill-Spector, a psychologist at Stanford University, <a href="https://arstechnica.com/science/2019/05/theres-a-brain-region-for-pokemon-characters-if-you-played-a-lot-as-a-kid/">told Jennifer Ouellette at <i>Ars Technica</i></a>.</p><p>This same Pokécentric brain region might also play some role in processing images of animals, which makes sense for animated characters modeled on wildlife. In a way, this hints at just how malleable and versatile the brain really is, Grill-Spector said in a statement.</p><p>The results also shouldn’t necessarily spark concern about the lasting effects of playing video games in childhood, Grill-Spector said. “The visual cortex is made up of hundreds of millions of neurons...we have the capacity to encode many, many patterns.”</p></div>
  

  
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<p>For those who still hold a special place in their hearts for Pikachu, rest assured that the brain’s getting in on some of the action, too.</p>

Pokémon Characters Activate A Special Region in the Brains of Veteran Players





  
      <div class="rich-text"><p>In 1994, physician-researcher <a href="http://www.ragoninstitute.org/portfolio-item/walker-lab/">Bruce Walker</a> was sure he’d stumbled upon the impossible.</p><p>Despite being HIV positive, the patient in his office was healthy—and had been for at least a decade, all without the help of drugs. But in a year when AIDS would <a href="https://www.amfar.org/thirty-years-of-hiv/aids-snapshots-of-an-epidemic/">kill 35,000 people</a> in the United States alone, all Walker’s patient wanted to know was when he would die, too.</p><p>Walker had no answer for him. It was the first time he had seen someone subvert what he’d been certain was a death sentence. “I was stunned,” Walker recalls. “I just thought, ‘This is unbelievable. This means HIV doesn’t kill everyone.’”</p></div>
  

  
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      <div class="rich-text"><p>In the years that followed, Walker, now a researcher at the Ragon Institute, would come to realize that this remarkable patient wasn’t a fluke. Thousands more like him existed, many of whom were completely unaware they harbored the virus in the first place—all because their immune systems had somehow kept the deadly virus in check.</p><p>This singular riddle has driven Walker’s research for the past 25 years. But at long last, he and his team think they’re close to an answer. In a <a href="https://science.sciencemag.org/cgi/doi/10.1126/science.aax4989">study</a> published today in the journal <i>Science,</i> they propose an explanation for why, despite being exposed to the same virus, some individuals control infection (“controllers”), while others progress to disease (“progressors”). [Disclosure: Walker is also a relative of NOVA’s Deputy Executive Producer, Julia Cort.]</p><p>According to the study, hitting HIV’s Achilles heel might require leveraging the “social network” that governs the virus’ structure. HIV, like all viruses, is made up of several interconnected pieces. Much like the pieces in a chess game, those parts aren’t equally influential—which means an effective immune response is likely to be one that pinpoints the most pivotal players on the board.</p><p>“This is a very elegant piece of science that could identify potential weak spots in HIV,” says <a href="https://www.med.unc.edu/microimm/directory/nilu-goonetilleke-phd/">Nilu Goonetilleke</a>, an immunologist studying HIV at the University of North Carolina’s School of Medicine who was not involved in the study. “I look forward to seeing a design for a vaccine come out of this, and, hopefully, seeing it tested.”</p>
            <figure class="richtext-image full-width"><img alt="6813396647_b6c62b8f61_o.jpg" class="richtext-image full-width" height="600" width="800"
            src="/wgbh/nova/media/images/6813396647_b6c62b8f61_o.width-800.jpg"/><figcaption><p>A scanning electromicrograph of an HIV-infected cell. Image Credit: NIAID, flickr</p><div class="credit"><p></p></div></figcaption>
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            <p>HIV is particularly tricky for the immune system to deal with. Not only does the virus infect and incapacitate some of the very immune cells that might otherwise defend against it, but it also behaves a bit like a moving target.</p><p>When on the lookout for pathogens like viruses, the immune system scours the body for foreign molecules with incriminating features—the microscopic equivalent of passing a mugshot from cell to cell. But when the HIV virus invades cells to copy its genome, it does so sloppily, accumulating so many mutations it can change the way it appears to the immune system. The HIV of one cell might look completely different from the HIV of another—and any intel the immune system might have stored can quickly become obsolete, allowing the virus to slip by unnoticed.</p><p>As it passes from person to person, the virus shapeshifts further, generating many distinct subgroups within and across populations. And protection against one version of HIV doesn’t guarantee protection against another.</p><p>In the face of such staggering diversity, an effective HIV vaccine will have to accomplish what the typical immune system cannot—recognizing the virus in all its myriad forms, says <a href="https://www.hivresearch.org/our-scientists/morgane-rolland-phd">Morgane Rolland</a>, an HIV virologist and vaccinologist at the U.S. Military HIV Research Program who was not involved in the study.</p><p>But even across vastly different strains, certain features of HIV remain the same, and don’t mutate as easily as others. Researchers think these so-called “conserved” spots represent indispensable components of HIV anatomy—ones that help it break its way into cells, or manufacture more of itself once inside—that could cripple the virus if altered.</p><p>Several years ago, Walker’s group found that these immutable regions seemed to be the same ones targeted by the immune systems of many HIV controllers. But Walker was disappointed to find the relationship was imperfect: Some of the patients who were homing in on seemingly crucial pieces of the virus were still getting sick.</p><p>So his team decided to go deeper, and zoom in on some of the proteins that contained conserved regions. They quickly discovered that, while all conserved regions were slow to change, only some of them had something else in common: They wielded an enormous amount of influence on the rest of the protein.</p></div>
  

