D'OH! DHA Supplements Don't Reduce Alzheimer's Risks
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Streeter.","credit":null,"description":null,"imgSizes":{"thumbnail":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2014/10/Streeter_NPR_Sleep_640-400x224.jpg","width":400,"height":224,"mimeType":"image/jpeg"},"guest-author-32":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2014/10/Streeter_NPR_Sleep_640-32x32.jpg","width":32,"height":32,"mimeType":"image/jpeg"},"guest-author-64":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2014/10/Streeter_NPR_Sleep_640-64x64.jpg","width":64,"height":64,"mimeType":"image/jpeg"},"guest-author-96":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2014/10/Streeter_NPR_Sleep_640-96x96.jpg","width":96,"height":96,"mimeType":"image/jpeg"},"guest-author-128":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2014/10/Streeter_NPR_Sleep_640-128x128.jpg","width":128,"height":128,"mimeType":"image/jpeg"},"detail":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2014/10/Streeter_NPR_Sleep_640-75x75.jpg","width":75,"height":75,"mimeType":"image/jpeg"},"kqedFullSize":{"file":"https://ww2.kqed.org/app/uploads/sites/39/2014/10/Streeter_NPR_Sleep_640.jpg","width":640,"height":359}},"fetchFailed":false,"isLoading":false},"quest_13535":{"type":"attachments","id":"quest_13535","meta":{"index":"attachments_1591205162","site":"quest","id":"13535","found":true},"title":"alzheimer","publishDate":1302030819,"status":"inherit","parent":13504,"modified":1302030819,"caption":null,"credit":null,"description":"\u003cp class=\"attachment\">\u003ca href='http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/alzheimer2.jpg' title='alzheimer'>\u003cimg width=\"300\" height=\"200\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/alzheimer2.jpg\" class=\"attachment-medium\" alt=\"alzheimer\" title=\"alzheimer\" 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The program is part of an ongoing collaboration between the \u003ca href=\"http://genetics.stanford.edu/\">Stanford Department of Genetics\u003c/a> and \u003ca href=\"http://www.thetech.org/\">The Tech Museum of Innovation\u003c/a>. Together these two partners created the \u003ca href=\"http://www.thetech.org/exhibits/permanent/index.php?sGalKey=gtwt&galKey=lt\">Genetics: Technology with a Twist\u003c/a> exhibition.\r\n\r\nYou can also see \u003ca href=\"https://ww2.kqed.org/science/author/dr-barry-starr/\">additional posts by Barry at KQED Science\u003c/a>, and read his \u003ca href=\"http://science.kqed.org/quest/author/dr-barry-starr/\">previous contributions\u003c/a> to \u003ca href=\"http://science.kqed.org/quest/\">QUEST\u003c/a>, a project dedicated to exploring the Science of Sustainability.","avatar":"https://secure.gravatar.com/avatar/4a5680e4c642ea0f0f3041af16018969?s=600&d=blank&r=g","twitter":"geneticsboy","facebook":null,"instagram":null,"linkedin":null,"sites":[{"site":"science","roles":["author"]},{"site":"quest","roles":["subscriber"]}],"headData":{"title":"Dr. Barry Starr | KQED","description":null,"ogImgSrc":"https://secure.gravatar.com/avatar/4a5680e4c642ea0f0f3041af16018969?s=600&d=blank&r=g","twImgSrc":"https://secure.gravatar.com/avatar/4a5680e4c642ea0f0f3041af16018969?s=600&d=blank&r=g"},"isLoading":false,"link":"/author/dr-barry-starr"},"acurry":{"type":"authors","id":"6444","meta":{"index":"authors_1591205172","id":"6444","found":true},"name":"Arwen Curry","firstName":"Arwen","lastName":"Curry","slug":"acurry","email":"acurry@KQED.org","display_author_email":false,"staff_mastheads":[],"title":null,"bio":"Arwen Curry is Associate Producer of TV at KQED Science. She comes to KQED from documentary film, and is director of \u003cem>Worlds of Ursula K. Le Guin\u003c/em>, a feature documentary about the influential science fiction writer. She was Associate Producer of the films \u003cem>Regarding Susan Sontag\u003c/em>, \u003cem>American Jerusalem: Jews and the Making of San Francisco\u003c/em>, \u003cem>EAMES: The Architect & The Painter\u003c/em>, \u003cem>Utopia in Four Movements\u003c/em>, and co-produced and directed \u003cem>Stuffed\u003c/em>, a short film about compulsive hoarding. Arwen was editor of the punk magazine \u003cem>Maximum Rock 'n' Roll\u003c/em>, and has been a contributor to Radio Lab and McSweeney’s. She is a Bay Area native and a graduate of the UC Berkeley Graduate School of Journalism.","avatar":"https://secure.gravatar.com/avatar/59af0722ca76a9bcd9dd6da80e683e18?s=600&d=blank&r=g","twitter":null,"facebook":null,"instagram":null,"linkedin":null,"sites":[{"site":"science","roles":["editor"]},{"site":"quest","roles":["leadcoordinator","subscriber"]}],"headData":{"title":"Arwen