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Rejection. Now What?","publishDate":1550278825,"format":"audio","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>\u003cstrong>Originally published on Sept 27, 2018\u003c/strong>\u003c/p>\n\u003cp>A few months ago, I ordered a home genetic testing kit. I didn’t do it because I wanted to know about my ancestry. I did it because I’d heard about a genetic variation that can make people more sensitive to rejection — and I was convinced I had it.\u003c/p>\n\u003cp>I have always been a bit overly sensitive. I remember a particularly devastating moment in fourth grade. Ms. Brown had asked a question I knew the answer to. I raised my hand, stretching my whole body up so she would notice. She made eye contact with me, commented that I had already gotten to answer a question that day, and then called on a student behind me.\u003c/p>\n\u003caside class=\"pullquote alignright\">I have long struggled with bouts of depression; my relationships are typically a roller coaster of anxieties. If I were a G-carrier, it could explain so much of what I was experiencing.\u003c/aside>\n\u003cp>I could feel my face flush with embarrassment. A knot started to form in my throat as, almost in a whisper, I asked to be excused, the tears welling up in my eyes. Once I was safe behind the bathroom door, I used my shirt to muffle the sounds of my crying. Simply because the teacher hadn’t called on me.\u003c/p>\n\u003cp>A few years later in middle school, my friend Jennifer slipped a note into my locker saying that she wanted to play with another kid at recess, not me. That night — and for many nights after — I lay curled up in my bed for hours, the note on my nightstand.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>As I got older, it got worse. The emotional pain I experienced in social situations changed how I felt about myself and how I behaved with other people. As an adult, if a friend didn’t respond to a text, I would pull away and avoid them. When someone I barely knew ghosted me, I convinced myself that I wasn’t desirable to anyone.\u003c/p>\n\u003cp>Friends told me I was overreacting. Sure, everyone feels a little hurt by these things, but to become so debilitated each time was a bit over the top, they told me. Finally, in my late 20s, I started to wonder if maybe there was something wrong with me.\u003c/p>\n\u003cp>\u003cstrong>Is Oversensitivity Biological?\u003c/strong>\u003c/p>\n\u003cp>In 2009, \u003ca href=\"http://www.pnas.org/content/106/35/15079\">a ground-breaking study\u003c/a> investigated the link between emotional sensitivity and our genetics. Scientists already knew that a particular gene, the OPRM1 gene, could influence our sensitivity to physical pain. \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/18719451\">Previous studies\u003c/a> had shown that people with a G allele on this gene required higher doses of morphine to curb pain, suggesting they experience pain more intensely than others. Because \u003ca href=\"https://www.kqed.org/futureofyou/175807/can-taking-tylenol-help-you-get-over-a-romantic-breakup-maybe\">physical pain and emotional pain are processed in similar regions of the brain\u003c/a>, researchers wondered if G-allele carriers might also experience more intense \u003cem>emotional \u003c/em>pain.\u003c/p>\n\u003cp>To test the question, neuroscientists at the University of California Los Angeles recruited 122 people, 49 of whom were G-carriers, the rest of whom were not. Participants came into the lab and played a computer game intended to evoke feelings of rejection. In the game, each participant would toss a ball back and forth to two other virtual players on a screen. The two players would, at some point, exclude the participant. Meanwhile, the participant lay in a functional magnetic resonance imaging (fMRI) brain scanner that measured blood flow to the pain regions of the brain.\u003c/p>\n\u003cfigure id=\"attachment_443244\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003cimg class=\"size-large wp-image-443244\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-1020x381.jpg\" alt=\"Brain scan showing yellow dots\" width=\"640\" height=\"239\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-1020x381.jpg 1020w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-160x60.jpg 160w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-800x299.jpg 800w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-768x287.jpg 768w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-1200x448.jpg 1200w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-1920x717.jpg 1920w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-1180x441.jpg 1180w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-960x359.jpg 960w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-240x90.jpg 240w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-375x140.jpg 375w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-520x194.jpg 520w\" sizes=\"(max-width: 640px) 100vw, 640px\">\u003cfigcaption class=\"wp-caption-text\">fMRI scan of brain showing activation of pain regions (including the dorsal anterior cingulate cortex). The image comes from a study in which participants played “Cyberball” while lying in the fMRI scanner—a game designed to induce feelings of rejection. \u003ccite>(Baldwin Way)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>“What the researchers found was that there was an exaggerated response [in G carriers],” says Jon-Kar Zubieta, a psychiatric researcher at the University of Utah. “Individuals who were G-allele carriers had greater responses to the negative emotional challenge, which was associated with greater activation of the anterior cingulate cortex,” a pain region of the brain.\u003c/p>\n\u003cp>I had called up Zubieta to get his take on the research for this story — but my questions were also personally motivated.\u003c/p>\n\u003cp>“G-carriers seem to have less capacity to compensate for negative emotion,” he told me. And it doesn’t matter whether that negative emotion is in response to physical pain or the social pain of rejection, like what study participants experienced during the ball-tossing game.\u003c/p>\n\u003cp>Zubieta also told me that G-carriers — who make up 15 to 20 percent of the general population — not only feel more hurt in everyday social interactions, “these individuals \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4330509/\">have traits\u003c/a> that make them more prone to developing conditions such as depression and anxiety.”\u003c/p>\n\u003cfigure id=\"attachment_443245\" class=\"wp-caption aligncenter\" style=\"max-width: 600px\">\u003cimg class=\"wp-image-443245 size-full\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2018/07/Zubieta.jpg\" alt=\"A man speaks in front of a white board.\" width=\"600\" height=\"400\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2018/07/Zubieta.jpg 600w, https://ww2.kqed.org/app/uploads/sites/13/2018/07/Zubieta-160x107.jpg 160w, https://ww2.kqed.org/app/uploads/sites/13/2018/07/Zubieta-240x160.jpg 240w, https://ww2.kqed.org/app/uploads/sites/13/2018/07/Zubieta-375x250.jpg 375w, https://ww2.kqed.org/app/uploads/sites/13/2018/07/Zubieta-520x347.jpg 520w\" sizes=\"(max-width: 600px) 100vw, 600px\">\u003cfigcaption class=\"wp-caption-text\">Jon-Kar Zubieta, Chairman of the Department of Psychiatry and Psychiatrist-in-Chief of the University of Utah Neuropsychiatric Institute. \u003ccite>(University of Utah Health)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Listening to Zubieta recount such findings, I found myself nodding my head. All of it resonated with me. I have long struggled with bouts of depression; my relationships are typically a roller coaster of anxieties. If I were a G-carrier, it could explain so much of what I was experiencing.\u003c/p>\n\u003cp>\u003cstrong>Why Do G-Carriers Feel More Pain?\u003c/strong>\u003c/p>\n\u003cp>When the genetic kit finally arrived at my house, I opened it and pulled out the clear test tube. I collected my saliva, sealed it back up, and shipped it off to the lab to be tested.\u003c/p>\n\u003cp>In the weeks I spent waiting for my results, I looked up more research on how the OPRM1 gene could lead to a heightened sense of pain.\u003c/p>\n\u003cp>[emailsignup newslettername='science' align='right']As it turns out, the gene controls the number of opioid receptors in the brain. In a typical brain, when a person is experiencing pain, neurons fire in regions such as the anterior cingulate cortex. In response, the body releases endorphins — our natural pain killers. The endorphins rush into the brain and attach to neuron receptors, inhibiting those cells from firing, effectively stopping the pain signal. This process is actually what happens during the “runner’s high,” and the same process occurs for most people when they experience the pain of rejection.\u003c/p>\n\u003cp>However, if a person doesn’t have enough opioid receptors or doesn’t release a sufficient amount of endorphins, they could experience more suffering than others. Zubieta says this is likely what happens to G-carriers; they appear to have fewer receptors in critical areas of the brain and, he adds, “they may have less capacity to release natural opioids in general.” This means, Zubieta says, that G-carriers “have less capacity to suppress responses to pain.”\u003c/p>\n\u003cp>\u003cstrong>So … Am I A G-Carrier?\u003c/strong>\u003c/p>\n\u003cp>Several weeks after shipping off my saliva, I was at home when an email popped up in my inbox; my results had come in. My stomach dropped and I sat staring at the unopened email for a few minutes.\u003c/p>\n\u003cp>What would it mean if I were a G-carrier? It would feel validating, of course. For so long I had felt like I was emotionally weak. If I were a G-carrier then it would mean there was a biological explanation for my feelings. It would mean that I hadn’t been overreacting all these years; rather, I had been reacting proportionally to the pain I was feeling — pain that 80 to 85 percent of the population simply doesn’t feel.\u003c/p>\n\u003cp>On the other hand, if I weren’t a G-carrier, I wasn’t sure where that would leave me. I could feel my heart beating faster. My hands shook slightly as I struggled to steady my breathing.\u003c/p>\n\u003cp>I opened the email and scrolled through lines of the genetic code until I found the OPRM1 gene on chromosome 6. Typed in small font was a “G.”\u003c/p>\n\u003cfigure id=\"attachment_442608\" class=\"wp-caption alignright\" style=\"max-width: 240px\">\u003cimg class=\"size-full wp-image-442608\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2018/06/RS31383_CANTRELL_003-sfi.jpg\" alt=\"\" width=\"240\" height=\"360\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2018/06/RS31383_CANTRELL_003-sfi.jpg 240w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/RS31383_CANTRELL_003-sfi-160x240.jpg 160w\" sizes=\"(max-width: 240px) 100vw, 240px\">\u003cfigcaption class=\"wp-caption-text\">Lisa Cantrell stretches prior to running at Dolores Park in San Francisco, Calif., on Monday, June 11, 2018. \u003ccite>(Lauren Hanussak/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>\u003cstrong>What Now?\u003c/strong>\u003c/p>\n\u003cp>So am I stuck with unbearable pain forever? A prisoner to my genetics? On the phone with Zubieta, I ask him if a G-carrier like me could do anything about it.\u003c/p>\n\u003cp>“You have to remember that the opioid system becomes active when there are things like exercise or stressors,” so when you do physically demanding sports or activities that in some way cause pain “you are training the system.” In other words, Zubieta says, you can modify your brain’s response.\u003c/p>\n\u003cp>The advice makes sense. Exercise not only releases endorphins that decrease pain in the moment, regularly challenging your body with physical activity can strengthen the overall functioning of the opioid system, potentially prompting your brain to create new receptors and urging your body to increase the amount of endorphins released each time you experience a stressor.\u003c/p>\n\u003cp>All of this could make the system more optimal, more prepared to kick into full gear when it encounters pain, be it physical or emotional. Interestingly, \u003ca href=\"https://www.sciencedirect.com/science/article/abs/pii/003193849190418N\">chocolate\u003c/a> and \u003ca href=\"http://rspb.royalsocietypublishing.org/content/early/2011/09/12/rspb.2011.1373.short\">laughter\u003c/a> may also help — they bump up endorphin release, which could alleviate pain in the moment as well as have longer term effects.\u003c/p>\n\u003cp>Zubieta continued with his suggestions. “So you could do yoga… or run marathons.” Something physically demanding, he says.\u003c/p>\n\u003cp>“I’m not sure about a marathon,” I laugh.\u003c/p>\n\u003cp>But the idea stuck with me as I hung up the phone.\u003c/p>\n\u003cp>I do envision a life for myself someday in which I have slightly thicker skin — a life in which I don’t cry because a friend forgets to return my text. So, after a few days of mulling it over, I decide to take Zubieta’s advice.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>For the past two months I have been on a strict running schedule, gradually increasing my miles, preparing for a half marathon I’m signed up to run next month. Is the physical training helping me tame my emotions? It’s hard to say. I have definitely experienced moments of rejection over the last few weeks that I feel have been easier to deal with. But it’s hard to know if the marathon training is the cause of my increased ability to cope, or if it’s just the power of having a label. Maybe just knowing I’m a G-carrier — knowing that my pain might be more intense than others — is what I have needed all along. My own self-awareness might just be the first real step in changing how I react to the world.\u003c/p>\n\n","blocks":[],"excerpt":"Fifteen to 20 percent of the population carry the gene that causes acute emotional pain in response to social rejection. Will a genetic test to reveal the gene offer validation or hopelessness?","status":"publish","parent":0,"modified":1550281257,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":37,"wordCount":1795},"headData":{"title":"One Gene Makes Me Painfully Sensitive to Rejection. Now What? | KQED","description":"Fifteen to 20 percent of the population carry the gene that causes acute emotional pain in response to social rejection. Will a genetic test to reveal the gene offer validation or hopelessness?","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"442604 https://ww2.kqed.org/futureofyou/?p=442604","disqusUrl":"https://ww2.kqed.org/futureofyou/2019/02/15/i-found-out-my-genetics-makes-me-painfully-sensitive-to-rejection-now-what/","disqusTitle":"One Gene Makes Me Painfully Sensitive to Rejection. Now What?","source":"Your Genes","audioUrl":"https://www.kqed.org/.stream/anon/radio/tcrmag/2019/02/CantrellRejectionGene.mp3","nprByline":"Lisa Cantrell","audioTrackLength":315,"path":"/futureofyou/442604/i-found-out-my-genetics-makes-me-painfully-sensitive-to-rejection-now-what","audioDuration":330000,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cstrong>Originally published on Sept 27, 2018\u003c/strong>\u003c/p>\n\u003cp>A few months ago, I ordered a home genetic testing kit. I didn’t do it because I wanted to know about my ancestry. I did it because I’d heard about a genetic variation that can make people more sensitive to rejection — and I was convinced I had it.\u003c/p>\n\u003cp>I have always been a bit overly sensitive. I remember a particularly devastating moment in fourth grade. Ms. Brown had asked a question I knew the answer to. I raised my hand, stretching my whole body up so she would notice. She made eye contact with me, commented that I had already gotten to answer a question that day, and then called on a student behind me.\u003c/p>\n\u003caside class=\"pullquote alignright\">I have long struggled with bouts of depression; my relationships are typically a roller coaster of anxieties. If I were a G-carrier, it could explain so much of what I was experiencing.\u003c/aside>\n\u003cp>I could feel my face flush with embarrassment. A knot started to form in my throat as, almost in a whisper, I asked to be excused, the tears welling up in my eyes. Once I was safe behind the bathroom door, I used my shirt to muffle the sounds of my crying. Simply because the teacher hadn’t called on me.\u003c/p>\n\u003cp>A few years later in middle school, my friend Jennifer slipped a note into my locker saying that she wanted to play with another kid at recess, not me. That night — and for many nights after — I lay curled up in my bed for hours, the note on my nightstand.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>As I got older, it got worse. The emotional pain I experienced in social situations changed how I felt about myself and how I behaved with other people. As an adult, if a friend didn’t respond to a text, I would pull away and avoid them. When someone I barely knew ghosted me, I convinced myself that I wasn’t desirable to anyone.\u003c/p>\n\u003cp>Friends told me I was overreacting. Sure, everyone feels a little hurt by these things, but to become so debilitated each time was a bit over the top, they told me. Finally, in my late 20s, I started to wonder if maybe there was something wrong with me.\u003c/p>\n\u003cp>\u003cstrong>Is Oversensitivity Biological?\u003c/strong>\u003c/p>\n\u003cp>In 2009, \u003ca href=\"http://www.pnas.org/content/106/35/15079\">a ground-breaking study\u003c/a> investigated the link between emotional sensitivity and our genetics. Scientists already knew that a particular gene, the OPRM1 gene, could influence our sensitivity to physical pain. \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/18719451\">Previous studies\u003c/a> had shown that people with a G allele on this gene required higher doses of morphine to curb pain, suggesting they experience pain more intensely than others. Because \u003ca href=\"https://www.kqed.org/futureofyou/175807/can-taking-tylenol-help-you-get-over-a-romantic-breakup-maybe\">physical pain and emotional pain are processed in similar regions of the brain\u003c/a>, researchers wondered if G-allele carriers might also experience more intense \u003cem>emotional \u003c/em>pain.\u003c/p>\n\u003cp>To test the question, neuroscientists at the University of California Los Angeles recruited 122 people, 49 of whom were G-carriers, the rest of whom were not. Participants came into the lab and played a computer game intended to evoke feelings of rejection. In the game, each participant would toss a ball back and forth to two other virtual players on a screen. The two players would, at some point, exclude the participant. Meanwhile, the participant lay in a functional magnetic resonance imaging (fMRI) brain scanner that measured blood flow to the pain regions of the brain.\u003c/p>\n\u003cfigure id=\"attachment_443244\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003cimg class=\"size-large wp-image-443244\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-1020x381.jpg\" alt=\"Brain scan showing yellow dots\" width=\"640\" height=\"239\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-1020x381.jpg 1020w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-160x60.jpg 160w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-800x299.jpg 800w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-768x287.jpg 768w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-1200x448.jpg 1200w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-1920x717.jpg 1920w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-1180x441.jpg 1180w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-960x359.jpg 960w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-240x90.jpg 240w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-375x140.jpg 375w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/4_dACC-and-aI-labelled-520x194.jpg 520w\" sizes=\"(max-width: 640px) 100vw, 640px\">\u003cfigcaption class=\"wp-caption-text\">fMRI scan of brain showing activation of pain regions (including the dorsal anterior cingulate cortex). The image comes from a study in which participants played “Cyberball” while lying in the fMRI scanner—a game designed to induce feelings of rejection. \u003ccite>(Baldwin Way)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>“What the researchers found was that there was an exaggerated response [in G carriers],” says Jon-Kar Zubieta, a psychiatric researcher at the University of Utah. “Individuals who were G-allele carriers had greater responses to the negative emotional challenge, which was associated with greater activation of the anterior cingulate cortex,” a pain region of the brain.\u003c/p>\n\u003cp>I had called up Zubieta to get his take on the research for this story — but my questions were also personally motivated.\u003c/p>\n\u003cp>“G-carriers seem to have less capacity to compensate for negative emotion,” he told me. And it doesn’t matter whether that negative emotion is in response to physical pain or the social pain of rejection, like what study participants experienced during the ball-tossing game.