  
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      <div class="rich-text"><p>Whether they’re mingling with coworkers or counting degrees of separation from Kevin Bacon, every human is a member of a social network: a complex constellation of interpersonal relationships. For better or worse, social networks tend to distribute power unequally, with certain members who are better connected, more well liked, or who simply hold more sway over others.</p><p>The same, Walker says, is true of proteins like the ones that make up HIV. Though each protein is first synthesized as a linear chain of subunits called amino acids, it eventually takes the form of a three-dimensional structure, transforming what’s essentially a string of molecular “beads” into a web of convoluted loops and whorls. Amino acids that are nowhere near each other in the chain can come close enough to touch, creating an intricate nexus of associations that can bridge enormous divides. In other words, a network.</p><p>But clout can be a double-edged sword: In any network, the same pieces that hold it together are the ones it can least afford to lose. Walker’s team found that the more partners an amino acid had, the more central it was to a protein’s structural integrity—which meant snipping at just one of these critical threads could be enough to unravel the entire viral tapestry. Using a computer algorithm, the researchers analyzed the sequence of several HIV proteins and assigned each amino acid a “score” denoting how networked it was. When the team then mutated the amino acids with the highest scores, the entire virus “basically fell apart,” Walker says.</p><p>“Networked amino acids are the ones that are touching everything else,” says <a href="https://scholar.harvard.edu/alquraishi/home">Mohammed AlQuraishi</a>, a structural biologist at Harvard University who was not involved in the study. “If you want to target a large number of strains, these are your best bets.”</p>
            <figure class="richtext-image full-width"><img alt="Screen Shot 2019-05-02 at 1.43.03 PM.psd" class="richtext-image full-width" height="293" width="800"
            src="/wgbh/nova/media/images/gag120_p24.width-800.jpg"/><figcaption><p>An HIV protein’s 3D structure (left) is analyzed to produce a map of the connections between amino acids (center). At right, the larger circular nodes represent the more connected amino acids. Image Credit: Adapted from Gaiha et al., Science, 2019</p><div class="credit"><p></p></div></figcaption>
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            <p>In a final test, the team discovered that the immune cells of HIV controllers, but not progressors, consistently zeroed in on highly networked amino acids. It seemed the team had finally found what distinguished the patients who could fight off infection: their ability to root out the Kevin Bacons of the HIV protein grid.</p><p>Walker’s team is now working to design a vaccine based on these same principles. The hope is to develop something that can train just about any immune system to single out these highly networked amino acids, says study author <a href="https://www.massgeneral.org/doctors/doctor.aspx?id=20532">Gaurav Gaiha</a>, a physician at Massachusetts General Hospital. This would saddle HIV with a serious dilemma: Mutate into impotence, or stay the same and be caught red handed.</p><p>That’s still a long way off. Vaccine design involves a lot more than earmarking an immunological bulls-eye, Rolland says. In the coming years, the team will have to show that they can actually redirect a person’s immune response without compromising safety. What’s more, the best vaccines will ideally rouse multiple branches of the immune system, including those that produce antibodies, which were not tested in this study.</p><p>Additionally, there are person-to-person differences to consider. “Even if two people target the exact same things, the quality of the immune response can still be very different,” Goonetilleke says.</p><p>For now, though, Walker is optimistic. Vaccine or not, the end of a 25-year odyssey could finally be in sight. “After years of searching, we’re finally able to understand this remarkable outcome in some people who are HIV infected,” he says. “I feel like I finally understand what was going on in that patient I first met in 1994.”</p></div>
  

  
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<p>A new computational analysis identifies weak spots in the virus that causes AIDS, and could someday inform the development of a long-awaited vaccine.</p>

HIV Proteins’ ‘Social Networks’ Reveal Why Some Patients Control Infection Better Than Others





  
      <div class="rich-text"><p>With the development of a decoder that translates brain signals into synthetic speech, a team of neuroscientists has now taken crucial steps toward someday restoring the voices of people who have lost the ability to speak.</p><p>The new technology, described in a <a href="https://www.nature.com/articles/s41586-019-1119-1">study</a> published today in the journal <i>Nature,</i> has yet to leave the lab. If successful, however, a similar brain-machine interface could be a major windfall for those who have no means of producing language, such as patients who have suffered strokes, throat cancer, amyotrophic lateral sclerosis (ALS), or Parkinson’s disease.</p><p>In its current iteration, the decoder relies on monitoring brain regions that are active during conscious vocalizations—meaning it won’t pick up on unspoken thoughts. It also hasn’t yet been tested in patients who don’t have the ability to speak.</p><p>Regardless, because it seems to successfully eavesdrop on how the brain dictates speech, the research represents a “huge advance,” Kate Watkins, a cognitive neuroscientist at the University of Oxford who was not involved in the study, <a href="https://www.theguardian.com/science/2019/apr/24/scientists-create-decoder-to-turn-brain-activity-into-speech-parkinsons-als-throat-cancer">told Hannah Devlin at <i>The Guardian</i></a>.</p></div>
  