Curry | KQED","description":null,"ogImgSrc":"https://secure.gravatar.com/avatar/59af0722ca76a9bcd9dd6da80e683e18?s=600&d=blank&r=g","twImgSrc":"https://secure.gravatar.com/avatar/59af0722ca76a9bcd9dd6da80e683e18?s=600&d=blank&r=g"},"isLoading":false,"link":"/author/acurry"},"darya-pino":{"type":"authors","id":"10218","meta":{"index":"authors_1591205172","id":"10218","found":true},"name":"Darya Pino","firstName":"Darya","lastName":"Pino","slug":"darya-pino","email":"darya@summertomato.com","display_author_email":false,"staff_mastheads":[],"title":null,"bio":"Darya Pino is a Ph.D trained scientist, San Francisco foodie, food and health writer and advocate of local, seasonal foods. She shares her unique scientific perspective on health and enthusiasm for delicious foods at her website Summer Tomato. Follow her on Twitter @summertomato.","avatar":"https://secure.gravatar.com/avatar/b5303fe7938a19bb9d4baa7837fb8390?s=600&d=blank&r=g","twitter":null,"facebook":null,"instagram":null,"linkedin":null,"sites":[{"site":"quest","roles":["subscriber"]}],"headData":{"title":"Darya Pino | KQED","description":null,"ogImgSrc":"https://secure.gravatar.com/avatar/b5303fe7938a19bb9d4baa7837fb8390?s=600&d=blank&r=g","twImgSrc":"https://secure.gravatar.com/avatar/b5303fe7938a19bb9d4baa7837fb8390?s=600&d=blank&r=g"},"isLoading":false,"link":"/author/darya-pino"}},"breakingNewsReducer":{},"campaignFinanceReducer":{},"firebase":{"requesting":{},"requested":{},"timestamps":{},"data":{},"ordered":{},"auth":{"isLoaded":false,"isEmpty":true},"authError":null,"profile":{"isLoaded":false,"isEmpty":true},"listeners":{"byId":{},"allIds":[]},"isInitializing":false,"errors":[]},"navBarReducer":{"navBarId":"home","fullView":true,"showPlayer":false},"navMenuReducer":{"menus":[{"key":"menu1","items":[{"name":"News","link":"/","type":"title"},{"name":"Politics","link":"/politics"},{"name":"Science","link":"/science"},{"name":"Education","link":"/educationnews"},{"name":"Housing","link":"/housing"},{"name":"Immigration","link":"/immigration"},{"name":"Criminal Justice","link":"/criminaljustice"},{"name":"Silicon Valley","link":"/siliconvalley"},{"name":"Forum","link":"/forum"},{"name":"The California Report","link":"/californiareport"}]},{"key":"menu2","items":[{"name":"Arts & Culture","link":"/arts","type":"title"},{"name":"Critics’ Picks","link":"/thedolist"},{"name":"Cultural Commentary","link":"/artscommentary"},{"name":"Food & Drink","link":"/food"},{"name":"Bay Area Hip-Hop","link":"/bayareahiphop"},{"name":"Rebel Girls","link":"/rebelgirls"},{"name":"Arts Video","link":"/artsvideos"}]},{"key":"menu3","items":[{"name":"Podcasts","link":"/podcasts","type":"title"},{"name":"Bay Curious","link":"/podcasts/baycurious"},{"name":"Rightnowish","link":"/podcasts/rightnowish"},{"name":"The Bay","link":"/podcasts/thebay"},{"name":"On Our Watch","link":"/podcasts/onourwatch"},{"name":"Mindshift","link":"/podcasts/mindshift"},{"name":"Consider This","link":"/podcasts/considerthis"},{"name":"Political Breakdown","link":"/podcasts/politicalbreakdown"}]},{"key":"menu4","items":[{"name":"Live Radio","link":"/radio","type":"title"},{"name":"TV","link":"/tv","type":"title"},{"name":"Events","link":"/events","type":"title"},{"name":"For Educators","link":"/education","type":"title"},{"name":"Support KQED","link":"/support","type":"title"},{"name":"About","link":"/about","type":"title"},{"name":"Help Center","link":"https://kqed-helpcenter.kqed.org/s","type":"title"}]}]},"pagesReducer":{},"postsReducer":{"stream_live":{"type":"live","id":"stream_live","audioUrl":"https://streams.kqed.org/kqedradio","title":"Live Stream","excerpt":"Live Stream information currently unavailable.","link":"/radio","featImg":"","label":{"name":"KQED Live","link":"/"}},"stream_kqedNewscast":{"type":"posts","id":"stream_kqedNewscast","audioUrl":"https://www.kqed.org/.stream/anon/radio/RDnews/newscast.mp3?_=1","title":"KQED Newscast","featImg":"","label":{"name":"88.5 FM","link":"/"}},"quest_17514":{"type":"posts","id":"quest_17514","meta":{"index":"posts_1591205157","site":"quest","id":"17514","score":null,"sort":[1415804432000]},"guestAuthors":[],"slug":"catching-up-on-sleep-science","title":"Catching Up on Sleep Science","publishDate":1415804432,"format":"video","headTitle":"QUEST | KQED Science","labelTerm":{},"content":"\u003cp>\u003cem>This video story was originally produced by \u003ca href=\"http://ww2.kqed.org/quest/author/sheraz-sadiq/\">Sheraz Sadiq\u003c/a> and was updated by\u003ca href=\"http://ww2.kqed.org/quest/author/lisalanders/\"> Lisa Landers\u003c/a> and \u003ca href=\"http://ww2.kqed.org/quest/author/acurry/\">Arwen Curry.