\u003c/p>\n\u003cp>Zubieta also told me that G-carriers — who make up 15 to 20 percent of the general population — not only feel more hurt in everyday social interactions, “these individuals \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4330509/\">have traits\u003c/a> that make them more prone to developing conditions such as depression and anxiety.”\u003c/p>\n\u003cfigure id=\"attachment_443245\" class=\"wp-caption aligncenter\" style=\"max-width: 600px\">\u003cimg class=\"wp-image-443245 size-full\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2018/07/Zubieta.jpg\" alt=\"A man speaks in front of a white board.\" width=\"600\" height=\"400\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2018/07/Zubieta.jpg 600w, https://ww2.kqed.org/app/uploads/sites/13/2018/07/Zubieta-160x107.jpg 160w, https://ww2.kqed.org/app/uploads/sites/13/2018/07/Zubieta-240x160.jpg 240w, https://ww2.kqed.org/app/uploads/sites/13/2018/07/Zubieta-375x250.jpg 375w, https://ww2.kqed.org/app/uploads/sites/13/2018/07/Zubieta-520x347.jpg 520w\" sizes=\"(max-width: 600px) 100vw, 600px\">\u003cfigcaption class=\"wp-caption-text\">Jon-Kar Zubieta, Chairman of the Department of Psychiatry and Psychiatrist-in-Chief of the University of Utah Neuropsychiatric Institute. \u003ccite>(University of Utah Health)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Listening to Zubieta recount such findings, I found myself nodding my head. All of it resonated with me. I have long struggled with bouts of depression; my relationships are typically a roller coaster of anxieties. If I were a G-carrier, it could explain so much of what I was experiencing.\u003c/p>\n\u003cp>\u003cstrong>Why Do G-Carriers Feel More Pain?\u003c/strong>\u003c/p>\n\u003cp>When the genetic kit finally arrived at my house, I opened it and pulled out the clear test tube. I collected my saliva, sealed it back up, and shipped it off to the lab to be tested.\u003c/p>\n\u003cp>In the weeks I spent waiting for my results, I looked up more research on how the OPRM1 gene could lead to a heightened sense of pain.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"emailsignup","attributes":{"named":{"newslettername":"science","align":"right","label":""},"numeric":[]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>As it turns out, the gene controls the number of opioid receptors in the brain. In a typical brain, when a person is experiencing pain, neurons fire in regions such as the anterior cingulate cortex. In response, the body releases endorphins — our natural pain killers. The endorphins rush into the brain and attach to neuron receptors, inhibiting those cells from firing, effectively stopping the pain signal. This process is actually what happens during the “runner’s high,” and the same process occurs for most people when they experience the pain of rejection.\u003c/p>\n\u003cp>However, if a person doesn’t have enough opioid receptors or doesn’t release a sufficient amount of endorphins, they could experience more suffering than others. Zubieta says this is likely what happens to G-carriers; they appear to have fewer receptors in critical areas of the brain and, he adds, “they may have less capacity to release natural opioids in general.” This means, Zubieta says, that G-carriers “have less capacity to suppress responses to pain.”\u003c/p>\n\u003cp>\u003cstrong>So … Am I A G-Carrier?\u003c/strong>\u003c/p>\n\u003cp>Several weeks after shipping off my saliva, I was at home when an email popped up in my inbox; my results had come in. My stomach dropped and I sat staring at the unopened email for a few minutes.\u003c/p>\n\u003cp>What would it mean if I were a G-carrier? It would feel validating, of course. For so long I had felt like I was emotionally weak. If I were a G-carrier then it would mean there was a biological explanation for my feelings. It would mean that I hadn’t been overreacting all these years; rather, I had been reacting proportionally to the pain I was feeling — pain that 80 to 85 percent of the population simply doesn’t feel.\u003c/p>\n\u003cp>On the other hand, if I weren’t a G-carrier, I wasn’t sure where that would leave me. I could feel my heart beating faster. My hands shook slightly as I struggled to steady my breathing.\u003c/p>\n\u003cp>I opened the email and scrolled through lines of the genetic code until I found the OPRM1 gene on chromosome 6. Typed in small font was a “G.”\u003c/p>\n\u003cfigure id=\"attachment_442608\" class=\"wp-caption alignright\" style=\"max-width: 240px\">\u003cimg class=\"size-full wp-image-442608\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2018/06/RS31383_CANTRELL_003-sfi.jpg\" alt=\"\" width=\"240\" height=\"360\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2018/06/RS31383_CANTRELL_003-sfi.jpg 240w, https://ww2.kqed.org/app/uploads/sites/13/2018/06/RS31383_CANTRELL_003-sfi-160x240.jpg 160w\" sizes=\"(max-width: 240px) 100vw, 240px\">\u003cfigcaption class=\"wp-caption-text\">Lisa Cantrell stretches prior to running at Dolores Park in San Francisco, Calif., on Monday, June 11, 2018. \u003ccite>(Lauren Hanussak/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>\u003cstrong>What Now?\u003c/strong>\u003c/p>\n\u003cp>So am I stuck with unbearable pain forever? A prisoner to my genetics? On the phone with Zubieta, I ask him if a G-carrier like me could do anything about it.\u003c/p>\n\u003cp>“You have to remember that the opioid system becomes active when there are things like exercise or stressors,” so when you do physically demanding sports or activities that in some way cause pain “you are training the system.” In other words, Zubieta says, you can modify your brain’s response.\u003c/p>\n\u003cp>The advice makes sense. Exercise not only releases endorphins that decrease pain in the moment, regularly challenging your body with physical activity can strengthen the overall functioning of the opioid system, potentially prompting your brain to create new receptors and urging your body to increase the amount of endorphins released each time you experience a stressor.\u003c/p>\n\u003cp>All of this could make the system more optimal, more prepared to kick into full gear when it encounters pain, be it physical or emotional. Interestingly, \u003ca href=\"https://www.sciencedirect.com/science/article/abs/pii/003193849190418N\">chocolate\u003c/a> and \u003ca href=\"http://rspb.royalsocietypublishing.org/content/early/2011/09/12/rspb.2011.1373.short\">laughter\u003c/a> may also help — they bump up endorphin release, which could alleviate pain in the moment as well as have longer term effects.\u003c/p>\n\u003cp>Zubieta continued with his suggestions. “So you could do yoga… or run marathons.” Something physically demanding, he says.\u003c/p>\n\u003cp>“I’m not sure about a marathon,” I laugh.\u003c/p>\n\u003cp>But the idea stuck with me as I hung up the phone.\u003c/p>\n\u003cp>I do envision a life for myself someday in which I have slightly thicker skin — a life in which I don’t cry because a friend forgets to return my text. So, after a few days of mulling it over, I decide to take Zubieta’s advice.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"floatright"},"numeric":["floatright"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>For the past two months I have been on a strict running schedule, gradually increasing my miles, preparing for a half marathon I’m signed up to run next month. Is the physical training helping me tame my emotions? It’s hard to say. I have definitely experienced moments of rejection over the last few weeks that I feel have been easier to deal with. But it’s hard to know if the marathon training is the cause of my increased ability to cope, or if it’s just the power of having a label. Maybe just knowing I’m a G-carrier — knowing that my pain might be more intense than others — is what I have needed all along. My own self-awareness might just be the first real step in changing how I react to the world.\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/442604/i-found-out-my-genetics-makes-me-painfully-sensitive-to-rejection-now-what","authors":["byline_futureofyou_442604"],"categories":["futureofyou_73","futureofyou_1064"],"tags":["futureofyou_1275","futureofyou_120","futureofyou_80"],"featImg":"futureofyou_444781","label":"source_futureofyou_442604"},"futureofyou_445019":{"type":"posts","id":"futureofyou_445019","meta":{"index":"posts_1591205157","site":"futureofyou","id":"445019","score":null,"sort":[1539363244000]},"guestAuthors":[],"slug":"easy-dna-identifications-with-genealogy-databases-raise-privacy-concerns","title":"Easy DNA Identifications With Genealogy Databases Raise Privacy Concerns","publishDate":1539363244,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>Police in California \u003ca href=\"https://www.npr.org/sections/thetwo-way/2018/04/27/606624218/in-hunt-for-golden-state-killer-investigators-uploaded-his-dna-to-genealogy-site\" target=\"_blank\" rel=\"noopener\">made headlines\u003c/a> this spring when they charged a former police officer with being the Golden State Killer, a man who allegedly committed a series of notorious rapes and murders in the 1970s and '80s.[contextly_sidebar id=\"wnxqjWPunPnkNxirmoKmxB8OyxTBzMuy\"]\u003c/p>\n\u003cp>Authorities revealed they used DNA from a publicly available genealogy website to crack the case.\u003c/p>\n\u003cp>Since then, police around the country have started doing the same sort of thing to solve other cold cases.\u003c/p>\n\u003cp>That prompted \u003ca href=\"https://www.myheritage.com/management/yaniv_erlich\" target=\"_blank\" rel=\"noopener\">Yaniv Erlich, \u003c/a>the chief science officer at the Israeli company \u003ca href=\"https://www.myheritage.com/\" target=\"_blank\" rel=\"noopener\">MyHeritage\u003c/a>, to investigate just how easy it is to use public genealogy databases to track down people.\u003c/p>\n\u003cp>\"We wanted to quantify how powerful this technique is to identify individuals,\" Erlich says. So he and his colleagues analyzed the genomes of 1.28 million people in the company's database.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>In a \u003ca href=\"http://science.sciencemag.org/lookup/doi/10.1126/science.aau4832\" target=\"_blank\" rel=\"noopener\">paper \u003c/a>published Thursday in the journal \u003cem>Science\u003c/em>, the researchers projected that they could identify third cousins and more closely related relatives in more than 60 percent of people of European descent. (They chose this group because most people in their database have that ancestry.)\u003c/p>\n\u003cp>\"It's kind of like each person in this database is a beacon that illuminates hundreds of distant relatives,\" Erlich says. \"So it's enough to have your third cousin or your second cousin once-removed in these databases to actually identify you.\"[contextly_sidebar id=\"B44UUm4fmJ0qJhwetu8JjvUYBxbNVQtq\"]\u003c/p>\n\u003cp>And when the researchers combined their strategy with other information, such a specific geographic area or the approximate age of a person, they could quickly reduce a list of possibilities to just a few people.\u003c/p>\n\u003cp>\"Of course, you need the genealogical records. You need to do the work. But you have enough power to to get very close,\" Erlich says.\u003c/p>\n\u003cp>And that's not all. Erlich estimates that as his and other databases grow, investigators will essentially be able to identify anyone in the United States within that ethnic background within a few years.\u003c/p>\n\u003cp>\"It seems that very quickly we can get virtually to nearly everyone,\" Erlich says.\u003c/p>\n\u003cp>In another part of the study, the researchers went even further to see if they could do the same thing with other DNA databases. They were able to use their techniques to identify a supposedly anonymous woman whose DNA was stored in the \u003ca href=\"https://www.genome.gov/27528684/1000-genomes-project/\" target=\"_blank\" rel=\"noopener\">1,000 Genomes Project\u003c/a>, a National Institutes of Health research database.\u003c/p>\n\u003cp>\"This technique doesn't only get you criminals,\" Erlich says. \"You can also use this technique for other purposes — maybe purposes that could be illegitimate.\"\u003c/p>\n\u003cp>And that, he says, raises serious questions about privacy.\u003c/p>\n\u003cp>\"The police currently [are] using these techniques to find ... [murderers] and bad people,\" Erlich says. \"But are we OK with using this technique to identify people in a political demonstration who left their DNA behind? There are many scenarios that you can think about misuse.\"[contextly_sidebar id=\"EdtIiFNqDOAH81r6zsse3iX6ZCM6PiDN\"]\u003c/p>\n\u003cp>But some people involved in genealogical forensics defend the use of the techniques to help solves serious crimes.\u003c/p>\n\u003cp>\"I was excited to see this demonstration that genetic genealogy is so powerful,\" says \u003ca href=\"https://www.parabon-nanolabs.com/nanolabs/news-events/2015/10/snapshot-ishi-presentation.html\" target=\"_blank\" rel=\"noopener\">Ellen Greytak\u003c/a>, director of bioinformatics at \u003ca href=\"https://parabon-nanolabs.com/\" target=\"_blank\" rel=\"noopener\">Parabon Nanolabs, Inc.\u003c/a>, which helps police solve crimes this way.\u003c/p>\n\u003cp>\"We're working on these cases that haven't been able to be solved for decades. They are all either homicide or sexual assault. And some of these are horrific,\" she says.\u003c/p>\n\u003cp>But Greytak and her colleagues caution that this study suggests the process is easier than it seems.\u003c/p>\n\u003cp>\"There are a number of problematic assumptions made in the study that do not reflect the reality of the work I am doing,\" writes \u003ca href=\"http://www.yourgeneticgenealogist.com/p/about-me.html\" target=\"_blank\" rel=\"noopener\">CeCe Moore\u003c/a>, who works with Parabon, in an e-mail. \"The study demonstrates the power of genetic genealogy in a theoretical way, but does not fully capture the challenges of the work in practice.\"\u003c/p>\n\u003cp>But others argue that the findings underscore the need to make sure people know what they're getting into when they provide their genetic information to genealogy services and other databases.\u003c/p>\n\u003cp>\"When you make those decisions to put the genome out in the world it's really hard to dial it back,\" \u003ca href=\"https://its.law.nyu.edu/facultyprofiles/index.cfm?fuseaction=profile.overview&personid=31567\" target=\"_blank\" rel=\"noopener\">Erin Murphy\u003c/a>, a professor at the New York University School of Law.\u003c/p>\n\u003cp>\"And more importantly,\" she says, \"you've made a decision not just for yourself but for your siblings, for your distant cousins, people you don't even know you're related to, for your children, for your children's children.\"\u003c/p>\n\u003cp>A second \u003ca href=\"http://www.cell.com/cell/fulltext/S0092-8674(18)31180-2\" target=\"_blank\" rel=\"noopener\">paper\u003c/a> published Thursday in the journal \u003cem>Cell\u003c/em> found that it could be possible to link ancestry databases to older law enforcement DNA databases, giving police yet another potential tool.\u003c/p>\n\u003cp>\"We were trying to pose the question of whether a newer, more modern system of genetic markers could be tested against the old system and still get matches and find relatives,\" says \u003ca href=\"https://profiles.stanford.edu/noah-rosenberg\" target=\"_blank\" rel=\"noopener\">Noah Rosenberg\u003c/a>, a biology professor at Stanford University.\u003c/p>\n\u003cp>Taking these studies together, some bioethicists and legal experts say they show that it's important to take steps to protect genetic information and make sure people providing DNA samples are aware of the risks.\u003c/p>\n\u003cp>\"We can tell people that we can de-identify their data,\" says \u003ca href=\"https://www.bioethics.nih.gov/people/berkman-bio.shtml\" target=\"_blank\" rel=\"noopener\">Benjamin Berkman\u003c/a>, a bioethicist at the National Institutes of Health, who was speaking for himself, not NIH. \"We can tell them about all the procedural and technical safeguards that we've put in place to protect the confidentiality of their data. But I don't think we can promise people anonymity.\"\u003c/p>\n\u003cp>As a result, Berkman says, \"it's incumbent on anyone collecting and aggregating and sharing genomic data to be clear exactly how the data will be treated and whether there are any risks to genomic privacy.\"\u003c/p>\n\u003cp>For his part, Erlich proposes that all genetic information be encrypted to protect the information and enable people to explicitly provide consent for using their data.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"It sounds geeky and complicated, but it's very simple in practice,\" Erlich says.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Easy+DNA+Identifications+With+Genealogy+Databases+Raise+Privacy+Concerns&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n","blocks":[],"excerpt":"A majority of Americans of European descent could be linked to third cousins, or closer relatives, using genealogy databases, a study finds. Soon it may be possible to identify nearly everyone by DNA.","status":"publish","parent":0,"modified":1539363353,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":32,"wordCount":989},"headData":{"title":"Easy DNA Identifications With Genealogy Databases Raise Privacy Concerns | KQED","description":"A majority of Americans of European descent could be linked to third cousins, or closer relatives, using genealogy databases, a study finds. Soon it may be possible to identify nearly everyone by DNA.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"445019 https://ww2.kqed.org/futureofyou/?p=445019","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/10/12/easy-dna-identifications-with-genealogy-databases-raise-privacy-concerns/","disqusTitle":"Easy DNA Identifications With Genealogy Databases Raise Privacy Concerns","source":"DIY Health","nprByline":"Rob Stein, NPR","nprImageAgency":"Randy Pench/Sacramento Bee/TNS via Getty Images","nprStoryId":"656268742","nprApiLink":"http://api.npr.org/query?id=656268742&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2018/10/11/656268742/easy-dna-identifications-with-genealogy-databases-raise-privacy-concerns?ft=nprml&f=656268742","nprRetrievedStory":"1","nprPubDate":"Thu, 11 Oct 2018 18:53:00 -0400","nprStoryDate":"Thu, 11 Oct 2018 15:58:00 -0400","nprLastModifiedDate":"Thu, 11 Oct 2018 16:51:42 -0400","nprAudio":"https://ondemand.npr.org/anon.npr-mp3/npr/atc/2018/10/20181011_atc_easy_dna_identifications_with_genealogy_databases_raise_privacy_concerns.mp3?orgId=1&topicId=1128&d=251&p=2&story=656268742&ft=nprml&f=656268742","nprAudioM3u":"http://api.npr.org/m3u/1656682250-420468.m3u?orgId=1&topicId=1128&d=251&p=2&story=656268742&ft=nprml&f=656268742","audioTrackLength":251,"path":"/futureofyou/445019/easy-dna-identifications-with-genealogy-databases-raise-privacy-concerns","audioUrl":"https://ondemand.npr.org/anon.npr-mp3/npr/atc/2018/10/20181011_atc_easy_dna_identifications_with_genealogy_databases_raise_privacy_concerns.mp3?orgId=1&topicId=1128&d=251&p=2&story=656268742&ft=nprml&f=656268742","parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Police in California \u003ca href=\"https://www.npr.org/sections/thetwo-way/2018/04/27/606624218/in-hunt-for-golden-state-killer-investigators-uploaded-his-dna-to-genealogy-site\" target=\"_blank\" rel=\"noopener\">made headlines\u003c/a> this spring when they charged a former police officer with being the Golden State Killer, a man who allegedly committed a series of notorious rapes and murders in the 1970s and '80s.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Authorities revealed they used DNA from a publicly available genealogy website to crack the case.\u003c/p>\n\u003cp>Since then, police around the country have started doing the same sort of thing to solve other cold cases.\u003c/p>\n\u003cp>That prompted \u003ca href=\"https://www.myheritage.com/management/yaniv_erlich\" target=\"_blank\" rel=\"noopener\">Yaniv Erlich, \u003c/a>the chief science officer at the Israeli company \u003ca href=\"https://www.myheritage.com/\" target=\"_blank\" rel=\"noopener\">MyHeritage\u003c/a>, to investigate just how easy it is to use public genealogy databases to track down people.\u003c/p>\n\u003cp>\"We wanted to quantify how powerful this technique is to identify individuals,\" Erlich says. So he and his colleagues analyzed the genomes of 1.28 million people in the company's database.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>In a \u003ca href=\"http://science.sciencemag.org/lookup/doi/10.1126/science.aau4832\" target=\"_blank\" rel=\"noopener\">paper \u003c/a>published Thursday in the journal \u003cem>Science\u003c/em>, the researchers projected that they could identify third cousins and more closely related relatives in more than 60 percent of people of European descent. (They chose this group because most people in their database have that ancestry.)\u003c/p>\n\u003cp>\"It's kind of like each person in this database is a beacon that illuminates hundreds of distant relatives,\" Erlich says. \"So it's enough to have your third cousin or your second cousin once-removed in these databases to actually identify you.\"\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>And when the researchers combined their strategy with other information, such a specific geographic area or the approximate age of a person, they could quickly reduce a list of possibilities to just a few people.