  
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      <div class="rich-text"><p>This is far from the first computer-based effort to recapitulate speech—but previous efforts, some of which relied on the reading of facial movements or painstakingly typed out words letter by letter, maxed out at a rate of <a href="https://preview-www.nature.com/platform/rh/preview/page/nature/brain-implants-that-let-you-speak-your-mind/16645644?view=fragmentPreview">about eight words per minute</a>. Natural spoken speech, on the other hand, averages 150 words per minute.</p><p>To bridge this gap, a team led by Edward Chang, a neurosurgeon at the University of California, San Francisco, decided to tackle the process further upstream—by listening in on the brain itself.</p><p>“The brain is the most efficient machine that has evolved over millennia, and speech is one of the hallmarks of behavior of humans that sets us apart,” study author Gopala Anumanchipalli, a neuroscientist at the University of California, San Francisco <a href="https://www.nationalgeographic.com/science/2019/04/new-computer-brain-interface-translates-activity-into-speech/">told Michael Greshko and Maya Wei-Haas at <i>National Geographic</i></a>.</p></div>
  

  
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      <div class="rich-text"><p>When a person speaks, the vocal tract acts as an ambassador between brain and speech, translating electrical activity from the motor cortex into the movements of the lips, tongue, and jaw. For many patients who have lost the ability to vocalize, the brain’s speech centers are still intact, but the machinery that makes sounds is no longer functional. So the researchers designed a computer program to mimic the decrypting abilities of the vocal tract.</p><p>To tune into the brain’s inner electrical monologue, the researchers hooked electrodes directly up to the brains of five people while they read sentences aloud. They then fed the data to a computer program that matched patterns in the brain’s signals with the vocal movements they would produce, like pressing the lips together. Finally, the algorithm turned the movements into fast-paced synthetic speech.</p><p>The sounds produced by the program were passable enough to be roughly transcribed by hundreds of listeners, who could understand, on average, 70 percent of the words spoken. But the results varied widely: Depending on the complexity of the syllables and words in each sentence, some phrases came through perfectly each time, while others were almost universally unintelligible.</p><p>Clearly, the synthetic speech is still a far cry from what humans can produce. The technique is limited to cases in which the speech centers of the brain haven’t been damaged, which can happen after traumatic brain injuries. Additionally, the method still relies on opening up the skull to implant electrodes in the brain—something that won’t be practical or safe on any large scale.</p><p>The study’s results are also based on a program that was trained only on people who retained the capability to speak—which means there’s no guarantee that it will work for patients who have lost their voice, or the ability to move their face and tongue.</p><p>But Chang and his team remain hopeful. When the researchers tested their program on a participant who silently mouthed sentences, it was still able to generate synthetic speech. However, intelligibility suffered.</p><p>All in all, there’s a lot to address, Marc Slutzky, a neurologist at Northwestern University, <a href="https://www.nature.com/articles/d41586-019-01328-x">told Giorgia Guglielmi at <i>Nature News</i></a><i>.</i> The study still represents “a really important step,” he said, “but there’s still a long way to go before synthesized speech is easily intelligible.”</p></div>
  

  
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<p>With a “virtual vocal tract,” researchers might someday be able to help people who have lost the ability to speak.</p>

Using Artificial Intelligence, Scientists Translate Brain Signals into Speech





  
      <div class="rich-text"><p>Plenty of people suffer from at least one irksome dietary dilemma—and I’m one of them. A few bites of cantaloupe will set my mouth and throat afire with an itchy, prickling sensation. Eating too much gluten gives me splitting migraines. And <a href="https://www.storycollider.org/stories/2017/11/10/dna-stories-about-family?rq=dna%20family">one gulp of milk</a> is all it takes to guarantee me the kind of gastrointestinal distress that can clear out an entire auditorium.</p><p>It might come as a surprise that I’m not allergic to any of these foods.</p><p>An undoubtedly complex lingo surrounds food allergies and intolerances, and many people <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2720064">incorrectly self-diagnose</a> without input from a medical professional. But the confusion can have far worse consequences than a misuse of terminology: For food service staff, misconceptions about dietary restrictions can lead to real-world mix-ups—a serious risk in a country where an allergic reaction to food sends someone to the emergency room <a href="https://www.foodallergy.org/life-with-food-allergies/food-allergy-101/facts-and-statistics">every three minutes</a>.</p></div>
  