\u003c/a>\u003c/em>\u003c/p>\n\u003cp>Be honest – do you ever brag about how little sleep you get? If so, you’re not alone. Humans are the only species that seems to deliberately deprive themselves of sleep. But if you’ve ever uttered a phrase like “I’ll sleep when I’m dead,” it’s time for a wake-up call, scientists say.\u003c/p>\n\u003cfigure id=\"attachment_72675\" class=\"wp-caption alignright\" style=\"max-width: 300px\">\u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/803_SLEEP_polar_bear.jpg\">\u003cimg class=\"size-thumbnail wp-image-72675\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/803_SLEEP_polar_bear-300x169.jpg\" alt=\"Sleep is common to all species that have been studied to date.\" width=\"300\" height=\"169\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Sleep is common to all species that have been studied to date.\u003c/figcaption>\u003c/figure>\n\u003cp>Researchers have long known that adequate sleep is critical for good health. Insufficient sleep \u003ca href=\"http://www.mayoclinic.org/diseases-conditions/insomnia/expert-answers/lack-of-sleep/faq-20057757\">impairs the immune system\u003c/a>, and is associated with everything from \u003ca href=\"http://www.hsph.harvard.edu/nutritionsource/sleep/\">obesity\u003c/a> to cardiovascular disease, stroke to cancer, depression to schizophrenia and \u003ca href=\"http://news.temple.edu/news/2014-03-18/chronic-sleep-disturbance-might-trigger-onset-alzheimer%E2%80%99s\">Alzheimer’s disease\u003c/a>. Now scientists are several steps closer to knowing how sleep keeps us healthy.\u003c/p>\n\u003cp>An important clue about sleep’s function surfaced in \u003ca href=\"http://www.nature.com/neuro/journal/v16/n2/full/nn.3303.html\">a 2013 study\u003c/a> published in the journal \u003cem>\u003ca href=\"http://www.nature.com/neuro/index.html\">Nature Neuroscience\u003c/a> \u003c/em>and conducted at the University of California-Berkeley. The study, by neuroscience professor Matthew Walker and his colleagues, showed that the structural changes the brain experiences as we age damage the quality of deep sleep. This hinders the brain’s ongoing ability to store memories.\u003c/p>\n\u003cfigure id=\"attachment_72671\" class=\"wp-caption alignleft\" style=\"max-width: 264px\">\u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/Matthew_Walker_AC_800.jpg\">\u003cimg class=\"wp-image-72671 size-thumbnail\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/Matthew_Walker_AC_800-264x169.jpg\" alt=\"Professor Matthew Walker runs the Sleep and Neuroimaging Lab at the University of California-Berkeley Photo by Arwen Curry.\" width=\"264\" height=\"169\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Professor Matthew Walker runs the Sleep and Neuroimaging Lab at the University of California-Berkeley.\u003cbr> Photo by Arwen Curry.\u003c/figcaption>\u003c/figure>\n\u003cp>Scientists were already aware of a connection between sleep and memory – now they are developing a working hypothesis about how the mechanism actually works.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“It’s almost as though your learning system is like a USB stick,” Walker said. “During the day you’re acquiring lots of information rapidly.” This information is lodged in an area of the brain called the hippocampus.\u003c/p>\n\u003cp>But when we sleep, this data is exported to “the hard drive of our brain,” a larger storage space called the cortex.\u003c/p>\n\u003cp>“When we wake up the next day, our USB stick has now been cleared out, so we can start to learn new information anew,” Walker said. “We’ve refreshed our learning capacity.”\u003c/p>\n\u003cp>The idea that we need less sleep as we age is a fallacy, he added. It now appears that the brain is physically unable to achieve the amount of slow-wave, non-rapid-eye-movement sleep needed to consolidate memories as we grow older. By the time we’re 50 years old, non-REM sleep has reduced by half compared to when we were 18 years old. By the time we’re 70, deep sleep is down to about 5 percent.\u003c/p>\n\u003cfigure id=\"attachment_72668\" class=\"wp-caption alignright\" style=\"max-width: 288px\">\u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/402a_sleep_640-288x162.jpg\">\u003cimg class=\"wp-image-72668 size-full\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/402a_sleep_640-288x162.jpg\" alt=\"Scientists use electric pulses to copy the rhythm of slow-wave sleep, which declines as we age.