\u003c/p>\n\u003cp>\"Of course, you need the genealogical records. You need to do the work. But you have enough power to to get very close,\" Erlich says.\u003c/p>\n\u003cp>And that's not all. Erlich estimates that as his and other databases grow, investigators will essentially be able to identify anyone in the United States within that ethnic background within a few years.\u003c/p>\n\u003cp>\"It seems that very quickly we can get virtually to nearly everyone,\" Erlich says.\u003c/p>\n\u003cp>In another part of the study, the researchers went even further to see if they could do the same thing with other DNA databases. They were able to use their techniques to identify a supposedly anonymous woman whose DNA was stored in the \u003ca href=\"https://www.genome.gov/27528684/1000-genomes-project/\" target=\"_blank\" rel=\"noopener\">1,000 Genomes Project\u003c/a>, a National Institutes of Health research database.\u003c/p>\n\u003cp>\"This technique doesn't only get you criminals,\" Erlich says. \"You can also use this technique for other purposes — maybe purposes that could be illegitimate.\"\u003c/p>\n\u003cp>And that, he says, raises serious questions about privacy.\u003c/p>\n\u003cp>\"The police currently [are] using these techniques to find ... [murderers] and bad people,\" Erlich says. \"But are we OK with using this technique to identify people in a political demonstration who left their DNA behind? There are many scenarios that you can think about misuse.\"\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>But some people involved in genealogical forensics defend the use of the techniques to help solves serious crimes.\u003c/p>\n\u003cp>\"I was excited to see this demonstration that genetic genealogy is so powerful,\" says \u003ca href=\"https://www.parabon-nanolabs.com/nanolabs/news-events/2015/10/snapshot-ishi-presentation.html\" target=\"_blank\" rel=\"noopener\">Ellen Greytak\u003c/a>, director of bioinformatics at \u003ca href=\"https://parabon-nanolabs.com/\" target=\"_blank\" rel=\"noopener\">Parabon Nanolabs, Inc.\u003c/a>, which helps police solve crimes this way.\u003c/p>\n\u003cp>\"We're working on these cases that haven't been able to be solved for decades. They are all either homicide or sexual assault. And some of these are horrific,\" she says.\u003c/p>\n\u003cp>But Greytak and her colleagues caution that this study suggests the process is easier than it seems.\u003c/p>\n\u003cp>\"There are a number of problematic assumptions made in the study that do not reflect the reality of the work I am doing,\" writes \u003ca href=\"http://www.yourgeneticgenealogist.com/p/about-me.html\" target=\"_blank\" rel=\"noopener\">CeCe Moore\u003c/a>, who works with Parabon, in an e-mail. \"The study demonstrates the power of genetic genealogy in a theoretical way, but does not fully capture the challenges of the work in practice.\"\u003c/p>\n\u003cp>But others argue that the findings underscore the need to make sure people know what they're getting into when they provide their genetic information to genealogy services and other databases.\u003c/p>\n\u003cp>\"When you make those decisions to put the genome out in the world it's really hard to dial it back,\" \u003ca href=\"https://its.law.nyu.edu/facultyprofiles/index.cfm?fuseaction=profile.overview&personid=31567\" target=\"_blank\" rel=\"noopener\">Erin Murphy\u003c/a>, a professor at the New York University School of Law.\u003c/p>\n\u003cp>\"And more importantly,\" she says, \"you've made a decision not just for yourself but for your siblings, for your distant cousins, people you don't even know you're related to, for your children, for your children's children.\"\u003c/p>\n\u003cp>A second \u003ca href=\"http://www.cell.com/cell/fulltext/S0092-8674(18)31180-2\" target=\"_blank\" rel=\"noopener\">paper\u003c/a> published Thursday in the journal \u003cem>Cell\u003c/em> found that it could be possible to link ancestry databases to older law enforcement DNA databases, giving police yet another potential tool.\u003c/p>\n\u003cp>\"We were trying to pose the question of whether a newer, more modern system of genetic markers could be tested against the old system and still get matches and find relatives,\" says \u003ca href=\"https://profiles.stanford.edu/noah-rosenberg\" target=\"_blank\" rel=\"noopener\">Noah Rosenberg\u003c/a>, a biology professor at Stanford University.\u003c/p>\n\u003cp>Taking these studies together, some bioethicists and legal experts say they show that it's important to take steps to protect genetic information and make sure people providing DNA samples are aware of the risks.\u003c/p>\n\u003cp>\"We can tell people that we can de-identify their data,\" says \u003ca href=\"https://www.bioethics.nih.gov/people/berkman-bio.shtml\" target=\"_blank\" rel=\"noopener\">Benjamin Berkman\u003c/a>, a bioethicist at the National Institutes of Health, who was speaking for himself, not NIH. \"We can tell them about all the procedural and technical safeguards that we've put in place to protect the confidentiality of their data. But I don't think we can promise people anonymity.\"\u003c/p>\n\u003cp>As a result, Berkman says, \"it's incumbent on anyone collecting and aggregating and sharing genomic data to be clear exactly how the data will be treated and whether there are any risks to genomic privacy.\"\u003c/p>\n\u003cp>For his part, Erlich proposes that all genetic information be encrypted to protect the information and enable people to explicitly provide consent for using their data.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"It sounds geeky and complicated, but it's very simple in practice,\" Erlich says.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Easy+DNA+Identifications+With+Genealogy+Databases+Raise+Privacy+Concerns&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/445019/easy-dna-identifications-with-genealogy-databases-raise-privacy-concerns","authors":["byline_futureofyou_445019"],"categories":["futureofyou_1060","futureofyou_1","futureofyou_73","futureofyou_1064"],"tags":["futureofyou_464","futureofyou_17","futureofyou_197"],"collections":["futureofyou_1093","futureofyou_1094"],"featImg":"futureofyou_445020","label":"source_futureofyou_445019"},"futureofyou_444641":{"type":"posts","id":"futureofyou_444641","meta":{"index":"posts_1591205157","site":"futureofyou","id":"444641","score":null,"sort":[1538075041000]},"guestAuthors":[],"slug":"governments-decision-to-review-research-of-fetal-tissue-blasted-as-political-move","title":"Is the Federal Government Politicizing Research Involving Fetal Tissue?","publishDate":1538075041,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>\u003cstrong>Updated at 3:45 pm ET\u003c/strong>\u003c/p>\n\u003cp>The Department of Health and Human Services says it is reviewing all medical research involving human fetal tissue.\u003c/p>\n\u003cp>HHS \u003ca href=\"https://www.hhs.gov/about/news/2018/09/24/statement-from-the-department-of-health-and-human-services.html\" target=\"_blank\" rel=\"noopener\">said this week\u003c/a> that it will conduct an audit of \"all acquisitions involving human fetal tissue\" as well as \"all research involving fetal tissue to ensure consistency with statutes and regulations governing such research and to ensure the adequacy of procedures and oversight of this research in light of the serious regulatory, moral, and ethical considerations involved.\"[contextly_sidebar id=\"SsrZIxp3cgGelsMqmovjR5mXFrobSZOz\"]\u003c/p>\n\u003cp>In addition, HHS announced that it has canceled \u003ca href=\"https://www.fpds.gov/ezsearch/search.do?q=advanced+bioscience+resources+VENDOR_DUNS_NUMBER%3A%22786845982%22&s=FPDSNG.COM&templateName=1.4.4&indexName=awardfull&sortBy=SIGNED_DATE&desc=Y\" target=\"_blank\" rel=\"noopener\">a $15,000 contract\u003c/a> for a California-based company called Advanced Bioscience Resources to provide the Food and Drug Administration with human fetal tissue to develop testing protocols. The contract was terminated, HHS said, because the department \"was not sufficiently assured that the contract included the appropriate protections applicable to fetal tissue research or met all other procurement requirements.\"\u003c/p>\n\u003cp>Scientists use fetal tissue in medical research because it grows quickly and is highly versatile and long-lasting.\u003c/p>\n\u003cp>\"It allows us to answer specific questions that can't be answered by adult tissue, which is far more specialized,\"\u003c/p>\n\u003cp>NIH Associate Director for Science Policy Carrie Wolinetz \u003ca href=\"https://www.npr.org/sections/health-shots/2015/09/29/444214443/research-on-fetal-tissue-draws-renewed-political-scientific-scrutiny\" target=\"_blank\" rel=\"noopener\">told NPR's Rob Stein\u003c/a> in 2015. \"Fetal tissue can contain information — about structural features, or the architecture of organs — that cells in a dish alone can't provide. And this is sometimes very important to our understanding of disease.\"\u003c/p>\n\u003cp>Fetal tissue used in scientific research often comes from aborted fetuses. In an email to NPR, \u003ca href=\"https://law.wisc.edu/profiles/racharo\" target=\"_blank\" rel=\"noopener\">Alta Charo\u003c/a>, a professor of law and bioethics at the University of Wisconsin, explains why that is.[contextly_sidebar id=\"G1kyrCYVpzDmWCInUE7H0cF8gc9zn4Ce\"]\u003c/p>\n\u003cp>\"Miscarriages are not often an available source, as they do not take place in a controlled environment and may be due to genetic or other anomalies that would render the cadaveric tissues useless,\" she says. \"Therefore, the tissue usually comes from a fetus that has been aborted.\"\u003c/p>\n\u003cp>Despite the small size of the canceled FDA contract, some observers said the larger political symbolism is evident.\u003c/p>\n\u003cp>\"My instinct is that this is driven by politics, and is part of the overall effort to stigmatize and eventually criminalize abortion, as well as part of a larger campaign to roll-back the clock on sexual and reproductive rights,\" Charo says.\u003c/p>\n\u003cp>However, \u003ca href=\"https://lozierinstitute.org/team-member/david-prentice/\" target=\"_blank\" rel=\"noopener\">David Prentice\u003c/a>, vice president and research director for the Charlotte Lozier Institute, a conservative think tank opposed to abortion, says the HHS announcement doesn't go far enough.\u003c/p>\n\u003cp>\"Canceling a small FDA contract ... seems designed to mollify some Members of Congress and groups who were outraged by the continuing funding of fetal tissue research with taxpayer dollars,\" Prentice writes in an email to NPR. \"But what's needed is wholesale reform across the breadth of HHS. Use of fetal tissue is antiquated research, and [HHS Secretary Alex] Azar should redirect those funds to modern science and better alternatives, including adult stem cells.\"\u003c/p>\n\u003cp>\u003cem>Science\u003c/em> notes that on earlier this month, 45 groups opposed to abortion \u003ca href=\"https://www.sba-list.org/wp-content/uploads/2018/09/Group-Letter-to-Azar-FDA-and-fetal-tissue-FINAL-with-Signatures.pdf\" target=\"_blank\" rel=\"noopener\">sent a letter\u003c/a> to Azar calling the FDA contract for fetal tissue \"shocking\" and \"unacceptable.\" A few days later, 85 members of Congress \u003ca href=\"https://chrissmith.house.gov/uploadedfiles/2018-09-17_-chs-hartzler-walker_letter_on_fda_fetal_tissue_contract.pdf\" target=\"_blank\" rel=\"noopener\">sent a letter\u003c/a> to the FDA's commissioner, urging the agency to cancel the contract.\u003c/p>\n\u003cp>The National Institutes of Health, which also falls under HHS, spent $98 million last fiscal year on research that involved human fetal tissue. The NIH said it \"concurs that it is important that research involving human fetal tissue should be consistent with the statutes and regulation governing such research and that it is important to have adequate procedures for oversight.\"[contextly_sidebar id=\"xJs8IF14XoPynhHrniTrS5E5qgAhyVmm\"]\u003c/p>\n\u003cp>Use of fetal tissue in research has been controversial for some time, \u003cem>Science\u003c/em> magazine reported on Tuesday:\u003c/p>\n\u003cblockquote>\u003cp>\"In 2016, \u003ca href=\"https://energycommerce.house.gov/news/press-release/house-creates-select-panel-investigate-handling-infant-lives/\" target=\"_blank\" rel=\"noopener\">Republican members of the House of Representatives\u003c/a>, led by Representative Marsha Blackburn (TN), \u003ca href=\"https://www.sciencemag.org/news/2017/01/fact-checking-congress-s-fetal-tissue-report\">produced a report\u003c/a> that urged the federal government to transition to obtaining fetal tissue from miscarriages and stillbirths. But opponents of fetal tissue research have failed repeatedly to pass legislation that would end funding for research using tissue from electively aborted fetuses — most recently earlier this month, when language prohibiting such funding was stripped from a 2019 HHS spending bill.\"\u003c/p>\u003c/blockquote>\n\u003cp>\u003ca href=\"https://trentcenter.duke.edu/node/221\" target=\"_blank\" rel=\"noopener\">Ross McKinney\u003c/a>, chief scientific officer at the Association of American Medical Colleges, says fetal tissue was key in the development of major medical advances such as vaccines for polio, rubella, measles, chickenpox, adenovirus and rabies, as well as treatments for diseases such as rheumatoid arthritis, cystic fibrosis and hemophilia.\u003c/p>\n\u003cp>\"The unique characteristics of this tissue are essential to the study of fetal diseases, like those caused by Zika virus, and hold promise for advancing biomedical research in other areas as well, bringing hope to patients struggling with diseases such as Alzheimer's, Parkinson's, and multiple sclerosis,\" he writes in an email to NPR.\u003c/p>\n\u003cp>\"Fetal tissue continues to be an important resource for biomedical research, and the Association of American Medical Colleges fully supports its availability as one of the scientific methods that could save and improve lives.\"[contextly_sidebar id=\"GY9wMG5EY8EjMrFWoS2AArgcQmiE5UTu\"]\u003c/p>\n\u003cp>During \u003ca href=\"https://www.npr.org/2016/01/28/464594826/in-wake-of-videos-planned-parenthood-investigations-find-no-fetal-tissue-sales\" target=\"_blank\" rel=\"noopener\">a 2015 brouhaha\u003c/a>, the Obama-era HHS \u003ca href=\"https://www.plannedparenthood.org/files/3514/4709/3497/HHS_Letter_2015_08_14_-_FT_Research.pdf\" target=\"_blank\" rel=\"noopener\">sent a letter\u003c/a> to two Republican senators calling the use of fetal tissue in medical research \"an instrumental component of our attempts to understand, treat, and cure a number of conditions and diseases that affect millions of Americans,\" noting that scientists in the U.S. have been working with fetal tissue \u003ca href=\"https://fas.org/sgp/crs/misc/R44129.pdf\" target=\"_blank\" rel=\"noopener\">since the 1930s\u003c/a>.\u003c/p>\n\u003cp>\u003cem>NPR science correspondent Rob Stein contributed to this report.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Health+And+Human+Services+Says+It%27s+Reviewing+Use+Of+Fetal+Tissue+For+Research&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003c/p>\n","blocks":[],"excerpt":"The audit has been called a political gesture to placate anti-abortion groups that oppose use of the tissue. Fetal tissue has played a part in developing vaccines and medical treatments.","status":"publish","parent":0,"modified":1538075106,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":24,"wordCount":917},"headData":{"title":"Is the Federal Government Politicizing Research Involving Fetal Tissue? | KQED","description":"The audit has been called a political gesture to placate anti-abortion groups that oppose use of the tissue. Fetal tissue has played a part in developing vaccines and medical treatments.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"444641 https://ww2.kqed.org/futureofyou/?p=444641","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/09/27/governments-decision-to-review-research-of-fetal-tissue-blasted-as-political-move/","disqusTitle":"Is the Federal Government Politicizing Research Involving Fetal Tissue?","source":"Health","nprImageCredit":"Chip Somodevilla","nprByline":"Laurel Wamsley, NPR","nprImageAgency":"Getty Images","nprStoryId":"651838889","nprApiLink":"http://api.npr.org/query?id=651838889&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/2018/09/26/651838889/health-and-human-services-says-its-reviewing-use-of-fetal-tissue-for-research?ft=nprml&f=651838889","nprRetrievedStory":"1","nprPubDate":"Wed, 26 Sep 2018 16:17:00 -0400","nprStoryDate":"Wed, 26 Sep 2018 15:12:00 -0400","nprLastModifiedDate":"Wed, 26 Sep 2018 16:18:07 -0400","path":"/futureofyou/444641/governments-decision-to-review-research-of-fetal-tissue-blasted-as-political-move","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cstrong>Updated at 3:45 pm ET\u003c/strong>\u003c/p>\n\u003cp>The Department of Health and Human Services says it is reviewing all medical research involving human fetal tissue.\u003c/p>\n\u003cp>HHS \u003ca href=\"https://www.hhs.gov/about/news/2018/09/24/statement-from-the-department-of-health-and-human-services.html\" target=\"_blank\" rel=\"noopener\">said this week\u003c/a> that it will conduct an audit of \"all acquisitions involving human fetal tissue\" as well as \"all research involving fetal tissue to ensure consistency with statutes and regulations governing such research and to ensure the adequacy of procedures and oversight of this research in light of the serious regulatory, moral, and ethical considerations involved.\"\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>In addition, HHS announced that it has canceled \u003ca href=\"https://www.fpds.gov/ezsearch/search.do?q=advanced+bioscience+resources+VENDOR_DUNS_NUMBER%3A%22786845982%22&s=FPDSNG.COM&templateName=1.4.4&indexName=awardfull&sortBy=SIGNED_DATE&desc=Y\" target=\"_blank\" rel=\"noopener\">a $15,000 contract\u003c/a> for a California-based company called Advanced Bioscience Resources to provide the Food and Drug Administration with human fetal tissue to develop testing protocols. The contract was terminated, HHS said, because the department \"was not sufficiently assured that the contract included the appropriate protections applicable to fetal tissue research or met all other procurement requirements.\"\u003c/p>\n\u003cp>Scientists use fetal tissue in medical research because it grows quickly and is highly versatile and long-lasting.\u003c/p>\n\u003cp>\"It allows us to answer specific questions that can't be answered by adult tissue, which is far more specialized,\"\u003c/p>\n\u003cp>NIH Associate Director for Science Policy Carrie Wolinetz \u003ca href=\"https://www.npr.org/sections/health-shots/2015/09/29/444214443/research-on-fetal-tissue-draws-renewed-political-scientific-scrutiny\" target=\"_blank\" rel=\"noopener\">told NPR's Rob Stein\u003c/a> in 2015. \"Fetal tissue can contain information — about structural features, or the architecture of organs — that cells in a dish alone can't provide. And this is sometimes very important to our understanding of disease.\"\u003c/p>\n\u003cp>Fetal tissue used in scientific research often comes from aborted fetuses. In an email to NPR, \u003ca href=\"https://law.wisc.edu/profiles/racharo\" target=\"_blank\" rel=\"noopener\">Alta Charo\u003c/a>, a professor of law and bioethics at the University of Wisconsin, explains why that is.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\"Miscarriages are not often an available source, as they do not take place in a controlled environment and may be due to genetic or other anomalies that would render the cadaveric tissues useless,\" she says. \"Therefore, the tissue usually comes from a fetus that has been aborted.\"\u003c/p>\n\u003cp>Despite the small size of the canceled FDA contract, some observers said the larger political symbolism is evident.\u003c/p>\n\u003cp>\"My instinct is that this is driven by politics, and is part of the overall effort to stigmatize and eventually criminalize abortion, as well as part of a larger campaign to roll-back the clock on sexual and reproductive rights,\" Charo says.\u003c/p>\n\u003cp>However, \u003ca href=\"https://lozierinstitute.org/team-member/david-prentice/\" target=\"_blank\" rel=\"noopener\">David Prentice\u003c/a>, vice president and research director for the Charlotte Lozier Institute, a conservative think tank opposed to abortion, says the HHS announcement doesn't go far enough.\u003c/p>\n\u003cp>\"Canceling a small FDA contract ... seems designed to mollify some Members of Congress and groups who were outraged by the continuing funding of fetal tissue research with taxpayer dollars,\" Prentice writes in an email to NPR. \"But what's needed is wholesale reform across the breadth of HHS. Use of fetal tissue is antiquated research, and [HHS Secretary Alex] Azar should redirect those funds to modern science and better alternatives, including adult stem cells.\"\u003c/p>\n\u003cp>\u003cem>Science\u003c/em> notes that on earlier this month, 45 groups opposed to abortion \u003ca href=\"https://www.sba-list.org/wp-content/uploads/2018/09/Group-Letter-to-Azar-FDA-and-fetal-tissue-FINAL-with-Signatures.pdf\" target=\"_blank\" rel=\"noopener\">sent a letter\u003c/a> to Azar calling the FDA contract for fetal tissue \"shocking\" and \"unacceptable.