  
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      <div class="rich-text"><p>In the past decade, studies from around the globe have revealed consistent gaps in knowledge in the food service industry. <a href="https://www.annallergy.org/article/S1081-1206(10)60880-0/fulltext">Around a quarter</a> of <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0214625">food establishment personnel</a> are under the <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2222.2011.03748.x">false impression</a> that customers can <a href="https://core.ac.uk/download/pdf/30608527.pdf">safely consume</a> a <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6122805/">small amount</a> of the foods they’re allergic to. And <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2222.2011.03748.x">about a third</a> think <a href="https://onlinelibrary.wiley.com/doi/abs/10.1002/alr.21427">drinking</a> <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0214625">water</a> can <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5321626/">dampen the severity</a> of an <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6122805/">ongoing reaction</a>.</p><p>Given the <a href="https://www.jacionline.org/article/S0091-6749(17)31794-3/fulltext#sec1.1">increasing prevalence of food allergies</a>, these findings are “very concerning,” says <a href="https://www.luriechildrens.org/en/doctors/gupta-ruchi-s-2448/">Ruchi Gupta</a>, an allergist and pediatrician at Lurie Children&#x27;s Hospital Chicago. But there’s little point in assigning blame to one party or another. “Food allergies are complex, and the symptoms can affect almost any organ system in the body,” she says. “It’s hard for the general public to know what they have [when] there are so many food-related conditions.”</p><h3>Nothing to sneeze at</h3><p>When it comes to food, the terms “allergy,” “intolerance,” and “sensitivity” are often used interchangeably, but they each mean different things. Most critical are food <i>allergies,</i> which involve an inappropriate immune system response to a specific food. A person with a severe nut allergy, for instance, might manufacture molecules called IgE antibodies that incorrectly identify proteins present in almonds as dangerous and rouse immune cells into action. This can trigger a cascade of symptoms, sometimes culminating in life-threatening anaphylaxis.</p><p>But the symptoms of such “classic” food allergies aren’t always clear cut, Gupta says. Because the immune system is linked up to so many other parts of the body, allergies can manifest differently from person to person.</p><p>Currently, there are <a href="https://www.pbs.org/wgbh/nova/article/peanut-allergies-new-treatment-antibody">no cures for food allergies</a>, and they can develop (or even resolve) at almost any age. Definitive diagnoses can only be made by allergists, who will look for a reaction after injecting a tiny dose of the allergen under the skin. But these tests also sometimes misidentify patients as allergic who actually aren’t, says <a href="https://www.northshore.org/apps/findadoctor/physicians/jennifer-s.-kim">Jennifer Kim</a>, an allergist at NorthShore Medical Group in Illinois.</p>
            <figure class="richtext-image full-width"><img alt="iStock-927057490.jpg" class="richtext-image full-width" height="533" width="800"
            src="/wgbh/nova/media/images/iStock-927057490.width-800.jpg"/><figcaption><p>Fish, tree nuts, peanuts, milk, eggs, and wheat are among the most common food allergens. Image Credit: colnihko, iStock</p><div class="credit"><p></p></div></figcaption>
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            <p>Complicating matters are related, but separate, conditions like <a href="https://acaai.org/allergies/types/food-allergies/types-food-allergy/oral-allergy-syndrome">oral allergy syndrome</a>. People who suffer from pollen allergies have mild reactions to certain fruits or vegetables that make proteins resembling pollen. This immunological imposter act happens with ragweed and cantaloupe—that’s why my mouth tingles when I eat fruit salad, even though I’m not technically allergic to its ingredients.</p><p>Another common mix-up happens with <a href="https://acaai.org/resources/connect/ask-allergist/wheat-allergy-or-celiac-disease">celiac disease</a>, an autoimmune condition that<i> involves</i> gluten (a protein found in wheat, barley, and rye), but has some clear-cut distinctions compared to, say, an actual wheat allergy. In people who have celiac, the presence of gluten in the digestive tract prompts the production of IgA antibodies, which are distinct from the IgE antibodies active in classic food allergies. Problems arise when IgA antibodies target not gluten, but the lining of the small intestine. With continued exposure to gluten, this can lead to a chronic condition in which the body has trouble absorbing nutrients—but a single encounter with gluten won’t spark an immediate allergic response.</p><p>Food <i>intolerances</i> are more of a gray area. These refer to a negative reaction to a food, like bloating, nausea, or headaches, that <i>doesn’t</i> involve the immune system. My gluten and lactose intolerances, for instance, don’t make me allergic to either of these foods—but they do cause me quite a bit of discomfort. Unlike the case with allergies, trace amounts of these foods <a href="https://acaai.org/allergies/allergy-symptoms/nausea-and-vomiting">don’t carry the risk of an immediate, life-threatening reaction</a>. And, barring a false positive, intolerances won’t flare up after an allergy skin test.</p><p>In other words, intolerances are defined by what they <i>aren’t,</i> rather than what they <i>are</i>, making them a challenge to diagnose and explain. Part of the reason is that there’s no clear-cut constellation of symptoms or rapid fire test that can distinguish an intolerance from an allergy, causing many to conflate the two, says <a href="https://www.med.unc.edu/tarc/directory/onyinye-iweala-md-phd/">Onyinye Iweala</a>, an allergist at the Division of Rheumatology, Allergy, and Immunology of the University of North Carolina’s School of Medicine.</p><p>Last and definitely least, food <i>sensitivity</i> is “kind of a blanket term that doesn’t really mean anything specific,” Gupta says. In most cases, this phrasing is too vague to be helpful.</p><h3>Lost in translation</h3><p>Unfortunately, “food allergy” has become a catchall phrase. Gupta’s <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2720064">own research</a> found that, in a survey of 40,000 United States adults, 19 percent of participants claimed to suffer from a food allergy—but only about half of these people actually reported allergic symptoms.</p><p>While these statistics might seem to cast an unflattering light on some Americans, the more important takeaway is that up to a fifth of people could have <i>some</i> condition—perhaps an intolerance—that’s probably causing them to avoid certain foods, Gupta says.</p></div>
  