\" width=\"288\" height=\"162\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Scientists use electrical pulses to copy the rhythm of slow-wave sleep, which declines as we age.\u003c/figcaption>\u003c/figure>\n\u003cp>This research suggests that improving slow-wave sleep, which takes up about a quarter of the night, could slow the decline of memory as we age. Scientists are investigating \u003ca href=\"http://www.sciencedirect.com/science/article/pii/016643289390140L\">ways to use electrical stimulation to improve deep sleep in older people\u003c/a> by attaching electrodes to the scalp to create a mild current that mimics the pattern of slow-wave sleep.\u003c/p>\n\u003cp>The science of sleep has traditionally been abstract, but advances in imaging technology now allow scientists to peek inside the sleeping brain. In \u003ca href=\"http://www.urmc.rochester.edu/news/story/index.cfm?id=3956\">a groundbreaking 2013 study\u003c/a>, researchers at the University of Rochester Medical Center injected dyes into the brains of sleeping mice, and watched in real-time as the neurons in their brains shrank dramatically by about 60 percent. This increased the spaces between the brain cells, allowing cerebrospinal fluid to easily flow through and cleanse the brain of naturally occurring toxic waste.\u003c/p>\n\u003cfigure id=\"attachment_72672\" class=\"wp-caption alignleft\" style=\"max-width: 640px\">\u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/Rochester_Brain_Flushing_800.jpg\">\u003cimg class=\"wp-image-72672 size-large\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/Rochester_Brain_Flushing_800-640x360.jpg\" alt=\"This photograph shows cerebrospinal fluid (in blue) rinsing toxins from the brain of a sleeping mouse.\" width=\"640\" height=\"360\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">This photograph shows cerebrospinal fluid (in blue) rinsing toxins from the brain of a sleeping mouse. Photo courtesy of the University of Rochester Medical Center.\u003c/figcaption>\u003c/figure>\n\u003cp>“It’s almost as though you’re sort of walking past one of those delightful posh hotels and during the day there’s lots of dirt that happens on the sidewalk,” said Walker. “And then at night, someone comes out with one of those pressure-jet washers and cleans it all out, so that it’s fresh and functional the next day. That’s exactly what we think is now happening during sleep at night.”\u003c/p>\n\u003cp>Of particular note is that chronic sleep deprivation contributes to \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/24887018\">the buildup of a toxic protein called beta-amyloid\u003c/a>, which is a predictor of Alzheimer’s disease.\u003c/p>\n\u003cp>Walker’s research also suggests strong connections between sleep and creativity and emotional regulation. But with all we’ve learned about sleep, there remains much more to be discovered.\u003c/p>\n\u003cp>“If you think about it,” said Walker, “we’ve understood the other three main biological drives – eating, drinking and reproducing – for many tens, if not hundreds, of years. But the fourth main biological drive, common across all species that we’ve studied, which is to sleep, remains that quintessential mystery.”\u003c/p>\n\u003cp>One thing is clear: \u003ca href=\"http://www.gallup.com/poll/166553/less-recommended-amount-sleep.aspx\">People are sleeping demonstrably less than they did 70 years ago\u003c/a>. An estimated 70 million Americans suffer from some form of chronic sleep disorder, and 40 percent get less than the recommended amount of sleep – seven and a half to eight hours a night.\u003c/p>\n\u003cp>Contributing factors include multi-tasking, the invasion of technology in the bedroom and long commute times, which rob us of precious free hours, Walker said. But the biggest culprit may be our own attitudes.\u003c/p>\n\u003cp>“I think where we’re at in modern-day society is a problematic relationship with sleep,” he said.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“We know that sleep is fundamentally important at the most basic of biological levels,” he said. “But something strange has happened – sleep has received a stigma. There’s some kind of intonation which suggests that getting sufficient sleep is equivalent to being lazy. We wear this badge of sleep deprivation like some kind of honor emblem on our arm, and that’s profoundly misguided.”\u003c/p>\n\u003ch2>Additional Links\u003c/h2>\n\u003cul>\n\u003cli>\u003ca href=\"https://www.youtube.com/watch?v=yTIDkj9Tn58\">Watch the full episode of QUEST.