\" A few days later, 85 members of Congress \u003ca href=\"https://chrissmith.house.gov/uploadedfiles/2018-09-17_-chs-hartzler-walker_letter_on_fda_fetal_tissue_contract.pdf\" target=\"_blank\" rel=\"noopener\">sent a letter\u003c/a> to the FDA's commissioner, urging the agency to cancel the contract.\u003c/p>\n\u003cp>The National Institutes of Health, which also falls under HHS, spent $98 million last fiscal year on research that involved human fetal tissue. The NIH said it \"concurs that it is important that research involving human fetal tissue should be consistent with the statutes and regulation governing such research and that it is important to have adequate procedures for oversight.\"\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Use of fetal tissue in research has been controversial for some time, \u003cem>Science\u003c/em> magazine reported on Tuesday:\u003c/p>\n\u003cblockquote>\u003cp>\"In 2016, \u003ca href=\"https://energycommerce.house.gov/news/press-release/house-creates-select-panel-investigate-handling-infant-lives/\" target=\"_blank\" rel=\"noopener\">Republican members of the House of Representatives\u003c/a>, led by Representative Marsha Blackburn (TN), \u003ca href=\"https://www.sciencemag.org/news/2017/01/fact-checking-congress-s-fetal-tissue-report\">produced a report\u003c/a> that urged the federal government to transition to obtaining fetal tissue from miscarriages and stillbirths. But opponents of fetal tissue research have failed repeatedly to pass legislation that would end funding for research using tissue from electively aborted fetuses — most recently earlier this month, when language prohibiting such funding was stripped from a 2019 HHS spending bill.\"\u003c/p>\u003c/blockquote>\n\u003cp>\u003ca href=\"https://trentcenter.duke.edu/node/221\" target=\"_blank\" rel=\"noopener\">Ross McKinney\u003c/a>, chief scientific officer at the Association of American Medical Colleges, says fetal tissue was key in the development of major medical advances such as vaccines for polio, rubella, measles, chickenpox, adenovirus and rabies, as well as treatments for diseases such as rheumatoid arthritis, cystic fibrosis and hemophilia.\u003c/p>\n\u003cp>\"The unique characteristics of this tissue are essential to the study of fetal diseases, like those caused by Zika virus, and hold promise for advancing biomedical research in other areas as well, bringing hope to patients struggling with diseases such as Alzheimer's, Parkinson's, and multiple sclerosis,\" he writes in an email to NPR.\u003c/p>\n\u003cp>\"Fetal tissue continues to be an important resource for biomedical research, and the Association of American Medical Colleges fully supports its availability as one of the scientific methods that could save and improve lives.\"\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>During \u003ca href=\"https://www.npr.org/2016/01/28/464594826/in-wake-of-videos-planned-parenthood-investigations-find-no-fetal-tissue-sales\" target=\"_blank\" rel=\"noopener\">a 2015 brouhaha\u003c/a>, the Obama-era HHS \u003ca href=\"https://www.plannedparenthood.org/files/3514/4709/3497/HHS_Letter_2015_08_14_-_FT_Research.pdf\" target=\"_blank\" rel=\"noopener\">sent a letter\u003c/a> to two Republican senators calling the use of fetal tissue in medical research \"an instrumental component of our attempts to understand, treat, and cure a number of conditions and diseases that affect millions of Americans,\" noting that scientists in the U.S. have been working with fetal tissue \u003ca href=\"https://fas.org/sgp/crs/misc/R44129.pdf\" target=\"_blank\" rel=\"noopener\">since the 1930s\u003c/a>.\u003c/p>\n\u003cp>\u003cem>NPR science correspondent Rob Stein contributed to this report.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Health+And+Human+Services+Says+It%27s+Reviewing+Use+Of+Fetal+Tissue+For+Research&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003c/p>\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/444641/governments-decision-to-review-research-of-fetal-tissue-blasted-as-political-move","authors":["byline_futureofyou_444641"],"categories":["futureofyou_1","futureofyou_73","futureofyou_1064"],"tags":["futureofyou_342","futureofyou_1176","futureofyou_1615","futureofyou_294"],"collections":["futureofyou_1094"],"featImg":"futureofyou_444642","label":"source_futureofyou_444641"},"futureofyou_444281":{"type":"posts","id":"futureofyou_444281","meta":{"index":"posts_1591205157","site":"futureofyou","id":"444281","score":null,"sort":[1536178859000]},"guestAuthors":[],"slug":"historic-gene-editing-attempt-in-first-human-off-to-a-positive-start","title":"Historic Gene Editing Attempt in First Human Off to a Positive Start","publishDate":1536178859,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>Early, partial results from a historic gene editing study give encouraging signs that the treatment may be safe and having at least some of its hoped-for effect, but it’s too soon to know whether it ultimately will succeed.[contextly_sidebar id=\"nLB0LaskunDkFSzX8O5LVSxfj3Ayt7CZ\"]\u003c/p>\n\u003cp>The results announced Wednesday are from the first human \u003ca href=\"//mps2study.com/study-overview/?pn=\">test\u003c/a> of gene editing in the body, an attempt to permanently change someone’s DNA to cure a disease — in this case, a genetic disorder called \u003ca href=\"https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Mucopolysaccharidoses-Fact-Sheet\">Hunter syndrome\u003c/a> that often kills people in their teens.\u003c/p>\n\u003cp>In two patients who got a medium dose of the treatment, urine levels of large sugar compounds that are hallmarks of Hunter syndrome had fallen by half, on average, four months later — a possible sign the treatment is working. Two others who got a low dose have seen little change in these sugars so far.\u003c/p>\n\u003cp>There’s no way to know yet whether the change in the middle-dose patients is due to the gene editing or something else, but the fact their sugars have declined consistently since treatment suggests it might be.\u003c/p>\n\u003cp>“I cannot absolutely say it’s a treatment effect” but the drop is “really encouraging,” said the study leader, Dr. Joseph Muenzer of the University of North Carolina, Chapel Hill. The main goal of early treatment studies is to test safety, though researchers also look for hints that the therapy is working. Muenzer gave the results at a conference in Greece and consults for the treatment’s maker, California-based Sangamo Therapeutics.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The company’s president, Dr. Sandy Macrae, said tests in about five months will reveal more, but the change in the middle-dose group so far “looks really good.”[contextly_sidebar id=\"FMPymRVSamCP4f8RpmzlwSdu0yioj0rt\"]\u003c/p>\n\u003cp>“The most rational explanation for this is that what we hoped was going to happen has happened,” he said.\u003c/p>\n\u003cp>Several independent experts agreed.\u003c/p>\n\u003cp>“The results are exciting” and suggest that the gene editing is working to some degree, without safety concerns so far, said Dr. Howard Kaufman, a Boston scientist and member of a National Institutes of Health panel that reviewed the study before it began.\u003c/p>\n\u003cp>Dr. Matthew Porteus, a genetics expert at Stanford University who consults for two other companies developing gene therapies, said more time is needed to see how the patients’ immune system continues to react to the treatment and whether the effects last, but added, “I would be excited about continuing to push along” based on these results.\u003c/p>\n\u003cp>\u003cstrong>How It Works\u003c/strong>\u003c/p>\n\u003cp>Gene editing is intended as a more precise way to do gene therapy, to knock out a bad gene or supply a good one that’s missing. Doctors hope it will give a way to address a host of diseases that can’t be treated well now.\u003c/p>\n\u003cp>In November, a Phoenix-area man with Hunter syndrome, Brian Madeux, became the first person to test this inside the body. He lacks a gene that makes an enzyme that breaks down certain large sugar compounds called GAGs. These build up in cells and cause havoc throughout the body.\u003c/p>\n\u003cp>Through an IV, Madeux received many copies of a corrective gene and a gene-editing tool called zinc finger nucleases to help put it in a precise spot in his DNA. He was one of the two patients given a very low dose of the treatment, because this first-in-human testing called for extreme caution.\u003c/p>\n\u003cp>\u003cstrong>Early Results\u003c/strong>\u003c/p>\n\u003cp>In Madeux and the other low-dose patient, levels of the tell-tale sugar compounds in urine rose 9 percent on average after four months. Muenzer said it’s hard to know whether this is a significant change; little is known about the biology of these compounds, including whether they fluctuate during the day or before or after meals.[contextly_sidebar id=\"g6IAb2xjtv0z0Te9cBhCwQAn8pi68Yxx\"]\u003c/p>\n\u003cp>A liver biopsy on one patient given a low dose of the therapy found no evidence that the gene editing had occurred, but Sangamo scientists said this dose is far below the level at which such signs had been detected in research on primates.\u003c/p>\n\u003cp>Two other patients were given a middle dose that was twice what the first two patients received. Their GAG levels declined by 51 percent after four months, on average. Two of the main types of these sugars that accumulate in tissues declined 32 percent and 61 percent, respectively.\u003c/p>\n\u003cp>It is not yet known if declines like these can improve patients’ health or slow the progression of the disease.\u003c/p>\n\u003cp>“This is not proof that this is a successful therapy yet, that these patients had enough gene editing to now supply them with the enzyme they need for the rest of their life,” Muenzer said.\u003c/p>\n\u003cp>But he said an important goal was met: the treatment seems safe. There were two serious side effects — one patient was hospitalized for bronchitis and another for an irregular heartbeat — but those were deemed due to their disease and pre-existing conditions, not the gene treatment.\u003c/p>\n\u003cp>Blood tests did not detect the missing enzyme. Company scientists said this could be because any that was being made was rapidly used by cells rather than getting into the bloodstream — an explanation some outside experts agreed with. What counts, they said, was seeing the result of enzyme activity, the drop in sugars.\u003c/p>\n\u003cp>\u003cstrong>Next Steps\u003c/strong>\u003c/p>\n\u003cp>Two more patients have been given the highest dose being tested — 10 times the starting dose — for a total of six patients in the study. The next step is to start taking patients off the weekly enzyme treatments they’ve been receiving to see if the gene therapy has changed their bodies so they make enough of the enzyme themselves.\u003c/p>\n\u003cp>More results are expected at a medical meeting in February.\u003c/p>\n\u003cp>“We need to see sustained levels for this to be practical. If this only works for six months, that’s not very beneficial,” Muenzer said. “Time’s going to tell.”\u003c/p>\n\u003cp>In an interview at his home in Arizona last month, Madeux, 45, told The Associated Press he volunteered for the study in hope of being able to stop the weekly, three-hour enzyme infusions, but also to help find a treatment for future generations with the disease.\u003c/p>\n\u003cp>“I’m old and having Hunter’s has done a lot of damage to my body,” Madeux said. “I’m actually pretty lucky I’ve lived this long.”\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp> \u003c/p>\n\n","blocks":[],"excerpt":"Partial results for gene editing study give promising signs that the treatment may be safe and have at least some of its hoped - for effect.","status":"publish","parent":0,"modified":1536177185,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":30,"wordCount":1104},"headData":{"title":"Historic Gene Editing Attempt in First Human Off to a Positive Start | KQED","description":"Partial results for gene editing study give promising signs that the treatment may be safe and have at least some of its hoped - for effect.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"444281 https://ww2.kqed.org/futureofyou/?p=444281","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/09/05/historic-gene-editing-attempt-in-first-human-off-to-a-positive-start/","disqusTitle":"Historic Gene Editing Attempt in First Human Off to a Positive Start","source":"Your Genes","nprByline":"Marilynn Marchione\u003cbr />The Associated Press","path":"/futureofyou/444281/historic-gene-editing-attempt-in-first-human-off-to-a-positive-start","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Early, partial results from a historic gene editing study give encouraging signs that the treatment may be safe and having at least some of its hoped-for effect, but it’s too soon to know whether it ultimately will succeed.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>The results announced Wednesday are from the first human \u003ca href=\"//mps2study.com/study-overview/?pn=\">test\u003c/a> of gene editing in the body, an attempt to permanently change someone’s DNA to cure a disease — in this case, a genetic disorder called \u003ca href=\"https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Mucopolysaccharidoses-Fact-Sheet\">Hunter syndrome\u003c/a> that often kills people in their teens.\u003c/p>\n\u003cp>In two patients who got a medium dose of the treatment, urine levels of large sugar compounds that are hallmarks of Hunter syndrome had fallen by half, on average, four months later — a possible sign the treatment is working. Two others who got a low dose have seen little change in these sugars so far.\u003c/p>\n\u003cp>There’s no way to know yet whether the change in the middle-dose patients is due to the gene editing or something else, but the fact their sugars have declined consistently since treatment suggests it might be.\u003c/p>\n\u003cp>“I cannot absolutely say it’s a treatment effect” but the drop is “really encouraging,” said the study leader, Dr. Joseph Muenzer of the University of North Carolina, Chapel Hill. The main goal of early treatment studies is to test safety, though researchers also look for hints that the therapy is working. Muenzer gave the results at a conference in Greece and consults for the treatment’s maker, California-based Sangamo Therapeutics.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>The company’s president, Dr. Sandy Macrae, said tests in about five months will reveal more, but the change in the middle-dose group so far “looks really good.”\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>“The most rational explanation for this is that what we hoped was going to happen has happened,” he said.\u003c/p>\n\u003cp>Several independent experts agreed.\u003c/p>\n\u003cp>“The results are exciting” and suggest that the gene editing is working to some degree, without safety concerns so far, said Dr. Howard Kaufman, a Boston scientist and member of a National Institutes of Health panel that reviewed the study before it began.\u003c/p>\n\u003cp>Dr. Matthew Porteus, a genetics expert at Stanford University who consults for two other companies developing gene therapies, said more time is needed to see how the patients’ immune system continues to react to the treatment and whether the effects last, but added, “I would be excited about continuing to push along” based on these results.\u003c/p>\n\u003cp>\u003cstrong>How It Works\u003c/strong>\u003c/p>\n\u003cp>Gene editing is intended as a more precise way to do gene therapy, to knock out a bad gene or supply a good one that’s missing. Doctors hope it will give a way to address a host of diseases that can’t be treated well now.\u003c/p>\n\u003cp>In November, a Phoenix-area man with Hunter syndrome, Brian Madeux, became the first person to test this inside the body. He lacks a gene that makes an enzyme that breaks down certain large sugar compounds called GAGs. These build up in cells and cause havoc throughout the body.\u003c/p>\n\u003cp>Through an IV, Madeux received many copies of a corrective gene and a gene-editing tool called zinc finger nucleases to help put it in a precise spot in his DNA. He was one of the two patients given a very low dose of the treatment, because this first-in-human testing called for extreme caution.\u003c/p>\n\u003cp>\u003cstrong>Early Results\u003c/strong>\u003c/p>\n\u003cp>In Madeux and the other low-dose patient, levels of the tell-tale sugar compounds in urine rose 9 percent on average after four months. Muenzer said it’s hard to know whether this is a significant change; little is known about the biology of these compounds, including whether they fluctuate during the day or before or after meals.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>A liver biopsy on one patient given a low dose of the therapy found no evidence that the gene editing had occurred, but Sangamo scientists said this dose is far below the level at which such signs had been detected in research on primates.\u003c/p>\n\u003cp>Two other patients were given a middle dose that was twice what the first two patients received. Their GAG levels declined by 51 percent after four months, on average. Two of the main types of these sugars that accumulate in tissues declined 32 percent and 61 percent, respectively.\u003c/p>\n\u003cp>It is not yet known if declines like these can improve patients’ health or slow the progression of the disease.\u003c/p>\n\u003cp>“This is not proof that this is a successful therapy yet, that these patients had enough gene editing to now supply them with the enzyme they need for the rest of their life,” Muenzer said.\u003c/p>\n\u003cp>But he said an important goal was met: the treatment seems safe. There were two serious side effects — one patient was hospitalized for bronchitis and another for an irregular heartbeat — but those were deemed due to their disease and pre-existing conditions, not the gene treatment.\u003c/p>\n\u003cp>Blood tests did not detect the missing enzyme. Company scientists said this could be because any that was being made was rapidly used by cells rather than getting into the bloodstream — an explanation some outside experts agreed with. What counts, they said, was seeing the result of enzyme activity, the drop in sugars.\u003c/p>\n\u003cp>\u003cstrong>Next Steps\u003c/strong>\u003c/p>\n\u003cp>Two more patients have been given the highest dose being tested — 10 times the starting dose — for a total of six patients in the study. The next step is to start taking patients off the weekly enzyme treatments they’ve been receiving to see if the gene therapy has changed their bodies so they make enough of the enzyme themselves.\u003c/p>\n\u003cp>More results are expected at a medical meeting in February.\u003c/p>\n\u003cp>“We need to see sustained levels for this to be practical. If this only works for six months, that’s not very beneficial,” Muenzer said. “Time’s going to tell.”\u003c/p>\n\u003cp>In an interview at his home in Arizona last month, Madeux, 45, told The Associated Press he volunteered for the study in hope of being able to stop the weekly, three-hour enzyme infusions, but also to help find a treatment for future generations with the disease.\u003c/p>\n\u003cp>“I’m old and having Hunter’s has done a lot of damage to my body,” Madeux said. “I’m actually pretty lucky I’ve lived this long.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"floatright"},"numeric":["floatright"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp> \u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/444281/historic-gene-editing-attempt-in-first-human-off-to-a-positive-start","authors":["byline_futureofyou_444281"],"categories":["futureofyou_1062","futureofyou_1","futureofyou_73","futureofyou_1064"],"tags":["futureofyou_647","futureofyou_103","futureofyou_295"],"collections":["futureofyou_1097","futureofyou_1094"],"featImg":"futureofyou_444292","label":"source_futureofyou_444281"},"futureofyou_443977":{"type":"posts","id":"futureofyou_443977","meta":{"index":"posts_1591205157","site":"futureofyou","id":"443977","score":null,"sort":[1534348813000]},"guestAuthors":[],"slug":"multi-gene-test-may-find-risk-for-heart-disease-and-more","title":"Multi-Gene Test May Find Risk for Heart Disease and More","publishDate":1534348813,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>You know your cholesterol, your blood pressure ... your heart gene score? Researchers say a new way of analyzing genetic test data may one day help identify people at high risk of a youthful heart attack in time to help.\u003c/p>\n\u003cp>Today, gene testing mostly focuses on rare mutations in one or a few genes, like those that cause cystic fibrosis or sickle cell disease, or the BRCA gene responsible for a small fraction of breast cancer. It is less useful for some of the most common diseases, such as heart disease or diabetes, because they are influenced by vast numbers of genes-gone-wrong working together in complicated ways.\u003c/p>\n\u003cp>Monday, researchers reported a new way to measure millions of small genetic variations that add up to cause harm, letting them calculate someone’s inherited risk for the most common form of heart disease and four other serious disorders. The potential cardiac impact: They estimated that up to 25 million Americans may have triple the average person’s risk for coronary artery disease even if they haven’t yet developed warning signs like high cholesterol.