  
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      <div class="rich-text"><p>As these terms are bandied about, they can create a frustrating dialogue between those trying to eat out and the employees trying to serve them. In a <a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0214625">study</a> published today in the journal <i>PLOS ONE,</i> almost a fifth of restaurant staff surveyed in Germany indicated they would prefer not to serve patrons with food allergies.</p><p>The new study, like many before it, also underscored a persistent lack of knowledge in the restaurant industry—with potentially dire repercussions, says <a href="https://www.uniklinik-duesseldorf.de/patienten-besucher/klinikeninstitutezentren/institut-fuer-arbeits-sozial-und-umweltmedizin/team-kontakt/pd-dr-sc-hum-adrian-loerbroks">Adrian Loerbroks</a>, a social epidemiologist at the University of Düsseldorf in Germany who led the research. Of nearly 300 personnel surveyed, only 30 percent could name three food allergens, and almost 10 percent were unaware food allergies could be fatal. Almost 20 percent of participants thought removing an allergen from a finished dish (like picking the nuts off a salad) would render a meal safe for an allergic customer. And more than 40 percent believed some of the food allergies brought up by their patrons weren’t real.</p><p>Other incorrect beliefs have been highlighted by past research, such as the <a href="http://ssu.ac.ir/cms/fileadmin/user_upload/Mtahghighat/tfood/asil-article/amuzesh-Behdasht-Ghaza/Food_allergens_Knowledge_and_practices_of_food_handlers_in_restaurants.pdf">idea</a> that <a href="https://www.annallergy.org/article/S1081-1206(10)60880-0/fulltext">cooking</a> <a href="https://core.ac.uk/download/pdf/30608527.pdf">food</a> can <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2222.2011.03748.x">prevent</a> an <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6122805/">allergic reaction</a>. Despite these patterns, the new study is among <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2222.2011.03748.x">several</a> <a href="https://core.ac.uk/download/pdf/30608527.pdf">that</a> show <a href="https://www.annallergy.org/article/S1081-1206(10)60880-0/fulltext">a large majority</a> of restaurant staff <a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0214625">feel confident</a> in their ability to provide their customers an allergy-safe meal. Although <a href="http://ssu.ac.ir/cms/fileadmin/user_upload/Mtahghighat/tfood/asil-article/amuzesh-Behdasht-Ghaza/Food_allergens_Knowledge_and_practices_of_food_handlers_in_restaurants.pdf">managers</a> tend to be better informed than wait staff, it’s the latter who are “on the frontlines of interacting with customers,” Iweala points out.</p><h3>We reap what we sow (and sometimes, it gives us indigestion)</h3><p><a href="https://www.mountsinai.org/profiles/scott-h-sicherer">Scott Sicherer</a>, an allergist at Mount Sinai’s Icahn School of Medicine, cautions that none of this research should be used to demonize restaurants or their staff. “People in a restaurant don’t want you to get sick,” he says. “But they may not know everything they need to know to make sure you don’t get sick.”</p><p>After all, the logistics of juggling food allergies and intolerances aren’t trivial. In a typical food establishment, an order can pass through multiple servers before it reaches a team of chefs in a chaotic kitchen. If just one person in this complex chain misses the message, or underestimates the danger of the situation, the system can quickly break down.</p><p>“It’s frustrating for these people,” Kim says. “They’re not doctors, and even doctors can’t tell from a short, verbal interaction if [a customer] has an allergy or intolerance...it’s a challenge to make sure that every meal is safe.”</p><p>Part of the problem is that there isn’t a universal mandate for handling food allergies in dining establishments. While the United States Food and Drug Administration’s <a href="https://www.foodallergy.org/education-awareness/advocacy-resources/food-code-revisions">Food Code</a> includes information on allergies to guide members of the food service industry, it’s up to individual states to adopt the Code, and <a href="https://www.fda.gov/downloads/Food/GuidanceRegulation/RetailFoodProtection/FoodCode/UCM577858.pdf">participation varies</a> across the country.</p><p>Smaller scale hurdles exist as well. For one, with the sheer diversity of food establishments that exist in the United States, from pop-up food carts to Michelin-starred restaurants, it wouldn’t be practical to implement a one-size-fits-all strategy. And since the food industry has a very high turnover rate and many young employees, it’s difficult for eateries to keep their staff up-to-date, says <a href="https://ovc.uoguelph.ca/population-medicine/graduate-student/abhinand-thaivalappil">Abhinand Thaivalappil</a>, a public health researcher and food safety expert at the University of Guelph in Canada.</p>
            <figure class="richtext-image full-width"><img alt="iStock-537629516.jpg" class="richtext-image full-width" height="533" width="800"
            src="/wgbh/nova/media/images/iStock-537629516.width-800.jpg"/><figcaption><p>Despite what some might believe, simply picking an allergen off a finished meal isn&#x27;t a safe practice. Even trace amounts can put a person in a life-threatening situation. Image Credit: piotr_malczyk, iStock</p><div class="credit"><p></p></div></figcaption>
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            <p>That being said, things have vastly improved over the past 15 years, Gupta says. Many menus now list common allergens, or prompt patrons to inform their servers of any allergies. (On the flip side, some restaurants explicitly state that they can’t accommodate patrons with serious food allergies.) In many restaurants, wait staff will even explicitly ask about dietary restrictions before taking an order.</p><p>However, Gupta, Kim, and Sicherer agree that better training in eating establishments will be key to keeping people safe. Restaurant staff members who have undertaken formal education on food allergies remain <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6122805/">in the minority</a>, and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5321626/">several</a> <a href="https://www.annallergy.org/article/S1081-1206(10)60880-0/fulltext">studies</a> have <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2222.2011.03748.x">hinted</a> that <a href="https://onlinelibrary.wiley.com/doi/abs/10.1002/alr.21427">existing programs</a> <a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0214625">haven’t done much</a> to improve knowledge.</p><p>At a minimum, members of an establishment should have two basic sets of knowledge, Thaivalappil says. First, staff should feel comfortable asking about and handling common food allergies (the eight most common are milk, eggs, tree nuts, peanuts, shellfish, wheat, soy, and fish). Second, if exposure occurs, restaurant personnel should be able to pinpoint the typical symptoms of a reaction and take action by calling 911 or ensuring the patron uses their EpiPen.</p><p>Having these measures in place would probably alleviate a lot of concerns on both ends, Gupta says. “People [with allergies] <a href="https://acaai.org/news/safest-way-dine-out-those-food-allergies-using-15-strategies">definitely avoid</a> eating out, or have just a few safe places where they’ll go,” she says. “So restaurants do have something to gain from being food-allergy-friendly.”</p><p>At the same time, the burden shouldn’t fall entirely on the shoulders of restaurant staff, Thaivalappil says.</p><p>“If you’re the customer, don’t be afraid to ask questions,” he says. “Both parties need to do their best to minimize the risk of reaction. It’s your health on the line, and you’re just as responsible.”</p></div>
  