\u003c/a>\u003c/li>\n\u003cli>\u003ca href=\"http://www.kqed.org/a/forum/R201408261000\">Forum with Michael Krasny: sleep expert Matthew Walker\u003c/a>\u003c/li>\n\u003cli>\u003ca href=\"http://blogs.kqed.org/stateofhealth/2014/08/27/sleep-apps-myths-and-more-strategies-for-a-good-nights-rest/\">Sleep Apps, Myths and More: Strategies for a Good Night’s Rest\u003c/a>\u003c/li>\n\u003cli>\u003ca href=\"http://www.kqed.org/a/forum/R201311270930\">Forum with Dave Iverson: sleep therapy as a treatment for depression\u003c/a>\u003c/li>\n\u003c/ul>\n\n","blocks":[],"excerpt":"Sleep: It’s more important than you might think. Watch the video to see how sleep imprints memories, regulates emotions, and cleanses the brain of toxins. ","status":"publish","parent":0,"modified":1442634965,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":21,"wordCount":1052},"headData":{"title":"Catching Up on Sleep Science | KQED","description":"Sleep: It’s more important than you might think. Watch the video to see how sleep imprints memories, regulates emotions, and cleanses the brain of toxins. ","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"17514 http://science.kqed.org/quest/video/catching-up-on-sleep-science/","disqusUrl":"https://ww2.kqed.org/quest/2014/11/12/catching-up-on-sleep-science/","disqusTitle":"Catching Up on Sleep Science","videoEmbed":"https://www.youtube.com/watch?v=HW1HxGJAjqY","source":"Health","sourceUrl":"http://ww2.kqed.org/quest/category/health/","path":"/quest/17514/catching-up-on-sleep-science","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cem>This video story was originally produced by \u003ca href=\"http://ww2.kqed.org/quest/author/sheraz-sadiq/\">Sheraz Sadiq\u003c/a> and was updated by\u003ca href=\"http://ww2.kqed.org/quest/author/lisalanders/\"> Lisa Landers\u003c/a> and \u003ca href=\"http://ww2.kqed.org/quest/author/acurry/\">Arwen Curry.\u003c/a>\u003c/em>\u003c/p>\n\u003cp>Be honest – do you ever brag about how little sleep you get? If so, you’re not alone. Humans are the only species that seems to deliberately deprive themselves of sleep. But if you’ve ever uttered a phrase like “I’ll sleep when I’m dead,” it’s time for a wake-up call, scientists say.\u003c/p>\n\u003cfigure id=\"attachment_72675\" class=\"wp-caption alignright\" style=\"max-width: 300px\">\u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/803_SLEEP_polar_bear.jpg\">\u003cimg class=\"size-thumbnail wp-image-72675\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/803_SLEEP_polar_bear-300x169.jpg\" alt=\"Sleep is common to all species that have been studied to date.\" width=\"300\" height=\"169\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Sleep is common to all species that have been studied to date.\u003c/figcaption>\u003c/figure>\n\u003cp>Researchers have long known that adequate sleep is critical for good health. Insufficient sleep \u003ca href=\"http://www.mayoclinic.org/diseases-conditions/insomnia/expert-answers/lack-of-sleep/faq-20057757\">impairs the immune system\u003c/a>, and is associated with everything from \u003ca href=\"http://www.hsph.harvard.edu/nutritionsource/sleep/\">obesity\u003c/a> to cardiovascular disease, stroke to cancer, depression to schizophrenia and \u003ca href=\"http://news.temple.edu/news/2014-03-18/chronic-sleep-disturbance-might-trigger-onset-alzheimer%E2%80%99s\">Alzheimer’s disease\u003c/a>. Now scientists are several steps closer to knowing how sleep keeps us healthy.\u003c/p>\n\u003cp>An important clue about sleep’s function surfaced in \u003ca href=\"http://www.nature.com/neuro/journal/v16/n2/full/nn.3303.html\">a 2013 study\u003c/a> published in the journal \u003cem>\u003ca href=\"http://www.nature.com/neuro/index.html\">Nature Neuroscience\u003c/a> \u003c/em>and conducted at the University of California-Berkeley. The study, by neuroscience professor Matthew Walker and his colleagues, showed that the structural changes the brain experiences as we age damage the quality of deep sleep. This hinders the brain’s ongoing ability to store memories.\u003c/p>\n\u003cfigure id=\"attachment_72671\" class=\"wp-caption alignleft\" style=\"max-width: 264px\">\u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/Matthew_Walker_AC_800.jpg\">\u003cimg class=\"wp-image-72671 size-thumbnail\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/Matthew_Walker_AC_800-264x169.jpg\" alt=\"Professor Matthew Walker runs the Sleep and Neuroimaging Lab at the University of California-Berkeley Photo by Arwen Curry.