\u003c/p>\n\u003cp>“What I foresee is in five years, each person will know this risk number, this ‘polygenic risk score,’ similar to the way each person knows his or her cholesterol,” said Dr. Sekar Kathiresan who led the research team from the Broad Institute, Massachusetts General Hospital and Harvard Medical School.\u003c/p>\n\u003cp>If the approach pans out and doctors adopt it, a bad score wouldn’t mean you’d get a disease, just that your genetic makeup increases the chance — one more piece of information in deciding care. For example, when the researchers tested the system using a DNA database from Britain, less than 1 percent of people with the lowest risk scores were diagnosed with coronary artery disease, compared to 11 percent of people with the highest risk score.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“There are things you can do to lower the risk,” Kathiresan said — the usual advice about diet, exercise, cholesterol medication and not smoking helps.\u003c/p>\n\u003cp>On the flip side, a low-risk score “doesn’t give you a free pass,” he added. An unhealthy lifestyle could overwhelm the protection of good genes.\u003c/p>\n\u003cp>The scoring system also can predict an increased risk of Type 2 diabetes, inflammatory bowel disease, breast cancer and an irregular heartbeat called atrial fibrillation, the team reported in the journal Nature Genetics — noting that next steps include learning what might likewise lower those risks.\u003c/p>\n\u003cp>It doesn’t require the most sophisticated type of genetic testing. Instead, Kathiresan can calculate risk scores for those five diseases — eventually maybe more — simply by reanalyzing the kind of raw data people receive after sending a cheek swab to companies like 23andMe.\u003c/p>\n\u003cp>A geneticist who specializes in cardiovascular disease, he hopes to open a website where people can send in such data to learn their heart risk, as part of continuing research. Kathiresan and co-author Dr. Amit Khera, a Mass General cardiologist, are co-inventors on a patent application for the system.\u003c/p>\n\u003cp>Other scientists and companies have long sought ways to measure risk from multiple, additive gene effects — the “poly” in polygenic — and Myriad Genetics has begun selling a type of polygenic test for breast cancer risk.\u003c/p>\n\u003cp>But specialists in heart disease and genetics who weren’t involved with the research called the new findings exciting because of their scope.\u003c/p>\n\u003cp>“The results should be eye-opening for cardiologists,” said Dr. Charles C. Hong, director of cardiovascular research at the University of Maryland School of Medicine. “The only disappointment is that this score applies only to those with European ancestry, so I wonder if similar scores are in the works for the large majority of the world population that is not white.”\u003c/p>\n\u003cp>Hong pointed to a friend who recently died of a massive heart attack despite being a super-fit marathon runner who’d never smoked, the kind of puzzling death that doctors have long hoped that a better understanding of genetics could help to prevent.\u003c/p>\n\u003cp>“Most of the variation in disease risk comes from an enormous number of very tiny effects” in genes, agreed Stanford University genetics professor Jonathan Pritchard. “This is the first time polygenic scores have really been shown to reach the level of precision where they can have an impact” on patient health.\u003c/p>\n\u003cp>First, the Boston-based team combed previous studies that mapped the DNA of large numbers of people, looking for links to the five diseases — not outright mutations but minor misspellings in the genetic code.\u003c/p>\n\u003cp>Each variation alone would have only a tiny effect on health. They developed a computerized system that analyzed how those effects add up, and tested it using DNA and medical records from 400,000 people stored in Britain’s UK Biobank. Scores more than three times the average person’s risk were deemed high.\u003c/p>\n\u003cp>___\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>The Associated Press Health & Science Department receives \u003ca href=\"http://bit.ly/2G0n9w6\">support\u003c/a> from the Howard Hughes Medical Institute’s Department of Science Education. The AP is solely responsible for all content.\u003c/p>\n\n","blocks":[],"excerpt":"Researchers have reported a new way to measure millions of small genetic variations that add up to cause harm.","status":"publish","parent":0,"modified":1534320042,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":21,"wordCount":873},"headData":{"title":"Multi-Gene Test May Find Risk for Heart Disease and More | KQED","description":"Researchers have reported a new way to measure millions of small genetic variations that add up to cause harm.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"443977 https://ww2.kqed.org/futureofyou/?p=443977","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/08/15/multi-gene-test-may-find-risk-for-heart-disease-and-more/","disqusTitle":"Multi-Gene Test May Find Risk for Heart Disease and More","source":"Health","nprByline":"Lauran Neergaard\u003cbr />The Associated Press","path":"/futureofyou/443977/multi-gene-test-may-find-risk-for-heart-disease-and-more","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>You know your cholesterol, your blood pressure ... your heart gene score? Researchers say a new way of analyzing genetic test data may one day help identify people at high risk of a youthful heart attack in time to help.\u003c/p>\n\u003cp>Today, gene testing mostly focuses on rare mutations in one or a few genes, like those that cause cystic fibrosis or sickle cell disease, or the BRCA gene responsible for a small fraction of breast cancer. It is less useful for some of the most common diseases, such as heart disease or diabetes, because they are influenced by vast numbers of genes-gone-wrong working together in complicated ways.\u003c/p>\n\u003cp>Monday, researchers reported a new way to measure millions of small genetic variations that add up to cause harm, letting them calculate someone’s inherited risk for the most common form of heart disease and four other serious disorders. The potential cardiac impact: They estimated that up to 25 million Americans may have triple the average person’s risk for coronary artery disease even if they haven’t yet developed warning signs like high cholesterol.\u003c/p>\n\u003cp>“What I foresee is in five years, each person will know this risk number, this ‘polygenic risk score,’ similar to the way each person knows his or her cholesterol,” said Dr. Sekar Kathiresan who led the research team from the Broad Institute, Massachusetts General Hospital and Harvard Medical School.\u003c/p>\n\u003cp>If the approach pans out and doctors adopt it, a bad score wouldn’t mean you’d get a disease, just that your genetic makeup increases the chance — one more piece of information in deciding care. For example, when the researchers tested the system using a DNA database from Britain, less than 1 percent of people with the lowest risk scores were diagnosed with coronary artery disease, compared to 11 percent of people with the highest risk score.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“There are things you can do to lower the risk,” Kathiresan said — the usual advice about diet, exercise, cholesterol medication and not smoking helps.\u003c/p>\n\u003cp>On the flip side, a low-risk score “doesn’t give you a free pass,” he added. An unhealthy lifestyle could overwhelm the protection of good genes.\u003c/p>\n\u003cp>The scoring system also can predict an increased risk of Type 2 diabetes, inflammatory bowel disease, breast cancer and an irregular heartbeat called atrial fibrillation, the team reported in the journal Nature Genetics — noting that next steps include learning what might likewise lower those risks.\u003c/p>\n\u003cp>It doesn’t require the most sophisticated type of genetic testing. Instead, Kathiresan can calculate risk scores for those five diseases — eventually maybe more — simply by reanalyzing the kind of raw data people receive after sending a cheek swab to companies like 23andMe.\u003c/p>\n\u003cp>A geneticist who specializes in cardiovascular disease, he hopes to open a website where people can send in such data to learn their heart risk, as part of continuing research. Kathiresan and co-author Dr. Amit Khera, a Mass General cardiologist, are co-inventors on a patent application for the system.\u003c/p>\n\u003cp>Other scientists and companies have long sought ways to measure risk from multiple, additive gene effects — the “poly” in polygenic — and Myriad Genetics has begun selling a type of polygenic test for breast cancer risk.\u003c/p>\n\u003cp>But specialists in heart disease and genetics who weren’t involved with the research called the new findings exciting because of their scope.\u003c/p>\n\u003cp>“The results should be eye-opening for cardiologists,” said Dr. Charles C. Hong, director of cardiovascular research at the University of Maryland School of Medicine. “The only disappointment is that this score applies only to those with European ancestry, so I wonder if similar scores are in the works for the large majority of the world population that is not white.”\u003c/p>\n\u003cp>Hong pointed to a friend who recently died of a massive heart attack despite being a super-fit marathon runner who’d never smoked, the kind of puzzling death that doctors have long hoped that a better understanding of genetics could help to prevent.\u003c/p>\n\u003cp>“Most of the variation in disease risk comes from an enormous number of very tiny effects” in genes, agreed Stanford University genetics professor Jonathan Pritchard. “This is the first time polygenic scores have really been shown to reach the level of precision where they can have an impact” on patient health.\u003c/p>\n\u003cp>First, the Boston-based team combed previous studies that mapped the DNA of large numbers of people, looking for links to the five diseases — not outright mutations but minor misspellings in the genetic code.\u003c/p>\n\u003cp>Each variation alone would have only a tiny effect on health. They developed a computerized system that analyzed how those effects add up, and tested it using DNA and medical records from 400,000 people stored in Britain’s UK Biobank. Scores more than three times the average person’s risk were deemed high.\u003c/p>\n\u003cp>___\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>The Associated Press Health & Science Department receives \u003ca href=\"http://bit.ly/2G0n9w6\">support\u003c/a> from the Howard Hughes Medical Institute’s Department of Science Education. The AP is solely responsible for all content.\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/443977/multi-gene-test-may-find-risk-for-heart-disease-and-more","authors":["byline_futureofyou_443977"],"categories":["futureofyou_1060","futureofyou_1064"],"tags":["futureofyou_17","futureofyou_324","futureofyou_61","futureofyou_279"],"collections":["futureofyou_1093","futureofyou_1094"],"featImg":"futureofyou_443979","label":"source_futureofyou_443977"},"futureofyou_443829":{"type":"posts","id":"futureofyou_443829","meta":{"index":"posts_1591205157","site":"futureofyou","id":"443829","score":null,"sort":[1533675608000]},"guestAuthors":[],"slug":"genetic-tests-can-hurt-your-chances-of-getting-some-types-of-insurance","title":"Genetic Tests Can Hurt Your Chances Of Getting Some Types Of Insurance","publishDate":1533675608,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>Taking a genetic test in your 20s or 30s could, indeed, affect your ability to get long-term-care insurance later — or at least the price you'll pay. And people who are considering enrolling in Medicare \u003cem>after\u003c/em> age 65 would do well to read the fine print of the sign-up rules. Readers have insurance questions on these topics this month, and we have answers:\u003c/p>\n\u003cp>\u003cstrong>Q: Can getting a genetic test interfere with being able to buy long-term-care insurance in the future? If you do get a plan, can the insurer drop you after you find out the results of a genetic test?\u003c/strong>\u003c/p>\n\u003cp>In general, long-term-care insurers \u003ca href=\"https://www.npr.org/sections/health-shots/2018/07/11/627287642/has-genetic-privacy-been-strained-by-trumps-recent-aca-moves\" target=\"_blank\" rel=\"noopener\">can indeed use genetic test results\u003c/a> when they decide whether to offer you coverage. The federal Genetic Information Nondiscrimination Act does prohibit insurers from asking for or using your genetic information to make decisions about whether to sell you \u003cem>health\u003c/em> insurance or how much to charge you. But those privacy protections don't apply to long-term-care policies, life insurance or disability insurance.[contextly_sidebar id=\"qQSelkzIcg9rHvmpdeoo1Q3hIhLbJVzz\"]\u003c/p>\n\u003cp>When you apply for a long-term-care policy, the insurer is permitted to review your medical records and ask you questions about your health history and that of your family. It's all part of the underwriting process to determine whether to offer you a policy and how much to charge.\u003c/p>\n\u003cp>If the insurer asks you whether you've undergone genetic testing, you generally must disclose it, even if the testing was performed through a direct-to-consumer site like 23andMe, says Catherine Theroux, a spokeswoman for \u003ca href=\"https://www.limra.com/News_Center/\" target=\"_blank\" rel=\"noopener\">LIMRA\u003c/a>, an insurance industry trade group.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\"You need to release any medically relevant information,\" she says.\u003c/p>\n\u003cp>Some states provide extra consumer protections related to genetic testing and long-term-care insurance, says \u003ca href=\"https://www.law.gwu.edu/sonia-m-suter\" target=\"_blank\" rel=\"noopener\">Sonia Mateu Suter\u003c/a>, a law professor at George Washington University who specializes in genetics and the law. But most follow federal law.\u003c/p>\n\u003cp>If you get genetic testing after you have a policy, the results can't affect your coverage.\u003c/p>\n\u003cp>\"Once the policy has been underwritten and issued, the insurer doesn't revoke the policy if new medical information comes to light,\" Theroux says.\u003c/p>\n\u003cp>\u003cstrong>Q: Can I switch Medigap insurance companies midway through the year? I found a less expensive policy.\u003c/strong>\u003c/p>\n\u003cp>It depends. Under federal law, when people turn 65 and first enroll in Medicare Part B they have a six-month window to sign up for a \u003ca href=\"https://www.medicare.gov/supplement-other-insurance/medigap/whats-medigap.html\" target=\"_blank\" rel=\"noopener\">Medigap plan\u003c/a> — a commercial policy that picks up some of the out-of-pocket costs for services that Medicare doesn't cover. (\u003ca href=\"https://www.medicare.gov/what-medicare-covers/part-a/what-part-a-covers.html\" target=\"_blank\" rel=\"noopener\">Medicare Part A covers\u003c/a> hospitalization, and \u003ca href=\"https://www.medicare.gov/what-medicare-covers/part-b/what-medicare-part-b-covers.html\" target=\"_blank\" rel=\"noopener\">Medicare Part B covers\u003c/a> outpatient services.) During that six-month period, insurers have to accept enrollees, even if they have health problems.[contextly_sidebar id=\"AH3oYgfcAwGcfBrC61gPsQfir4oB7Yc7\"]\u003c/p>\n\u003cp>If you're still within that six-month period now and you want to switch plans, go right ahead.\u003c/p>\n\u003cp>But if you're past the six-month window, under federal law, insurers are required to sell you a plan only in certain circumstances — such as if you lose your retiree coverage or Medicare Advantage plan. If you don't meet the criteria, insurers can decline to cover you or charge you more for preexisting medical conditions.\u003c/p>\n\u003cp>Many states have provided more robust protections, however. Three states — Connecticut, Massachusetts and New York — have year-round open enrollment and require insurers to offer coverage. And Maine requires a one-month \"guaranteed issue\" open-enrollment period every year.\u003c/p>\n\u003cp>Some states guarantee current policyholders a chance to switch Medigap plans at certain points during the year. Other states have \u003ca href=\"https://www.kff.org/medicare/issue-brief/medigap-enrollment-and-consumer-protections-vary-across-states/\" target=\"_blank\" rel=\"noopener\">additional qualifying events\u003c/a> that allow people to switch Medigap plans, according to data from the Kaiser Family Foundation.\u003c/p>\n\u003cp>\"The first thing the person should do is check with her state insurance department to find out her rights related to buying a Medigap plan,\" says \u003ca href=\"https://www.ncoa.org/centerforbenefits/about-the-center/\" target=\"_blank\" rel=\"noopener\">Brandy Bauer\u003c/a>, associate director at the Center for Benefits Access at the National Council on Aging. If you decide to go ahead and switch, she says, it is wise to sign up for a new plan before terminating your current policy.[contextly_sidebar id=\"t6VA7YIl0My5E1I6mIhIw1XmFGiwNdrT\"]\u003c/p>\n\u003cp>\u003cstrong>Q: I did not enroll in Medicare Part B when I turned 65 because I already have a regular plan that covers everything. I was told that the insurer would keep paying as usual, but now the company says it will pay only part and that I have to buy Medicare Part B. I didn't want to pay for two policies. Is there anything I can do to avoid that?\u003c/strong>\u003c/p>\n\u003cp>From your description, it's hard to know exactly what's going on, but we can make educated guesses. Typically, when people turn 65, it makes sense to sign up for Medicare unless they or their spouse are working and getting health insurance from an employer. For others, at age 65, Medicare typically becomes their primary insurer and any other coverage they have becomes secondary, filling in gaps in Medicare coverage.\u003c/p>\n\u003cp>If you have an individual policy that you bought on the health insurance exchange, and decide to hang on to it instead of signing up for Medicare, your premiums and other costs could be higher than they would be on Medicare, depending on your income.\u003c/p>\n\u003cp>But if you're not receiving employee coverage and you don't enroll in Medicare Part B, you could be subject to a permanent \u003ca href=\"https://www.medicare.gov/your-medicare-costs/part-b-costs/penalty/part-b-late-enrollment-penalty.html\" target=\"_blank\" rel=\"noopener\">late enrollment penalty\u003c/a> of 10 percent of the policy's premium for every 12 months that you could have signed up for Part B but didn't.\u003c/p>\n\u003cp>You could also owe a premium penalty for not signing up for a Part D prescription drug plan. (Most people don't owe any premium for Medicare Part A, so there's no penalty for late sign-up.)\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Your best move now may be to call 800-Medicare or visit your local \u003ca href=\"https://www.medicare.gov/contacts/#resources/ships\" target=\"_blank\" rel=\"noopener\">state health insurance assistance program\u003c/a> to help sort out your coverage issues, including whether to drop your current coverage and sign up for Medicare Part B and Part D.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 Kaiser Health News. To see more, visit \u003ca href=\"http://www.kaiserhealthnews.org/\" target=\"_blank\" rel=\"noopener\">Kaiser Health News\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Genetic+Tests+Can+Hurt+Your+Chances+Of+Getting+Some+Types+Of+Insurance&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n","blocks":[],"excerpt":"Federal law keeps insurers from using genetic test results when pricing and issuing health insurance. But the tests might keep you from being able to get life insurance or a long-term-care policy.","status":"publish","parent":0,"modified":1533650118,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":24,"wordCount":1020},"headData":{"title":"Genetic Tests Can Hurt Your Chances Of Getting Some Types Of Insurance | KQED","description":"Federal law keeps insurers from using genetic test results when pricing and issuing health insurance. But the tests might keep you from being able to get life insurance or a long-term-care policy.