  
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<p>Up to one third of restaurant staff hold the mistaken belief that drinking cold water can dilute an allergic response to food.</p>

What Restaurants, and the Rest of Us, Get Wrong About Food Allergies





  
      <div class="rich-text"><p>Someday, in the not-so-distant future, new parents might have the option of having their children’s fates forecast at birth. These prophecies, which might reveal everything from an individual’s height to their risk of developing a certain disease, will arise not through readings of tea leaves or tarot cards, but of DNA.</p><p>Although there are many ethical and scientific hurdles to overcome, the toolkit of genetic prediction continues to grow. The latest addition? A <a href="https://www.cell.com/cell/fulltext/S0092-8674(19)30290-9">score</a> that tabulates an individual’s inborn risk for obesity, published today in the journal <i>Cell.</i></p><p>The metric, which compiles information from more than two million spots in the genome that affect a person’s weight, isn’t a perfect predictor of physique. But adults that score in the top 10 percent are, on average, almost 29 pounds heavier than those in the bottom 10 percent—and it appears that genetically driven differences in weight can materialize as early as age three.</p><p>“This work is, overall, an important contribution,” says <a href="https://irp.nih.gov/pi/charles-rotimi">Charles Rotimi</a>, a human geneticist at the National Institutes of Health who was not involved in the study. “It takes advantage of all the genetic resources we’re getting out of [studies of human genetics]...and takes into account a lot of the variation we’ve found with obesity.”</p><p>Regardless of its performance, however, Rotimi and other experts advise caution in interpreting the results. Weight is certainly <i>affected</i> by genes, but “a genetic score can never fully predict obesity,” says <a href="https://icahn.mssm.edu/profiles/ruth-loos">Ruth Loos</a>, a human geneticist at the Icahn School of Medicine at Mt. Sinai who was not involved in the study. “Lifestyle and environmental factors remain equally, if not more, important.”</p></div>
  

  
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      <div class="rich-text"><p>It’s long been clear that lifestyle changes like a healthy diet and regular exercise can help stave off weight gain. But the genetic side of this equation has always been far murkier. Like most traits, weight isn’t controlled by the flip of a single molecular switch. Dozens, possibly hundreds, of genes can affect a person’s risk of becoming obese—and scientists are nowhere close to finding and characterizing them all.</p><p>The score detailed in the study, however, has a workaround. In recent years, researchers have found over 2.1 million genetic alterations—equivalent to single-letter typos—that are more prevalent in obese individuals.</p><p>Even without knowing what the underlying genes actually do, scientists can still tally up the tweaks in any given individual. The result integrates information scattered across the genome into a single, interpretable number, “almost like a cholesterol score,” says study author <a href="http://www.kathiresanlab.org/about-sek/">Sekar Kathiresan</a>, a cardiologist and human geneticist at Massachusetts General Hospital.</p><p>When Kathiresan and his team put their score to the test in a population of 300,000 adults, it accurately stratified groups of individuals by weight, body mass index (BMI), and prevalence of obesity. For instance, when arrayed by score, people in the top 10 percent were 25 times more likely to be severely obese, with a BMI of at least 40 kilograms per square meter, than those in the bottom 10 percent.</p><p>“How striking these differences are...is what got us so excited,” Kathiresan says. “The tremendous differences between the two ends of the spectrum are remarkable.”</p>
            <figure class="richtext-image full-width"><img alt="iStock-910049866.jpg" class="richtext-image full-width" height="533" width="800"
            src="/wgbh/nova/media/images/iStock-910049866.width-800.jpg"/><figcaption><p>Environmental factors and genetics both play into weight. But while a lot is known about the lifestyle choices that can influence obesity, the genetic side is far murkier. Image Credit: Rostislav_Sedlacek, iStock</p><div class="credit"><p></p></div></figcaption>
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            <p>The technology isn’t ready for use in the clinic. But the researchers are hoping to create a low-cost test—maybe around $50 per patient—that could use an easy-to-take sample like blood to scour the genome for obesity-related variants.</p><p>Making this kind of information widely available could be an important step toward reducing cultural stigma around obesity, which can both cause undue emotional hardship and dissuade people from seeking effective treatment. “Obesity is viewed as a problem of willpower,” Kathiresan says. “We blame the patient. What this [score] says is, ‘There’s a big biological underpinning that’s not necessarily within their control.’”</p><p>Such stigma is frustrating, given that obesity isn’t always disease-related, Rotimi says. “Not all of these people have diseases like diabetes,” he says. “There are people who are very heavy, but are doing fine.”</p><p>But those individuals are the exception, rather than the norm. High-scoring adults in the study were also more likely to suffer from several heart-related conditions—including coronary artery disease, diabetes, heart failure, and stroke—and had higher rates of overall mortality.</p></div>
  