\" width=\"264\" height=\"169\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Professor Matthew Walker runs the Sleep and Neuroimaging Lab at the University of California-Berkeley.\u003cbr> Photo by Arwen Curry.\u003c/figcaption>\u003c/figure>\n\u003cp>Scientists were already aware of a connection between sleep and memory – now they are developing a working hypothesis about how the mechanism actually works.\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>“It’s almost as though your learning system is like a USB stick,” Walker said. “During the day you’re acquiring lots of information rapidly.” This information is lodged in an area of the brain called the hippocampus.\u003c/p>\n\u003cp>But when we sleep, this data is exported to “the hard drive of our brain,” a larger storage space called the cortex.\u003c/p>\n\u003cp>“When we wake up the next day, our USB stick has now been cleared out, so we can start to learn new information anew,” Walker said. “We’ve refreshed our learning capacity.”\u003c/p>\n\u003cp>The idea that we need less sleep as we age is a fallacy, he added. It now appears that the brain is physically unable to achieve the amount of slow-wave, non-rapid-eye-movement sleep needed to consolidate memories as we grow older. By the time we’re 50 years old, non-REM sleep has reduced by half compared to when we were 18 years old. By the time we’re 70, deep sleep is down to about 5 percent.\u003c/p>\n\u003cfigure id=\"attachment_72668\" class=\"wp-caption alignright\" style=\"max-width: 288px\">\u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/402a_sleep_640-288x162.jpg\">\u003cimg class=\"wp-image-72668 size-full\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/402a_sleep_640-288x162.jpg\" alt=\"Scientists use electric pulses to copy the rhythm of slow-wave sleep, which declines as we age.\" width=\"288\" height=\"162\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Scientists use electrical pulses to copy the rhythm of slow-wave sleep, which declines as we age.\u003c/figcaption>\u003c/figure>\n\u003cp>This research suggests that improving slow-wave sleep, which takes up about a quarter of the night, could slow the decline of memory as we age. Scientists are investigating \u003ca href=\"http://www.sciencedirect.com/science/article/pii/016643289390140L\">ways to use electrical stimulation to improve deep sleep in older people\u003c/a> by attaching electrodes to the scalp to create a mild current that mimics the pattern of slow-wave sleep.\u003c/p>\n\u003cp>The science of sleep has traditionally been abstract, but advances in imaging technology now allow scientists to peek inside the sleeping brain. In \u003ca href=\"http://www.urmc.rochester.edu/news/story/index.cfm?id=3956\">a groundbreaking 2013 study\u003c/a>, researchers at the University of Rochester Medical Center injected dyes into the brains of sleeping mice, and watched in real-time as the neurons in their brains shrank dramatically by about 60 percent. This increased the spaces between the brain cells, allowing cerebrospinal fluid to easily flow through and cleanse the brain of naturally occurring toxic waste.\u003c/p>\n\u003cfigure id=\"attachment_72672\" class=\"wp-caption alignleft\" style=\"max-width: 640px\">\u003ca href=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/Rochester_Brain_Flushing_800.jpg\">\u003cimg class=\"wp-image-72672 size-large\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2014/10/Rochester_Brain_Flushing_800-640x360.jpg\" alt=\"This photograph shows cerebrospinal fluid (in blue) rinsing toxins from the brain of a sleeping mouse.\" width=\"640\" height=\"360\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">This photograph shows cerebrospinal fluid (in blue) rinsing toxins from the brain of a sleeping mouse. Photo courtesy of the University of Rochester Medical Center.\u003c/figcaption>\u003c/figure>\n\u003cp>“It’s almost as though you’re sort of walking past one of those delightful posh hotels and during the day there’s lots of dirt that happens on the sidewalk,” said Walker. “And then at night, someone comes out with one of those pressure-jet washers and cleans it all out, so that it’s fresh and functional the next day. That’s exactly what we think is now happening during sleep at night.”\u003c/p>\n\u003cp>Of particular note is that chronic sleep deprivation contributes to \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/24887018\">the buildup of a toxic protein called beta-amyloid\u003c/a>, which is a predictor of Alzheimer’s disease.