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"443829 https://ww2.kqed.org/futureofyou/?p=443829","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/08/07/genetic-tests-can-hurt-your-chances-of-getting-some-types-of-insurance/","disqusTitle":"Genetic Tests Can Hurt Your Chances Of Getting Some Types Of Insurance","source":"Health","nprByline":"Michelle Andrews, KHN","nprImageAgency":"Science Photo Library RF/Getty Images","nprStoryId":"636026264","nprApiLink":"http://api.npr.org/query?id=636026264&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2018/08/07/636026264/genetic-tests-can-hurt-your-chances-of-getting-some-types-of-insurance?ft=nprml&f=636026264","nprRetrievedStory":"1","nprPubDate":"Tue, 07 Aug 2018 09:08:00 -0400","nprStoryDate":"Tue, 07 Aug 2018 09:00:18 -0400","nprLastModifiedDate":"Tue, 07 Aug 2018 09:08:23 -0400","path":"/futureofyou/443829/genetic-tests-can-hurt-your-chances-of-getting-some-types-of-insurance","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Taking a genetic test in your 20s or 30s could, indeed, affect your ability to get long-term-care insurance later — or at least the price you'll pay. And people who are considering enrolling in Medicare \u003cem>after\u003c/em> age 65 would do well to read the fine print of the sign-up rules. Readers have insurance questions on these topics this month, and we have answers:\u003c/p>\n\u003cp>\u003cstrong>Q: Can getting a genetic test interfere with being able to buy long-term-care insurance in the future? If you do get a plan, can the insurer drop you after you find out the results of a genetic test?\u003c/strong>\u003c/p>\n\u003cp>In general, long-term-care insurers \u003ca href=\"https://www.npr.org/sections/health-shots/2018/07/11/627287642/has-genetic-privacy-been-strained-by-trumps-recent-aca-moves\" target=\"_blank\" rel=\"noopener\">can indeed use genetic test results\u003c/a> when they decide whether to offer you coverage. The federal Genetic Information Nondiscrimination Act does prohibit insurers from asking for or using your genetic information to make decisions about whether to sell you \u003cem>health\u003c/em> insurance or how much to charge you. But those privacy protections don't apply to long-term-care policies, life insurance or disability insurance.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>When you apply for a long-term-care policy, the insurer is permitted to review your medical records and ask you questions about your health history and that of your family. It's all part of the underwriting process to determine whether to offer you a policy and how much to charge.\u003c/p>\n\u003cp>If the insurer asks you whether you've undergone genetic testing, you generally must disclose it, even if the testing was performed through a direct-to-consumer site like 23andMe, says Catherine Theroux, a spokeswoman for \u003ca href=\"https://www.limra.com/News_Center/\" target=\"_blank\" rel=\"noopener\">LIMRA\u003c/a>, an insurance industry trade group.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\"You need to release any medically relevant information,\" she says.\u003c/p>\n\u003cp>Some states provide extra consumer protections related to genetic testing and long-term-care insurance, says \u003ca href=\"https://www.law.gwu.edu/sonia-m-suter\" target=\"_blank\" rel=\"noopener\">Sonia Mateu Suter\u003c/a>, a law professor at George Washington University who specializes in genetics and the law. But most follow federal law.\u003c/p>\n\u003cp>If you get genetic testing after you have a policy, the results can't affect your coverage.\u003c/p>\n\u003cp>\"Once the policy has been underwritten and issued, the insurer doesn't revoke the policy if new medical information comes to light,\" Theroux says.\u003c/p>\n\u003cp>\u003cstrong>Q: Can I switch Medigap insurance companies midway through the year? I found a less expensive policy.\u003c/strong>\u003c/p>\n\u003cp>It depends. Under federal law, when people turn 65 and first enroll in Medicare Part B they have a six-month window to sign up for a \u003ca href=\"https://www.medicare.gov/supplement-other-insurance/medigap/whats-medigap.html\" target=\"_blank\" rel=\"noopener\">Medigap plan\u003c/a> — a commercial policy that picks up some of the out-of-pocket costs for services that Medicare doesn't cover. (\u003ca href=\"https://www.medicare.gov/what-medicare-covers/part-a/what-part-a-covers.html\" target=\"_blank\" rel=\"noopener\">Medicare Part A covers\u003c/a> hospitalization, and \u003ca href=\"https://www.medicare.gov/what-medicare-covers/part-b/what-medicare-part-b-covers.html\" target=\"_blank\" rel=\"noopener\">Medicare Part B covers\u003c/a> outpatient services.) During that six-month period, insurers have to accept enrollees, even if they have health problems.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>If you're still within that six-month period now and you want to switch plans, go right ahead.\u003c/p>\n\u003cp>But if you're past the six-month window, under federal law, insurers are required to sell you a plan only in certain circumstances — such as if you lose your retiree coverage or Medicare Advantage plan. If you don't meet the criteria, insurers can decline to cover you or charge you more for preexisting medical conditions.\u003c/p>\n\u003cp>Many states have provided more robust protections, however. Three states — Connecticut, Massachusetts and New York — have year-round open enrollment and require insurers to offer coverage. And Maine requires a one-month \"guaranteed issue\" open-enrollment period every year.\u003c/p>\n\u003cp>Some states guarantee current policyholders a chance to switch Medigap plans at certain points during the year. Other states have \u003ca href=\"https://www.kff.org/medicare/issue-brief/medigap-enrollment-and-consumer-protections-vary-across-states/\" target=\"_blank\" rel=\"noopener\">additional qualifying events\u003c/a> that allow people to switch Medigap plans, according to data from the Kaiser Family Foundation.\u003c/p>\n\u003cp>\"The first thing the person should do is check with her state insurance department to find out her rights related to buying a Medigap plan,\" says \u003ca href=\"https://www.ncoa.org/centerforbenefits/about-the-center/\" target=\"_blank\" rel=\"noopener\">Brandy Bauer\u003c/a>, associate director at the Center for Benefits Access at the National Council on Aging. If you decide to go ahead and switch, she says, it is wise to sign up for a new plan before terminating your current policy.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\u003cstrong>Q: I did not enroll in Medicare Part B when I turned 65 because I already have a regular plan that covers everything. I was told that the insurer would keep paying as usual, but now the company says it will pay only part and that I have to buy Medicare Part B. I didn't want to pay for two policies. Is there anything I can do to avoid that?\u003c/strong>\u003c/p>\n\u003cp>From your description, it's hard to know exactly what's going on, but we can make educated guesses. Typically, when people turn 65, it makes sense to sign up for Medicare unless they or their spouse are working and getting health insurance from an employer. For others, at age 65, Medicare typically becomes their primary insurer and any other coverage they have becomes secondary, filling in gaps in Medicare coverage.\u003c/p>\n\u003cp>If you have an individual policy that you bought on the health insurance exchange, and decide to hang on to it instead of signing up for Medicare, your premiums and other costs could be higher than they would be on Medicare, depending on your income.\u003c/p>\n\u003cp>But if you're not receiving employee coverage and you don't enroll in Medicare Part B, you could be subject to a permanent \u003ca href=\"https://www.medicare.gov/your-medicare-costs/part-b-costs/penalty/part-b-late-enrollment-penalty.html\" target=\"_blank\" rel=\"noopener\">late enrollment penalty\u003c/a> of 10 percent of the policy's premium for every 12 months that you could have signed up for Part B but didn't.\u003c/p>\n\u003cp>You could also owe a premium penalty for not signing up for a Part D prescription drug plan. (Most people don't owe any premium for Medicare Part A, so there's no penalty for late sign-up.)\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Your best move now may be to call 800-Medicare or visit your local \u003ca href=\"https://www.medicare.gov/contacts/#resources/ships\" target=\"_blank\" rel=\"noopener\">state health insurance assistance program\u003c/a> to help sort out your coverage issues, including whether to drop your current coverage and sign up for Medicare Part B and Part D.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 Kaiser Health News. To see more, visit \u003ca href=\"http://www.kaiserhealthnews.org/\" target=\"_blank\" rel=\"noopener\">Kaiser Health News\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Genetic+Tests+Can+Hurt+Your+Chances+Of+Getting+Some+Types+Of+Insurance&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/443829/genetic-tests-can-hurt-your-chances-of-getting-some-types-of-insurance","authors":["byline_futureofyou_443829"],"categories":["futureofyou_452","futureofyou_1","futureofyou_73","futureofyou_1064"],"tags":["futureofyou_1015","futureofyou_61","futureofyou_419","futureofyou_35"],"collections":["futureofyou_1094"],"featImg":"futureofyou_443830","label":"source_futureofyou_443829"},"futureofyou_443668":{"type":"posts","id":"futureofyou_443668","meta":{"index":"posts_1591205157","site":"futureofyou","id":"443668","score":null,"sort":[1533070821000]},"guestAuthors":[],"slug":"alzheimers-study-sparks-new-debate-over-amyloid-hypothesis","title":"Alzheimer’s Study Sparks New Debate Over Amyloid Hypothesis","publishDate":1533070821,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>In the long-running debate over just what causes Alzheimer’s disease, one side looks to have scored a victory with \u003ca href=\"https://www.statnews.com/2018/07/25/experimental-alzheimers-drug-biogen-eisai/\" target=\"_blank\" rel=\"noopener\">new results with an in-development drug\u003c/a>. But there’s enough variation in the data to ensure that the squabbling factions of Alzheimer’s will have plenty to fight about.[contextly_sidebar id=\"A04l79ZF49Fepp9ayXq47IfI7cWrtD3j\"]\u003c/p>\n\u003cp>At issue is the so-called amyloid hypothesis, a decades-old theory claiming that Alzheimer’s gradual degradation of the brain is caused by the accumulation of sticky plaques. And the new drug is BAN2401, designed by Biogen and Eisai to prevent those amyloid plaques from clustering and attack the clumps that already have.\u003c/p>\n\u003cp>In data presented last week, one group of patients receiving BAN2401 saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline compared with placebo.\u003c/p>\n\u003cp>To the amyloid-inclined, like Dr. Howard Fillit of the Alzheimer’s Drug Discovery Foundation, that marks a clear affirmation of the linkage between plaques and mental fortitude.\u003c/p>\n\u003cp>“I mean if you asked me five or 10 years ago if we’re going to have a drug that can remove the plaques from the brain, I would have thought this was space technology,” Fillit said. “And there was definitely a signal, in my opinion, on clinical outcomes, which is what we’ve all been looking for.”\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>But to skeptics, the trial was laden with confounding details that make it impossible to draw conclusions.\u003c/p>\n\u003cp>“These results are a mess,” wrote Baird biotech analyst Brian Skorney. “Not so much that they indicate an outright failure of the [amyloid] hypothesis, but they don’t really say anything informative at all.”\u003c/p>\n\u003cp>In the trial, every single tested dose had a significant effect on plaques as measured by a brain scan, and the more BAN2401 patients got, the less amyloid they had after 18 months. But looking at cognition, only the highest tested dose was significantly better than placebo at slowing down mental decline. And some of the patients who received lower doses actually declined faster than those who received no treatment at all.[contextly_sidebar id=\"TAyKNwsnIzWapwgWfQcwbB5f1ZW4XVH2\"]\u003c/p>\n\u003cp>If amyloid really is the driving factor behind Alzheimer’s, why didn’t each incremental reduction in plaques lead to a corresponding improvement in cognition?\u003c/p>\n\u003cp>Dr. Al Sandrock, Biogen’s chief scientific officer, said there is likely a threshold of amyloid reduction that must be reached before patients actually benefit. The low doses, despite their effect on plaques, might not have hit that threshold, Sandrock said, thus accounting for their poor performance on cognitive decline.\u003c/p>\n\u003cp>The divergence in the two curves is what gives Dr. Reisa Sperling, who was overall encouraged by the results, “the most pause.” But Sperling, director Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital, noted that some of the study’s arms had small numbers of patients, making it difficult to draw conclusions. She said while there is a biological argument that could underpin the threshold hypothesis, she wanted to see more data from a larger trial with a more traditional design.\u003c/p>\n\u003cp>Even if Sandrock’s theory holds up, what happened to BAN2401 is not a new phenomenon. This year a drug from Merck, meant to shut off the production of plaques by blocking an enzyme called BACE, was successful in reducing amyloid but fared so dismally on cognitive measures that researchers terminated the trial early. A second BACE drug, from Biogen and Eisai, had similar results in miniature, hitting the mark on plaque reduction in a Phase 2 trial but failing to significantly outperform placebo on cognition.\u003c/p>\n\u003cp>The underlying issue, according Dr. Lon Schneider, director of the California Alzheimer’s Disease Center at the University of Southern California, is that “the plaques are not the target — those are biomarkers.”\u003c/p>\n\u003cp>“A target is something that, as a result of hitting it, there will be change downstream in behavior, cognition, and illness course,” Schneider said. “So, yeah we’re knocking down amyloid, but so far we’re not changing behavior much.”\u003c/p>\n\u003cp>Even BAN2401’s saving grace — that its highest dose appeared to both reduce amyloid and improve patient’s clinical results — has come under scrutiny.\u003c/p>\n\u003cp>In the BAN2401 trial, about 70 percent of patients getting placebo had a genetic mutation that triples the risk of Alzheimer’s. But in the high-dose BAN2401 group, just 30 percent of patients had the mutation, called APOE4.[contextly_sidebar id=\"tcdS8fDReoUFY02DP3vnBwSqYDEV9wHe\"]\u003c/p>\n\u003cp>That could explain why BAN2401 seemed to outperform a saline injection in the high-dose group, skeptics say, as past trials suggest that APOE4 carriers have more rapidly progressing Alzheimer’s than patients without the mutation.\u003c/p>\n\u003cp>And it could mean that the drug’s seeming promise is a mirage.\u003c/p>\n\u003cp>Dr. Paul Aisen, who runs the Alzheimer’s Therapeutic Research Institute at the University of Southern California, said the discrepancy “does create a potential bias.” But in trials where patients are confirmed to have amyloid in their brains at the outset, as was the case with BAN2401, “the impact of [APOE4] on progression is modest,” Aisen wrote in an email. “I don’t think this accounts for the apparent slowing of cognitive decline in the high-dose arm.”\u003c/p>\n\u003cp>Sperling agreed that she did not think the arms’ different populations skewed the data, in part because the group that received the second highest dose of the drug had a larger share of APOE4 carriers and saw results that were similar — though not as substantial — as the high dose group.\u003c/p>\n\u003cp>“It’s a similar pattern,” she said. “For me that partially mitigates that concern.”\u003c/p>\n\u003cp>Biogen and Eisai have promised to dig into the data and parse out the effect APOE4 had on whether patients responded to BAN2401, but those results likely won’t be ready for months.\u003c/p>\n\u003cp>In the meantime, companies are still queueing up to take cracks at amyloid.\u003c/p>\n\u003cp>Eli Lilly, which has spent billions on failed Alzheimer’s drugs in recent years, has designed a trial that will test the amyloid hypothesis “in the most definitive way possible,” said Mark Mintun, the company’s vice president of neurodegeneration.\u003c/p>\n\u003cp>The plan is to take a BACE inhibitor and pair it with an injected treatment that targets amyloid already in the brain. That should address the two major concerns with each approach, Mintun said: BACE inhibitors prevent amyloid but don’t address plaques that already exist, while amyloid-targeting therapies don’t stem the flow of new toxic clumps.\u003c/p>\n\u003cp>“I equate it to going down to your basement and finding three feet of water and there’s been a slow drip for four weeks,” Mintun said. “You can turn off the spigot, but it won’t feel like you’ve made much progress, so you’ve got to pump it out, too.”\u003c/p>\n\u003cp>That study is enrolling 375 patients into three groups, planning to study whether the combination can improve cognition compared with placebo over 18 months.\u003c/p>\n\u003cp>\u003cem>Andrew Joseph contributed reporting.\u003c/em>\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2018/07/30/alzheimers-amyloid-hypothesis/\" target=\"_blank\" rel=\"noopener\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n","blocks":[],"excerpt":"In data presented recently, one group of patients receiving an experimental drug saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline.","status":"publish","parent":0,"modified":1532989851,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":31,"wordCount":1250},"headData":{"title":"Alzheimer’s Study Sparks New Debate Over Amyloid Hypothesis | KQED","description":"In data presented recently, one group of patients receiving an experimental drug saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"443668 https://ww2.kqed.org/futureofyou/?p=443668","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/07/31/alzheimers-study-sparks-new-debate-over-amyloid-hypothesis/","disqusTitle":"Alzheimer’s Study Sparks New Debate Over Amyloid Hypothesis","source":"Hope/Hype","nprByline":"Damian Garde\u003cbr />STAT","path":"/futureofyou/443668/alzheimers-study-sparks-new-debate-over-amyloid-hypothesis","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>In the long-running debate over just what causes Alzheimer’s disease, one side looks to have scored a victory with \u003ca href=\"https://www.statnews.com/2018/07/25/experimental-alzheimers-drug-biogen-eisai/\" target=\"_blank\" rel=\"noopener\">new results with an in-development drug\u003c/a>. But there’s enough variation in the data to ensure that the squabbling factions of Alzheimer’s will have plenty to fight about.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>At issue is the so-called amyloid hypothesis, a decades-old theory claiming that Alzheimer’s gradual degradation of the brain is caused by the accumulation of sticky plaques. And the new drug is BAN2401, designed by Biogen and Eisai to prevent those amyloid plaques from clustering and attack the clumps that already have.\u003c/p>\n\u003cp>In data presented last week, one group of patients receiving BAN2401 saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline compared with placebo.\u003c/p>\n\u003cp>To the amyloid-inclined, like Dr. Howard Fillit of the Alzheimer’s Drug Discovery Foundation, that marks a clear affirmation of the linkage between plaques and mental fortitude.\u003c/p>\n\u003cp>“I mean if you asked me five or 10 years ago if we’re going to have a drug that can remove the plaques from the brain, I would have thought this was space technology,” Fillit said. “And there was definitely a signal, in my opinion, on clinical outcomes, which is what we’ve all been looking for.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>But to skeptics, the trial was laden with confounding details that make it impossible to draw conclusions.\u003c/p>\n\u003cp>“These results are a mess,” wrote Baird biotech analyst Brian Skorney. “Not so much that they indicate an outright failure of the [amyloid] hypothesis, but they don’t really say anything informative at all.”\u003c/p>\n\u003cp>In the trial, every single tested dose had a significant effect on plaques as measured by a brain scan, and the more BAN2401 patients got, the less amyloid they had after 18 months. But looking at cognition, only the highest tested dose was significantly better than placebo at slowing down mental decline. And some of the patients who received lower doses actually declined faster than those who received no treatment at all.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>If amyloid really is the driving factor behind Alzheimer’s, why didn’t each incremental reduction in plaques lead to a corresponding improvement in cognition?\u003c/p>\n\u003cp>Dr. Al Sandrock, Biogen’s chief scientific officer, said there is likely a threshold of amyloid reduction that must be reached before patients actually benefit. The low doses, despite their effect on plaques, might not have hit that threshold, Sandrock said, thus accounting for their poor performance on cognitive decline.\u003c/p>\n\u003cp>The divergence in the two curves is what gives Dr. Reisa Sperling, who was overall encouraged by the results, “the most pause.” But Sperling, director Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital, noted that some of the study’s arms had small numbers of patients, making it difficult to draw conclusions. She said while there is a biological argument that could underpin the threshold hypothesis, she wanted to see more data from a larger trial with a more traditional design.\u003c/p>\n\u003cp>Even if Sandrock’s theory holds up, what happened to BAN2401 is not a new phenomenon. This year a drug from Merck, meant to shut off the production of plaques by blocking an enzyme called BACE, was successful in reducing amyloid but fared so dismally on cognitive measures that researchers terminated the trial early. A second BACE drug, from Biogen and Eisai, had similar results in miniature, hitting the mark on plaque reduction in a Phase 2 trial but failing to significantly outperform placebo on cognition.