  
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      <div class="rich-text"><p>Of course, most adults don’t need a genetic test to tell them whether or not they’re overweight, Kathiresan says. Genetic tests remain far more costly than stepping on a scale. These types of scores could still be explanatory, however—by offering someone perspective on why they’ve struggled to shed excess weight, for instance.</p><p>And there’s still a large contingent of people who might be able to use these scores to guide weight-based interventions—in themselves, or perhaps even their kids, says study author <a href="http://www.kathiresanlab.org/our-people/amit-khera/">Amit Khera</a>, a cardiologist and geneticist at Massachusetts General Hospital. The scores didn’t perform quite as well in children, but differences in body mass were discernible in individuals as young as three years old. “There’s no question that the impact takes effect very early in life,” Khera says. “A major goal is to use this info to empower people to offset inherited risk.”</p><p>Before any of that can happen, though, it’s important to acknowledge how much of obesity <i>can’t</i> be captured by this score, Loos says. In its current iteration, the test makes predictions that are often incorrect: About 40 percent of the highest-scoring adults were obese—but that leaves 60 percent that weren’t (and the accuracy drops further in younger populations). This could tread into tricky territory, especially if parents end up making lifestyle decisions on behalf of their children before the kids themselves can have a say, Rotimi says.</p><p>In the end, there are limits to what even the most rigorous genetic scans can tell us. A perfect, diversity-conscious genetic test would still capture only a fraction of what’s feeding the obesity epidemic, Loos says.</p><p>Altogether, these considerations could limit such a score’s utility in the clinic. “If we introduce a test into health care that is not predictive enough to be useful, then we are basically making health care more inefficient,” says <a href="http://www.cecilejanssens.org/">Cecile Janssens</a>, an epidemiologist and genomics researcher at Emory University who was not involved in the study. Even if the test is free, any interventions will require substantial public health investment, putting the onus on researchers to make these scores as accurate as possible, she says.</p>
            <figure class="richtext-image full-width"><img alt="iStock-1042024608.jpg" class="richtext-image full-width" height="533" width="800"
            src="/wgbh/nova/media/images/iStock-1042024608.width-800.jpg"/><figcaption><p>Human genetics research is accelerating at an unprecedented pace. But most studies are still done in populations of European ancestry. Image Credit: undefined, iStock</p><div class="credit"><p></p></div></figcaption>
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            <p>How this sort of information is doled out also needs to be carefully handled. The nature of the research reflects good intentions, Rotimi says, but “if we don’t carefully weigh the overall implications of these recommendations, we may indeed do more harm than good.”</p><p>While some individuals might be able to use a high score as motivation to be extra-conscious about their weight, others might feel like their fates are sealed by these genetic report cards, Loos says. Researchers have conducted similar risk assessments in the past with mixed results. In one study, disclosure actually backfired: People informed that they had a high genetic risk for obesity <a href="https://www.nejm.org/doi/full/10.1056/nejmoa1011893"><i>increased</i> their fat intake</a> in the months after receiving the news. The uptick was <a href="https://jmg.bmj.com/content/50/6/393.long">temporary</a>, but this kind of behavior, wherein people effectively resign themselves to what they see as genetic destiny, is definitely cause for concern, Loos says.</p><p>The converse could cause problems as well, Rotimi says. Just as there are individuals who might carry a higher risk for obesity, so, too, exist those who are a little more protected from it. Getting an ultra-low score might make some people think they can eat and do whatever they want, he says. And no one is immune to the repercussions of persistently unhealthy behavior.</p><p>There’s another big caveat. One of the largest limitations of the study is the fact that it was conducted exclusively with data from individuals of European ancestry. Based on previous research, these scores will apply to everyone, but will work best in those of European descent, Khera says. Leveling the playing field will require <a href="https://www.pbs.org/wgbh/nova/article/lack-diversity-genetic-research-could-be-costing-us-our-health/">expanding research to include other groups</a>.</p><p>With these issues in mind, the ultimate message is about striking a balance between nature and nurture. “This speaks to the fact that the endpoint of obesity is the result of genetics as well as lifestyle,” Kathiresan says.</p><p>And for many, that could actually be a silver lining: Genes are powerful—but we still have a lot of control over our own bodies. “People who are susceptible may have to work harder to keep weight off,” Kathiresan says. “But it’s important to know that they <i>can,</i> with great success.”</p></div>
  

  
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<p>There can be a 30-pound weight difference between people with low and high genetic risk. But genes aren’t everything.</p>

This Score Can Tell You Your Genetic Risk for Obesity. Is It Worth Knowing?