\u003c/p>\n\u003cp>Walker’s research also suggests strong connections between sleep and creativity and emotional regulation. But with all we’ve learned about sleep, there remains much more to be discovered.\u003c/p>\n\u003cp>“If you think about it,” said Walker, “we’ve understood the other three main biological drives – eating, drinking and reproducing – for many tens, if not hundreds, of years. But the fourth main biological drive, common across all species that we’ve studied, which is to sleep, remains that quintessential mystery.”\u003c/p>\n\u003cp>One thing is clear: \u003ca href=\"http://www.gallup.com/poll/166553/less-recommended-amount-sleep.aspx\">People are sleeping demonstrably less than they did 70 years ago\u003c/a>. An estimated 70 million Americans suffer from some form of chronic sleep disorder, and 40 percent get less than the recommended amount of sleep – seven and a half to eight hours a night.\u003c/p>\n\u003cp>Contributing factors include multi-tasking, the invasion of technology in the bedroom and long commute times, which rob us of precious free hours, Walker said. But the biggest culprit may be our own attitudes.\u003c/p>\n\u003cp>“I think where we’re at in modern-day society is a problematic relationship with sleep,” he said.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“We know that sleep is fundamentally important at the most basic of biological levels,” he said. “But something strange has happened – sleep has received a stigma. There’s some kind of intonation which suggests that getting sufficient sleep is equivalent to being lazy. We wear this badge of sleep deprivation like some kind of honor emblem on our arm, and that’s profoundly misguided.”\u003c/p>\n\u003ch2>Additional Links\u003c/h2>\n\u003cul>\n\u003cli>\u003ca href=\"https://www.youtube.com/watch?v=yTIDkj9Tn58\">Watch the full episode of QUEST.\u003c/a>\u003c/li>\n\u003cli>\u003ca href=\"http://www.kqed.org/a/forum/R201408261000\">Forum with Michael Krasny: sleep expert Matthew Walker\u003c/a>\u003c/li>\n\u003cli>\u003ca href=\"http://blogs.kqed.org/stateofhealth/2014/08/27/sleep-apps-myths-and-more-strategies-for-a-good-nights-rest/\">Sleep Apps, Myths and More: Strategies for a Good Night’s Rest\u003c/a>\u003c/li>\n\u003cli>\u003ca href=\"http://www.kqed.org/a/forum/R201311270930\">Forum with Dave Iverson: sleep therapy as a treatment for depression\u003c/a>\u003c/li>\n\u003c/ul>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/17514/catching-up-on-sleep-science","authors":["6444"],"categories":["quest_4","quest_12"],"tags":["quest_83","quest_135","quest_13038","quest_13048","quest_13044","quest_423","quest_13042","quest_13045","quest_13047","quest_13052","quest_13050","quest_13040","quest_13046","quest_12269","quest_13201","quest_13035","quest_1451","quest_11723","quest_10537","quest_1788","quest_13039","quest_13036","quest_1916","quest_13041","quest_9816","quest_13037","quest_2031","quest_13","quest_10538","quest_2655","quest_13034","quest_13051","quest_2893","quest_3021","quest_12094","quest_13043","quest_3071","quest_13049"],"featImg":"quest_72659","label":"source_quest_17514"},"quest_19244":{"type":"posts","id":"quest_19244","meta":{"index":"posts_1591205157","site":"quest","id":"19244","score":null,"sort":[1308587263000]},"guestAuthors":[],"slug":"the-cloud-in-the-silver-lining","title":"The Cloud in the Silver Lining","publishDate":1308587263,"format":"standard","headTitle":"QUEST | KQED Science","labelTerm":{"site":"quest"},"content":"\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/06/SilverLining.jpg\" alt=\"\">\u003c/a>\u003cem>My lower risk for Alzheimer's may be the silver lining\u003cbr>to being e2/e2 at APOE.\u003cbr>Image courtesy of \u003ca href=\"http://commons.wikimedia.org/wiki/File:Silver_Lining.JPG\">ImUnicke\u003c/a>\u003c/em>\u003c/span>\u003c/p>\n\u003cp>When last I left you in my \u003ca href=\"http://ww2.kqed.org/quest/2011/05/23/uncovering-risk-one-gene-at-a-time/\">personal genomic journey\u003c/a>, I had just discovered that I was e2/e2 at the APOE gene. I was quietly giddy* about this as it meant I was at a lower risk for getting Alzheimer’s. And even more importantly, it meant I didn’t have e4 which would have significantly increased my chances of getting this form of dementia.\u003c/p>\n\u003cp>Digging a bit deeper I found some more good news. People with e2/e2 usually have lower levels of LDL, the bad cholesterol that increases the risk for a heart attack. This is consistent with my low levels of LDL. Two good effects from one allele!