\u003c/p>\n\u003cp>The underlying issue, according Dr. Lon Schneider, director of the California Alzheimer’s Disease Center at the University of Southern California, is that “the plaques are not the target — those are biomarkers.”\u003c/p>\n\u003cp>“A target is something that, as a result of hitting it, there will be change downstream in behavior, cognition, and illness course,” Schneider said. “So, yeah we’re knocking down amyloid, but so far we’re not changing behavior much.”\u003c/p>\n\u003cp>Even BAN2401’s saving grace — that its highest dose appeared to both reduce amyloid and improve patient’s clinical results — has come under scrutiny.\u003c/p>\n\u003cp>In the BAN2401 trial, about 70 percent of patients getting placebo had a genetic mutation that triples the risk of Alzheimer’s. But in the high-dose BAN2401 group, just 30 percent of patients had the mutation, called APOE4.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>That could explain why BAN2401 seemed to outperform a saline injection in the high-dose group, skeptics say, as past trials suggest that APOE4 carriers have more rapidly progressing Alzheimer’s than patients without the mutation.\u003c/p>\n\u003cp>And it could mean that the drug’s seeming promise is a mirage.\u003c/p>\n\u003cp>Dr. Paul Aisen, who runs the Alzheimer’s Therapeutic Research Institute at the University of Southern California, said the discrepancy “does create a potential bias.” But in trials where patients are confirmed to have amyloid in their brains at the outset, as was the case with BAN2401, “the impact of [APOE4] on progression is modest,” Aisen wrote in an email. “I don’t think this accounts for the apparent slowing of cognitive decline in the high-dose arm.”\u003c/p>\n\u003cp>Sperling agreed that she did not think the arms’ different populations skewed the data, in part because the group that received the second highest dose of the drug had a larger share of APOE4 carriers and saw results that were similar — though not as substantial — as the high dose group.\u003c/p>\n\u003cp>“It’s a similar pattern,” she said. “For me that partially mitigates that concern.”\u003c/p>\n\u003cp>Biogen and Eisai have promised to dig into the data and parse out the effect APOE4 had on whether patients responded to BAN2401, but those results likely won’t be ready for months.\u003c/p>\n\u003cp>In the meantime, companies are still queueing up to take cracks at amyloid.\u003c/p>\n\u003cp>Eli Lilly, which has spent billions on failed Alzheimer’s drugs in recent years, has designed a trial that will test the amyloid hypothesis “in the most definitive way possible,” said Mark Mintun, the company’s vice president of neurodegeneration.\u003c/p>\n\u003cp>The plan is to take a BACE inhibitor and pair it with an injected treatment that targets amyloid already in the brain. That should address the two major concerns with each approach, Mintun said: BACE inhibitors prevent amyloid but don’t address plaques that already exist, while amyloid-targeting therapies don’t stem the flow of new toxic clumps.\u003c/p>\n\u003cp>“I equate it to going down to your basement and finding three feet of water and there’s been a slow drip for four weeks,” Mintun said. “You can turn off the spigot, but it won’t feel like you’ve made much progress, so you’ve got to pump it out, too.”\u003c/p>\n\u003cp>That study is enrolling 375 patients into three groups, planning to study whether the combination can improve cognition compared with placebo over 18 months.\u003c/p>\n\u003cp>\u003cem>Andrew Joseph contributed reporting.\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"floatright"},"numeric":["floatright"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2018/07/30/alzheimers-amyloid-hypothesis/\" target=\"_blank\" rel=\"noopener\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/443668/alzheimers-study-sparks-new-debate-over-amyloid-hypothesis","authors":["byline_futureofyou_443668"],"categories":["futureofyou_1062","futureofyou_1","futureofyou_1064"],"tags":["futureofyou_999","futureofyou_673","futureofyou_1023","futureofyou_141","futureofyou_61"],"collections":["futureofyou_1097"],"featImg":"futureofyou_443671","label":"source_futureofyou_443668"},"futureofyou_443063":{"type":"posts","id":"futureofyou_443063","meta":{"index":"posts_1591205157","site":"futureofyou","id":"443063","score":null,"sort":[1530222945000]},"guestAuthors":[],"slug":"the-age-plateau-study-suggests-at-certain-age-risk-of-death-no-longer-increases","title":"The Age Plateau: Study Suggests, At Certain Age, Risk of Death No Longer Increases","publishDate":1530222945,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{"term":1094,"site":"futureofyou"},"content":"\u003cp>Humans are living longer than ever before. But does our species have a fixed shelf life, or could we prolong our lives indefinitely?[contextly_sidebar id=\"SE82E4G0jfBm3Ty2BPZtQeC1Q2URGkhF\"]\u003c/p>\n\u003cp>A new study in \u003ca href=\"http://science.sciencemag.org/cgi/doi/10.1126/science.aat3119\" target=\"_blank\" rel=\"noopener\">Science\u003c/a> suggests that we haven’t yet hit our limit on longevity — findings that come amid a \u003ca href=\"https://www.nature.com/news/human-age-limit-claim-sparks-debate-1.20750\" target=\"_blank\" rel=\"noopener\">heated debate\u003c/a> on the question and that will almost surely be disputed by scientists who caution against putting too much hope in new advances in technology and medicine.\u003c/p>\n\u003cp>Demographers looked at data from nearly 4,000 Italians above the age of 105 and noticed that, with each passing year, they were no more likely to die than they had been before reaching that age. In other words, after a certain age, the risk for death plateaus.\u003c/p>\n\u003cp>“We’re seeing death rates, among extreme ages, go down a little bit,” said Ken Wachter, a professor of demography and statistics at University of California, Berkeley, who helped lead the study. “That means we’re not coming up against a limit to lifespan.”\u003c/p>\n\u003cp>A 2016 study examined global demographic data, and concluded that humans have an upper limit of 115 years — with an occasional outlier surpassing expectations. That paper, \u003ca href=\"https://www.nature.com/news/human-age-limit-claim-sparks-debate-1.20750\" target=\"_blank\" rel=\"noopener\">published in Nature\u003c/a>, was rebutted in subsequent papers — with this latest paper serving, potentially, as another.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Here’s what the Science paper found: A person’s risk of dying gets statistically higher with each passing year — until they hit 80. The idea is that those who were less fit, in a Darwinian sense, die out before they hit extreme old age. The survivors, who have proven their mettle as hardy stock, wind up less likely to die with each passing year. After 80, the death rates actually begin to decelerate — and after 105, the death rates plateau, according to the Science study.[contextly_sidebar id=\"YLSkNwloHkug4PGaOdi82m9E00o7xkuz\"]\u003c/p>\n\u003cp>Those who have survived to extreme old age — say, 110 years — aren’t any more likely to die than a person who is a few years younger. Rather, the idea is that the most genetically robust people survive into old age — and could potentially continue to live for an indefinite amount of time, if technology advances permit.\u003c/p>\n\u003cp>The paper’s methodology is “well-done,” but sheds little new light on the concept of mortality plateaus, said Tom Kirkwood, associate dean for aging at the Newcastle University Institute for Aging. Furthermore, it observes trends of aging but does nothing to explain why some people live for such long stretches.\u003c/p>\n\u003cp>“This kind of demographic study cannot identify the reasons for an apparent plateau, which are rooted in biology and which so far remain elusive,” Kirkwood said.\u003c/p>\n\u003cp>One scientific faction puts a hard stop on the human lifespan at 115 years. The 2016 paper in Nature found that the maximum reported age of death increased until the mid-1990s, then plateaued. That suggested that despite all the advances in technology since, the upper limit of age could not surpass 115. To increase the limit, scientists would have to develop interventions that would tackle aging on too many different fronts — and that’s just not possible with the current technology we have, said Jan Vijg, chair of genetics at the Albert Einstein College of Medicine and an author of the Nature paper.\u003c/p>\n\u003cp>Vijg thinks that a mortality plateau observed in the latest research doesn’t disprove his paper.[contextly_sidebar id=\"q3Z6RZoUG6JjLbtDvzjWH1Vt9KhybMkM\"]\u003c/p>\n\u003cp>“If you’re very lucky as a human, have good genes, and are lucky to avoid diseases, you probably do have a higher chance to live just a little longer than others — that’s selection,” Vijg said. “But this is far from saying ‘since mortality no longer increases, that means that humans can continue to live longer and longer.’\u003c/p>\n\u003cp>“These people are still very close to death.”\u003c/p>\n\u003cp>There’s a strong business incentive behind the idea that there’s no limit on human longevity. Case in point: Just this week, AbbVie and Google parent company Alphabet said they’d pour an \u003ca href=\"https://www.statnews.com/2018/06/26/google-calico-abbvie-aging/\">additional $1 billion\u003c/a> to fund Alphabet spinout Calico, which is working covertly on aging science. But not everyone accepts the premise.\u003c/p>\n\u003cp>“I’m not a believer that there is going to be some silver bullet, some magic drug or substance or intervention that will have a major impact on aging overall,” Wachter said. “The hope is that as we understand the interaction between genes and our behaviors, along with environments, toxins, and medicines, we’ll be able to better tune the life course for widespread improvements in lifespan.”\u003c/p>\n\u003cp>Humans have gradually been extending their lifespans over millennia — with the biggest leaps being made in the past century or so. But our genes, by and large, often date back to caveman times, he said.\u003c/p>\n\u003cp>“What that shows is that the way our bodies are put together, and our genetic heritage, is very permissive,” Wachter said. “We strongly believe that the patterns we’re seeing — which include this leveling out at extreme ages — partly reflect the processes of evolution.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2018/06/28/human-longevity-limits-aging/\" target=\"_blank\" rel=\"noopener\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n","blocks":[],"excerpt":"A new study suggests that we haven’t yet hit our limit on longevity, findings that come amid a heated debate on the question.","status":"publish","parent":0,"modified":1530222945,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":20,"wordCount":907},"headData":{"title":"The Age Plateau: Study Suggests, At Certain Age, Risk of Death No Longer Increases | KQED","description":"A new study suggests that we haven’t yet hit our limit on longevity, findings that come amid a heated debate on the question.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"443063 https://ww2.kqed.org/futureofyou/?p=443063","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/06/28/the-age-plateau-study-suggests-at-certain-age-risk-of-death-no-longer-increases/","disqusTitle":"The Age Plateau: Study Suggests, At Certain Age, Risk of Death No Longer Increases","nprByline":"Meghana Keshavan\u003cbr />STAT","path":"/futureofyou/443063/the-age-plateau-study-suggests-at-certain-age-risk-of-death-no-longer-increases","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Humans are living longer than ever before. But does our species have a fixed shelf life, or could we prolong our lives indefinitely?\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>A new study in \u003ca href=\"http://science.sciencemag.org/cgi/doi/10.1126/science.aat3119\" target=\"_blank\" rel=\"noopener\">Science\u003c/a> suggests that we haven’t yet hit our limit on longevity — findings that come amid a \u003ca href=\"https://www.nature.com/news/human-age-limit-claim-sparks-debate-1.20750\" target=\"_blank\" rel=\"noopener\">heated debate\u003c/a> on the question and that will almost surely be disputed by scientists who caution against putting too much hope in new advances in technology and medicine.\u003c/p>\n\u003cp>Demographers looked at data from nearly 4,000 Italians above the age of 105 and noticed that, with each passing year, they were no more likely to die than they had been before reaching that age. In other words, after a certain age, the risk for death plateaus.\u003c/p>\n\u003cp>“We’re seeing death rates, among extreme ages, go down a little bit,” said Ken Wachter, a professor of demography and statistics at University of California, Berkeley, who helped lead the study. “That means we’re not coming up against a limit to lifespan.”\u003c/p>\n\u003cp>A 2016 study examined global demographic data, and concluded that humans have an upper limit of 115 years — with an occasional outlier surpassing expectations. That paper, \u003ca href=\"https://www.nature.com/news/human-age-limit-claim-sparks-debate-1.20750\" target=\"_blank\" rel=\"noopener\">published in Nature\u003c/a>, was rebutted in subsequent papers — with this latest paper serving, potentially, as another.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Here’s what the Science paper found: A person’s risk of dying gets statistically higher with each passing year — until they hit 80. The idea is that those who were less fit, in a Darwinian sense, die out before they hit extreme old age. The survivors, who have proven their mettle as hardy stock, wind up less likely to die with each passing year. After 80, the death rates actually begin to decelerate — and after 105, the death rates plateau, according to the Science study.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Those who have survived to extreme old age — say, 110 years — aren’t any more likely to die than a person who is a few years younger. Rather, the idea is that the most genetically robust people survive into old age — and could potentially continue to live for an indefinite amount of time, if technology advances permit.\u003c/p>\n\u003cp>The paper’s methodology is “well-done,” but sheds little new light on the concept of mortality plateaus, said Tom Kirkwood, associate dean for aging at the Newcastle University Institute for Aging. Furthermore, it observes trends of aging but does nothing to explain why some people live for such long stretches.\u003c/p>\n\u003cp>“This kind of demographic study cannot identify the reasons for an apparent plateau, which are rooted in biology and which so far remain elusive,” Kirkwood said.\u003c/p>\n\u003cp>One scientific faction puts a hard stop on the human lifespan at 115 years. The 2016 paper in Nature found that the maximum reported age of death increased until the mid-1990s, then plateaued. That suggested that despite all the advances in technology since, the upper limit of age could not surpass 115. To increase the limit, scientists would have to develop interventions that would tackle aging on too many different fronts — and that’s just not possible with the current technology we have, said Jan Vijg, chair of genetics at the Albert Einstein College of Medicine and an author of the Nature paper.\u003c/p>\n\u003cp>Vijg thinks that a mortality plateau observed in the latest research doesn’t disprove his paper.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>“If you’re very lucky as a human, have good genes, and are lucky to avoid diseases, you probably do have a higher chance to live just a little longer than others — that’s selection,” Vijg said. “But this is far from saying ‘since mortality no longer increases, that means that humans can continue to live longer and longer.’\u003c/p>\n\u003cp>“These people are still very close to death.”\u003c/p>\n\u003cp>There’s a strong business incentive behind the idea that there’s no limit on human longevity. Case in point: Just this week, AbbVie and Google parent company Alphabet said they’d pour an \u003ca href=\"https://www.statnews.com/2018/06/26/google-calico-abbvie-aging/\">additional $1 billion\u003c/a> to fund Alphabet spinout Calico, which is working covertly on aging science. But not everyone accepts the premise.\u003c/p>\n\u003cp>“I’m not a believer that there is going to be some silver bullet, some magic drug or substance or intervention that will have a major impact on aging overall,” Wachter said. “The hope is that as we understand the interaction between genes and our behaviors, along with environments, toxins, and medicines, we’ll be able to better tune the life course for widespread improvements in lifespan.”\u003c/p>\n\u003cp>Humans have gradually been extending their lifespans over millennia — with the biggest leaps being made in the past century or so. But our genes, by and large, often date back to caveman times, he said.\u003c/p>\n\u003cp>“What that shows is that the way our bodies are put together, and our genetic heritage, is very permissive,” Wachter said. “We strongly believe that the patterns we’re seeing — which include this leveling out at extreme ages — partly reflect the processes of evolution.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2018/06/28/human-longevity-limits-aging/\" target=\"_blank\" rel=\"noopener\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/443063/the-age-plateau-study-suggests-at-certain-age-risk-of-death-no-longer-increases","authors":["byline_futureofyou_443063"],"categories":["futureofyou_1","futureofyou_73","futureofyou_1064"],"tags":["futureofyou_1564","futureofyou_532","futureofyou_141","futureofyou_1565","futureofyou_61"],"collections":["futureofyou_1094"],"featImg":"futureofyou_443067","label":"futureofyou_1094"},"futureofyou_442958":{"type":"posts","id":"futureofyou_442958","meta":{"index":"posts_1591205157","site":"futureofyou","id":"442958","score":null,"sort":[1529606096000]},"guestAuthors":[],"slug":"researchers-find-herpes-viruses-in-alzheimers-brains","title":"Researchers Find Herpes Viruses In Alzheimer's Brains","publishDate":1529606096,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>Two common herpes viruses appear to play a role in Alzheimer's disease.[contextly_sidebar id=\"xGMrgC5mfby5S92heGXjVDaxhvly8p6M\"]\u003c/p>\n\u003cp>The viruses, best known for causing a distinctive skin rash in young children, are abundant in brain tissue from people with Alzheimer's, a team of scientists \u003ca href=\"http://www.cell.com/neuron/fulltext/S0896-6273(18)30421-5\">reports\u003c/a> Thursday in \u003cem>Neuron.\u003c/em> The team also found evidence that the viruses can interact with brain cells in ways that could accelerate the disease.\u003c/p>\n\u003cp>\"Our hypothesis is that they put gas on the flame,\" says \u003ca href=\"https://www.mountsinai.org/profiles/joel-dudley\">Joel Dudley\u003c/a>, an author of the study and an associate professor of genetics and genomic sciences at the Icahn School of Medicine at Mt. Sinai in New York City.\u003c/p>\n\u003cp>The finding adds credence to a decades-old idea that an infection can cause Alzheimer's disease. It also suggests that it may be possible to prevent or \u003ca href=\"https://www.nia.nih.gov/alzheimers/clinical-trials/valacyclovir-mild-alzheimers-disease\">slow Alzheimer's using antiviral drugs\u003c/a>, or drugs that modulate how immune cells in the brain respond to an infection.\u003c/p>\n\u003cp>But the study doesn't prove that herpes viruses are involved in Alzheimer's, says \u003ca href=\"https://www.nia.nih.gov/about/staff/hodes-richard\">Dr. Richard Hodes\u003c/a>, director of the National Institute on Aging, which helped fund the research.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\"The data are very provocative, but fall short of showing a direct causal role,\" he says. \"And if viral infections are playing a part, they are not the sole actor.\"\u003c/p>\n\u003cp>Even so, the study offers strong evidence that viral infections can influence the course of Alzheimer's, Hodes says.\u003c/p>\n\u003cp>Like a lot of scientific discoveries, this one was an accident. \"Viruses were the last thing we were looking for,\" Dudley says.\u003c/p>\n\u003cp>He and a team of researchers were using genetic data to look for differences between healthy brain tissue and brain tissue from people who died with Alzheimer's.[contextly_sidebar id=\"8UKShQkLN6fHi6cnpzNKDWdZydXn4g8E\"]\u003c/p>\n\u003cp>The goal was to identify new targets for drugs. Instead, the team kept finding hints that that brain tissue from Alzheimer's patients contained higher levels of viruses.\u003c/p>\n\u003cp>\"When we started analyzing the differences, it just sort of came screaming out at us from the data,\" Dudley says.\u003c/p>\n\u003cp>The team found that levels of two human herpes viruses, HHV-6 and HHV-7, were up to twice as high in brain tissue from people with Alzheimer's. They confirmed the finding by analyzing data from a consortium of brain banks.