  
      <div class="rich-text"><p>The brain doesn’t last long after death. Deprived of blood and oxygen, the organ rapidly deteriorates and eventually shuts down completely.</p><p>That process is quick. But <i>quick</i> isn’t the same as <i>immediate</i>. If someone were to jumpstart electrical activity in the hours after death, a brain could maybe—just maybe—be salvaged.</p></div>
  

  
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      <div class="rich-text"><p>In a <a href="https://www.nature.com/articles/s41586-019-1099-1">study</a> published today in the journal <i>Nature,</i> a team of scientists has taken advantage of that critical window to partially revive the brains of dead pigs after slaughter. The brains didn’t regain the organized connectivity that they’d need for “consciousness,” but some neurons exhibited electrical activity. When coaxed with oxygen and glucose, the organs appeared to gobble them up, and even responded to drugs—clear signs that they had retained some metabolic function.</p><p>“This is a real advance,” Andrea Beckel-Mitchener, a neuroscientist at the National Institutes of Health who was not involved in the study, <a href="https://www.nytimes.com/2019/04/17/science/brain-dead-pigs.html">told Gina Kolata at <i>The New York Times</i></a>. “This has never been done before in a large intact mammalian brain.”</p><p>The ethical implications of the research—which has been described as <a href="https://www.washingtonpost.com/science/2019/04/17/scientists-restore-some-brain-cell-functions-pigs-four-hours-after-death/?utm_term=.890e3a731dd9">blurring the line</a> between life and death—have already sparked controversy. But scientifically, it presents a strong case for the idea that brain cells aren’t as fragile as previously thought.</p><p>Herein lies an important distinction, though: After their owners died, at no point did the brains come back to <i>life.</i> Restoring a subset of brain activity is not enough to constitute full reanimation, or even anything close. “This is not a living brain,” study author Nenad Sestan, a neuroscientist at Yale University, told the press. “This is a cellularly active brain.”</p><p>Regardless, “this is a huge breakthrough,” Nita Farahany, an ethicist at Duke Law School who was not involved in the study, <a href="https://www.washingtonpost.com/science/2019/04/17/scientists-restore-some-brain-cell-functions-pigs-four-hours-after-death/?utm_term=.189291333475">told Joel Achenbach at <i>The Washington Post</i></a>. “Our belief was there’s a point of no return. Certainly we would have believed that four hours after being decapitated, that was a point of no return. It turns out it’s not.”</p></div>
  

  
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      <div class="rich-text"><p>After sourcing 32 freshly decapitated pig heads from a local pork processing center, a team of researchers led by Sestan extracted the brains. While some were left to deteriorate, others were rejuvenated with a cocktail of nutrients and protective chemicals for six hours. It had only been four hours since the pigs had been slaughtered for their meat, but brain tissue is notoriously fickle and fragile. The goal was to maximize preservation—and, to an extent, it worked.</p><p>While some neurons continued their march toward death, others didn’t. Some kept consuming energy; a few even began to fire. But the researchers were unable to detect hints of awareness in any of the brains.</p><p>Or, at least, that’s what they think. During the experiment, the brains were infused with the anti-seizure drug lamotrigine, which subdues cellular activity, in the hopes that this would aid the preservation process. The drug could have masked the organized activity that’s often linked to consciousness, but it’s pretty unlikely, the researchers say. Besides, it was never the team’s goal to restore this type of awareness, and, had they seen any signals associated with it, they would have immediately administered anesthesia.</p><p>Still, consciousness is hard to define and measure under the best of circumstances—much less in a disembodied pig brain.</p><p>As such, the findings raise numerous ethical quandaries, including what this could mean for model organisms used in laboratories, or protocols of human organ transplants, which often rely on donors who have been declared dead and beyond resuscitation.</p><p>Any applications of the findings in human patients are a very, very long way off—and this isn’t going to pave the way to human brain transplants, Emory University neuroethicist Karen Rommelfanger, who was not involved in the study, <a href="https://www.theatlantic.com/science/archive/2019/04/scientists-partly-restore-activity-dead-pig-brains/587329/">told Ed Yong at <i>The Atlantic</i></a>. But there are less wild implications, including the advancement of new treatments for conditions ranging from Alzheimer’s to traumatic brain injury.</p><p>That’s not to minimize the ethical hurdles that stand in the way. In the meantime, the results of the study “should inform the discussion surrounding brain death,” Kathleen Fenton, a bioethicist and pediatric heart surgeon who was not involved in the study, <a href="https://www.statnews.com/2019/04/17/pig-brain-cellular-function-restored-after-death/">told Sharon Begley at <i>STAT</i></a>. “[What] was irreversible appears to not be irreversible...that’s important.”</p></div>
  

  
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<p>In a groundbreaking and controversial study, scientists have partially revived the brains of slaughtered pigs.</p>

Topic: Body & Brain

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