\u003c/p>\n\u003cp>These herpes viruses are extremely common, and can cause a skin rash called \u003ca href=\"http://kidshealth.org/en/parents/roseola.html\">roseola\u003c/a> in young children. But the viruses also can get into the brain, where they may remain inactive for decades.\u003c/p>\n\u003cp>Once the researchers knew the viruses were associated with Alzheimer's they started trying to figure out how a virus could affect the course of a brain disease. That meant identifying interactions between the virus genes and other genes in brain cells.\u003c/p>\n\u003cp>\"We mapped out the social network, if you will, of which genes the viruses are friends with and who they're talking to inside the brain,\" Dudley says. In essence, he says, they wanted to know: \"If the viruses are tweeting, who's tweeting back?\"\u003c/p>\n\u003cp>And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's.\u003c/p>\n\u003cp>They also found that these Alzheimer's risk genes seem to make a person's brain more vulnerable to infection with the two herpes viruses.\u003c/p>\n\u003cp>But just having herpes virus present in the brain isn't enough to cause Alzheimer's, Dudley says. Something needs to activate the viruses, which causes them to begin replicating.[contextly_sidebar id=\"gGYh4qorVVvYdrsEtJY48IAc6q49hNUX\"]\u003c/p>\n\u003cp>It's not clear what causes the activation, Dudley says, though he suspects some sort of change in the internal functions of brain cells.\u003c/p>\n\u003cp>Once the viruses do become active, they appear to influence things like the accumulation of the plaques and tangles in the brain associated with Alzheimer's. \"They are sort of throwing a wrench in the works,\" he says.\u003c/p>\n\u003cp>The herpes viruses also seem to trigger an immune response in certain brain cells, Hodes says. These cells are part of an ancient immune system that has \u003ca href=\"https://www.npr.org/sections/health-shots/2018/02/18/580475245/scientists-explore-ties-between-alzheimers-and-brains-ancient-immune-system\">previously been implicated\u003c/a> in Alzheimer's.\u003c/p>\n\u003cp>Most previous efforts to prevent or treat Alzheimer's have involved trying to reduce the plaques and tangles associated with the disease. Those efforts have failed to improve brain function even when they accomplished their immediate goal.\u003c/p>\n\u003cp>Those \"distressing and disappointing failures\" suggest it's time for some new approaches, Hodes says. And the new study suggests at least two.\u003c/p>\n\u003cp>One is to give antiviral drugs to people with high levels of herpes virus in their brains. The Institute on Aging is already funding a study to test this approach in people in the early stages of Alzheimer's, Hodes says.\u003c/p>\n\u003cp>Another approach is to prevent the brain's immune cells from reacting to the virus in ways that accelerate Alzheimer's, Hodes says. That's tricky, he says, because simply disabling the brain's immune cells could be harmful.\u003c/p>\n\u003cp>Even so, Hodes is optimistic.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"The more we learn about the disease process and the more targets we can address,\" he says, \"the greater the probability we are going to slow or prevent the progression of Alzheimer's disease.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Researchers+Find+Herpes+Viruses+In+Brains+Marked+By+Alzheimer%27s+Disease&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n","blocks":[],"excerpt":"Two herpes viruses that cause skin rashes in toddlers may accelerate Alzheimer's disease when they infect brain cells. The finding suggests antiviral drugs might help protect the brain.","status":"publish","parent":0,"modified":1529606195,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":29,"wordCount":866},"headData":{"title":"Researchers Find Herpes Viruses In Alzheimer's Brains | KQED","description":"Two herpes viruses that cause skin rashes in toddlers may accelerate Alzheimer's disease when they infect brain cells. The finding suggests antiviral drugs might help protect the brain.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"442958 https://ww2.kqed.org/futureofyou/?p=442958","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/06/21/researchers-find-herpes-viruses-in-alzheimers-brains/","disqusTitle":"Researchers Find Herpes Viruses In Alzheimer's Brains","source":"Health","nprByline":"Jon Hamilton, NPR","nprStoryId":"621908340","nprApiLink":"http://api.npr.org/query?id=621908340&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2018/06/21/621908340/researchers-find-herpes-viruses-in-brains-marked-by-alzheimers-disease?ft=nprml&f=621908340","nprRetrievedStory":"1","nprPubDate":"Thu, 21 Jun 2018 11:31:00 -0400","nprStoryDate":"Thu, 21 Jun 2018 11:16:00 -0400","nprLastModifiedDate":"Thu, 21 Jun 2018 11:31:51 -0400","path":"/futureofyou/442958/researchers-find-herpes-viruses-in-alzheimers-brains","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Two common herpes viruses appear to play a role in Alzheimer's disease.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>The viruses, best known for causing a distinctive skin rash in young children, are abundant in brain tissue from people with Alzheimer's, a team of scientists \u003ca href=\"http://www.cell.com/neuron/fulltext/S0896-6273(18)30421-5\">reports\u003c/a> Thursday in \u003cem>Neuron.\u003c/em> The team also found evidence that the viruses can interact with brain cells in ways that could accelerate the disease.\u003c/p>\n\u003cp>\"Our hypothesis is that they put gas on the flame,\" says \u003ca href=\"https://www.mountsinai.org/profiles/joel-dudley\">Joel Dudley\u003c/a>, an author of the study and an associate professor of genetics and genomic sciences at the Icahn School of Medicine at Mt. Sinai in New York City.\u003c/p>\n\u003cp>The finding adds credence to a decades-old idea that an infection can cause Alzheimer's disease. It also suggests that it may be possible to prevent or \u003ca href=\"https://www.nia.nih.gov/alzheimers/clinical-trials/valacyclovir-mild-alzheimers-disease\">slow Alzheimer's using antiviral drugs\u003c/a>, or drugs that modulate how immune cells in the brain respond to an infection.\u003c/p>\n\u003cp>But the study doesn't prove that herpes viruses are involved in Alzheimer's, says \u003ca href=\"https://www.nia.nih.gov/about/staff/hodes-richard\">Dr. Richard Hodes\u003c/a>, director of the National Institute on Aging, which helped fund the research.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\"The data are very provocative, but fall short of showing a direct causal role,\" he says. \"And if viral infections are playing a part, they are not the sole actor.\"\u003c/p>\n\u003cp>Even so, the study offers strong evidence that viral infections can influence the course of Alzheimer's, Hodes says.\u003c/p>\n\u003cp>Like a lot of scientific discoveries, this one was an accident. \"Viruses were the last thing we were looking for,\" Dudley says.\u003c/p>\n\u003cp>He and a team of researchers were using genetic data to look for differences between healthy brain tissue and brain tissue from people who died with Alzheimer's.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>The goal was to identify new targets for drugs. Instead, the team kept finding hints that that brain tissue from Alzheimer's patients contained higher levels of viruses.\u003c/p>\n\u003cp>\"When we started analyzing the differences, it just sort of came screaming out at us from the data,\" Dudley says.\u003c/p>\n\u003cp>The team found that levels of two human herpes viruses, HHV-6 and HHV-7, were up to twice as high in brain tissue from people with Alzheimer's. They confirmed the finding by analyzing data from a consortium of brain banks.\u003c/p>\n\u003cp>These herpes viruses are extremely common, and can cause a skin rash called \u003ca href=\"http://kidshealth.org/en/parents/roseola.html\">roseola\u003c/a> in young children. But the viruses also can get into the brain, where they may remain inactive for decades.\u003c/p>\n\u003cp>Once the researchers knew the viruses were associated with Alzheimer's they started trying to figure out how a virus could affect the course of a brain disease. That meant identifying interactions between the virus genes and other genes in brain cells.\u003c/p>\n\u003cp>\"We mapped out the social network, if you will, of which genes the viruses are friends with and who they're talking to inside the brain,\" Dudley says. In essence, he says, they wanted to know: \"If the viruses are tweeting, who's tweeting back?\"\u003c/p>\n\u003cp>And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's.\u003c/p>\n\u003cp>They also found that these Alzheimer's risk genes seem to make a person's brain more vulnerable to infection with the two herpes viruses.\u003c/p>\n\u003cp>But just having herpes virus present in the brain isn't enough to cause Alzheimer's, Dudley says. Something needs to activate the viruses, which causes them to begin replicating.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>It's not clear what causes the activation, Dudley says, though he suspects some sort of change in the internal functions of brain cells.\u003c/p>\n\u003cp>Once the viruses do become active, they appear to influence things like the accumulation of the plaques and tangles in the brain associated with Alzheimer's. \"They are sort of throwing a wrench in the works,\" he says.\u003c/p>\n\u003cp>The herpes viruses also seem to trigger an immune response in certain brain cells, Hodes says. These cells are part of an ancient immune system that has \u003ca href=\"https://www.npr.org/sections/health-shots/2018/02/18/580475245/scientists-explore-ties-between-alzheimers-and-brains-ancient-immune-system\">previously been implicated\u003c/a> in Alzheimer's.\u003c/p>\n\u003cp>Most previous efforts to prevent or treat Alzheimer's have involved trying to reduce the plaques and tangles associated with the disease. Those efforts have failed to improve brain function even when they accomplished their immediate goal.\u003c/p>\n\u003cp>Those \"distressing and disappointing failures\" suggest it's time for some new approaches, Hodes says. And the new study suggests at least two.\u003c/p>\n\u003cp>One is to give antiviral drugs to people with high levels of herpes virus in their brains. The Institute on Aging is already funding a study to test this approach in people in the early stages of Alzheimer's, Hodes says.\u003c/p>\n\u003cp>Another approach is to prevent the brain's immune cells from reacting to the virus in ways that accelerate Alzheimer's, Hodes says. That's tricky, he says, because simply disabling the brain's immune cells could be harmful.\u003c/p>\n\u003cp>Even so, Hodes is optimistic.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"The more we learn about the disease process and the more targets we can address,\" he says, \"the greater the probability we are going to slow or prevent the progression of Alzheimer's disease.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Researchers+Find+Herpes+Viruses+In+Brains+Marked+By+Alzheimer%27s+Disease&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/442958/researchers-find-herpes-viruses-in-alzheimers-brains","authors":["byline_futureofyou_442958"],"categories":["futureofyou_1","futureofyou_73","futureofyou_1064"],"tags":["futureofyou_999","futureofyou_673","futureofyou_952","futureofyou_1056","futureofyou_652"],"collections":["futureofyou_1094"],"featImg":"futureofyou_442960","label":"source_futureofyou_442958"}},"programsReducer":{"possible":{"id":"possible","title":"Possible","info":"Possible is hosted by entrepreneur Reid Hoffman and writer Aria Finger. Together in Possible, Hoffman and Finger lead enlightening discussions about building a brighter collective future. The show features interviews with visionary guests like Trevor Noah, Sam Altman and Janette Sadik-Khan. Possible paints an optimistic portrait of the world we can create through science, policy, business, art and our shared humanity. It asks: What if everything goes right for once? How can we get there? Each episode also includes a short fiction story generated by advanced AI GPT-4, serving as a thought-provoking springboard to speculate how humanity could leverage technology for good.","airtime":"SUN 2pm","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/Possible-Podcast-Tile-360x360-1.jpg","officialWebsiteLink":"https://www.possible.fm/","meta":{"site":"news","source":"Possible"},"link":"/radio/program/possible","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/possible/id1677184070","spotify":"https://open.spotify.com/show/730YpdUSNlMyPQwNnyjp4k"}},"1a":{"id":"1a","title":"1A","info":"1A is home to the national conversation. 1A brings on great guests and frames the best debate in ways that make you think, share and engage.","airtime":"MON-THU 11pm-12am","imageSrc":"https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/1a.jpg","officialWebsiteLink":"https://the1a.org/","meta":{"site":"news","source":"npr"},"link":"/radio/program/1a","subscribe":{"npr":"https://rpb3r.app.goo.gl/RBrW","apple":"https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?s=143441&mt=2&id=1188724250&at=11l79Y&ct=nprdirectory","tuneIn":"https://tunein.com/radio/1A-p947376/","rss":"https://feeds.npr.org/510316/podcast.xml"}},"all-things-considered":{"id":"all-things-considered","title":"All Things Considered","info":"Every weekday, \u003cem>All Things Considered\u003c/em> hosts Robert Siegel, Audie Cornish, Ari Shapiro, and Kelly McEvers present the program's trademark mix of news, interviews, commentaries, reviews, and offbeat features. 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But is this once sleepy suburb ready for them?","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/American-Suburb-Podcast-Tile-703x703-1.jpg","officialWebsiteLink":"/news/series/american-suburb-podcast","meta":{"site":"news","source":"kqed","order":"13"},"link":"/news/series/american-suburb-podcast/","subscribe":{"npr":"https://rpb3r.app.goo.gl/RBrW","apple":"https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?mt=2&id=1287748328","tuneIn":"https://tunein.com/radio/American-Suburb-p1086805/","rss":"https://ww2.kqed.org/news/series/american-suburb-podcast/feed/podcast","google":"https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkMzMDExODgxNjA5"}},"baycurious":{"id":"baycurious","title":"Bay Curious","tagline":"Exploring the Bay Area, one question at a time","info":"KQED’s new podcast, Bay Curious, gets to the bottom of the mysteries — both profound and peculiar — that give the Bay Area its unique identity. And we’ll do it with your help! You ask the questions. You decide what Bay Curious investigates. And you join us on the journey to find the answers.","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/Bay-Curious-Podcast-Tile-703x703-1.jpg","imageAlt":"\"KQED Bay Curious","officialWebsiteLink":"/news/series/baycurious","meta":{"site":"news","source":"kqed","order":"4"},"link":"/podcasts/baycurious","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/bay-curious/id1172473406","npr":"https://www.npr.org/podcasts/500557090/bay-curious","rss":"https://ww2.kqed.org/news/category/bay-curious-podcast/feed/podcast","google":"https://podcasts.google.com/feed/aHR0cHM6Ly93dzIua3FlZC5vcmcvbmV3cy9jYXRlZ29yeS9iYXktY3VyaW91cy1wb2RjYXN0L2ZlZWQvcG9kY2FzdA","stitcher":"https://www.stitcher.com/podcast/kqed/bay-curious","spotify":"https://open.spotify.com/show/6O76IdmhixfijmhTZLIJ8k"}},"bbc-world-service":{"id":"bbc-world-service","title":"BBC World Service","info":"The day's top stories from BBC News compiled twice daily in the week, once at weekends.","airtime":"MON-FRI 9pm-10pm, TUE-FRI 1am-2am","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/BBC-World-Service-Podcast-Tile-360x360-1.jpg","officialWebsiteLink":"https://www.bbc.co.uk/sounds/play/live:bbc_world_service","meta":{"site":"news","source":"BBC World Service"},"link":"/radio/program/bbc-world-service","subscribe":{"apple":"https://itunes.apple.com/us/podcast/global-news-podcast/id135067274?mt=2","tuneIn":"https://tunein.com/radio/BBC-World-Service-p455581/","rss":"https://podcasts.files.bbci.co.uk/p02nq0gn.rss"}},"code-switch-life-kit":{"id":"code-switch-life-kit","title":"Code Switch / Life Kit","info":"\u003cem>Code Switch\u003c/em>, which listeners will hear in the first part of the hour, has fearless and much-needed conversations about race. Hosted by journalists of color, the show tackles the subject of race head-on, exploring how it impacts every part of society — from politics and pop culture to history, sports and more.\u003cbr />\u003cbr />\u003cem>Life Kit\u003c/em>, which will be in the second part of the hour, guides you through spaces and feelings no one prepares you for — from finances to mental health, from workplace microaggressions to imposter syndrome, from relationships to parenting. The show features experts with real world experience and shares their knowledge. 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On Our Watch brings listeners into the rooms where officers are questioned and witnesses are interrogated to find out who this system is really protecting. 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For one hour a week, the show tries to lift the veil from the process of \"making media,\" especially news media, because it's through that lens that we see the world and the world sees us","airtime":"SUN 2pm-3pm, MON 12am-1am","imageSrc":"https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/onTheMedia.png","officialWebsiteLink":"https://www.wnycstudios.org/shows/otm","meta":{"site":"news","source":"wnyc"},"link":"/radio/program/on-the-media","subscribe":{"apple":"https://itunes.apple.com/us/podcast/on-the-media/id73330715?mt=2","tuneIn":"https://tunein.com/radio/On-the-Media-p69/","rss":"http://feeds.wnyc.org/onthemedia"}},"our-body-politic":{"id":"our-body-politic","title":"Our Body Politic","info":"Presented by KQED, KCRW and KPCC, and created and hosted by award-winning journalist Farai Chideya, Our Body Politic is unapologetically centered on reporting on not just how women of color experience the major political events of today, but how they’re impacting those very issues.","airtime":"SAT 6pm-7pm, SUN 1am-2am","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/Our-Body-Politic-Podcast-Tile-360x360-1.jpg","officialWebsiteLink":"https://our-body-politic.simplecast.com/","meta":{"site":"news","source":"kcrw"},"link":"/radio/program/our-body-politic","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/our-body-politic/id1533069868","google":"https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5zaW1wbGVjYXN0LmNvbS9feGFQaHMxcw","spotify":"https://open.spotify.com/show/4ApAiLT1kV153TttWAmqmc","rss":"https://feeds.simplecast.com/_xaPhs1s","tuneIn":"https://tunein.com/podcasts/News--Politics-Podcasts/Our-Body-Politic-p1369211/"}},"pbs-newshour":{"id":"pbs-newshour","title":"PBS NewsHour","info":"Analysis, background reports and updates from the PBS NewsHour putting today's news in context.","airtime":"MON-FRI 3pm-4pm","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/PBS-News-Hour-Podcast-Tile-360x360-1.jpg","officialWebsiteLink":"https://www.pbs.org/newshour/","meta":{"site":"news","source":"pbs"},"link":"/radio/program/pbs-newshour","subscribe":{"apple":"https://itunes.apple.com/us/podcast/pbs-newshour-full-show/id394432287?mt=2","tuneIn":"https://tunein.com/radio/PBS-NewsHour---Full-Show-p425698/","rss":"https://www.pbs.org/newshour/feeds/rss/podcasts/show"}},"perspectives":{"id":"perspectives","title":"Perspectives","tagline":"KQED's series of of daily listener commentaries since 1991","info":"KQED's series of of daily listener commentaries since 1991.","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/Perspectives-Podcast-Tile-703x703-1.jpg","officialWebsiteLink":"/perspectives/","meta":{"site":"radio","source":"kqed","order":"15"},"link":"/perspectives","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/id73801135","npr":"https://www.npr.org/podcasts/432309616/perspectives","rss":"https://ww2.kqed.org/perspectives/category/perspectives/feed/","google":"https://podcasts.google.com/feed/aHR0cHM6Ly93dzIua3FlZC5vcmcvcGVyc3BlY3RpdmVzL2NhdGVnb3J5L3BlcnNwZWN0aXZlcy9mZWVkLw"}},"planet-money":{"id":"planet-money","title":"Planet Money","info":"The economy explained. 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The result is stories that inform and inspire, arming our listeners with information to right injustices, hold the powerful accountable and improve lives.Reveal is hosted by Al Letson and showcases the award-winning work of CIR and newsrooms large and small across the nation. In a radio and podcast market crowded with choices, Reveal focuses on important and often surprising stories that illuminate the world for our listeners.","airtime":"SAT 4pm-5pm","imageSrc":"https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/reveal300px.png","officialWebsiteLink":"https://www.revealnews.org/episodes/","meta":{"site":"news","source":"npr"},"link":"/radio/program/reveal","subscribe":{"apple":"https://itunes.apple.com/us/podcast/reveal/id886009669","tuneIn":"https://tunein.com/radio/Reveal-p679597/","rss":"http://feeds.revealradio.org/revealpodcast"}},"says-you":{"id":"says-you","title":"Says You!","info":"Public radio's game show of bluff and bluster, words and whimsy. 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