\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>But there are no free lunches in genetics. For example, having two copies of the delta32 version of the CCR5 gene makes you \u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/ask.php?id=336\">pretty resistant to HIV infection\u003c/a>. But it makes you more susceptible to the West Nile Virus. Having one copy of the sickle cell version of the hemoglobin gene makes you \u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/ask.php?id=271\">resistant to malaria\u003c/a>. But your kids might end up with full blown sickle cell anemia. And so on.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The e2 version of the APOE gene is no different. It makes me less likely to get Alzheimer’s and, most of the time, to have a heart attack. But it means that I can end up with higher triglycerides from what I eat. This is consistent with what I have seen at the doctor’s. \u003c/p>\n\u003cp>Triglycerides are actually an independent predictor of heart attack risk. So even though my LDL is low, I need to watch my diet to keep the triglycerides down. If I am not careful, my increased triglycerides might cancel out my decreased LDL and so change my reduced heart attack risk to an increased one. \u003c/p>\n\u003cp>Being e2/e2 also puts me at risk for a relatively rare disease called \u003ca href=\"http://www.kimballgenetics.com/tests-apo_e.html\">hyperlipoproteinemia type III\u003c/a> (HLP type 3). One reason this disease is rare is because being e2/e2 is rare. For example, only around 0.4% of people of European background have this genetic combination.\u003c/p>\n\u003cp>But HLP type 3 is obviously more common for me since I am in that 0.4% group already. Still, only 2% of e2/e2 people end up with HLP type 3 so it is a low risk for me. I decided to look into it anyway.\u003c/p>\n\u003cp>This disease has various symptoms but the most worrisome ones for me are increased risk of heart attack and abnormal glucose tolerance. My fasting glucose levels are stubbornly high whenever I take my yearly blood test. Which makes me wonder if this genetic difference is affecting my glucose tolerance and I am on my way to HLP type 3.\u003c/p>\n\u003cp>Of course, lots of genetic differences are involved in establishing someone’s glucose tolerance. And the environment plays a role too. So my glucose tolerance might have nothing to do with me starting to get HLP type 3.\u003c/p>\n\u003cp>Still, I am definitely going to ask my doctor about it at my next visit. It is rare but there are specific blood tests I can ask for that can tell me if I have this condition. Who’d have thought that a lowered risk of Alzheimer’s would only be a silver lining…\u003c/p>\n\u003cp>*\u003cem>Well, more of a measured giddiness. I know this is just one of the many genes involved in Alzheimer’s but still, it was good news\u003c/em>.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.3393857 -121.8949555\u003c/p>\n\n","blocks":[],"excerpt":"There are no free lunches in genetics. Having a certain version of a gene may protect you from one thing, but make you susceptible to another.","status":"publish","parent":0,"modified":1308587263,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":16,"wordCount":598},"headData":{"title":"The Cloud in the Silver Lining | KQED","description":"There are no free lunches in genetics. Having a certain version of a gene may protect you from one thing, but make you susceptible to another.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"19244 http://www.kqed.org/quest/blog/2011/06/20/the-cloud-in-the-silver-lining/","disqusUrl":"https://ww2.kqed.org/quest/2011/06/20/the-cloud-in-the-silver-lining/","disqusTitle":"The Cloud in the Silver Lining","path":"/quest/19244/the-cloud-in-the-silver-lining","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/06/SilverLining.jpg\" alt=\"\">\u003c/a>\u003cem>My lower risk for Alzheimer's may be the silver lining\u003cbr>to being e2/e2 at APOE.\u003cbr>Image courtesy of \u003ca href=\"http://commons.wikimedia.org/wiki/File:Silver_Lining.JPG\">ImUnicke\u003c/a>\u003c/em>\u003c/span>\u003c/p>\n\u003cp>When last I left you in my \u003ca href=\"http://ww2.kqed.org/quest/2011/05/23/uncovering-risk-one-gene-at-a-time/\">personal genomic journey\u003c/a>, I had just discovered that I was e2/e2 at the APOE gene. I was quietly giddy* about this as it meant I was at a lower risk for getting Alzheimer’s. And even more importantly, it meant I didn’t have e4 which would have significantly increased my chances of getting this form of dementia.\u003c/p>\n\u003cp>Digging a bit deeper I found some more good news. People with e2/e2 usually have lower levels of LDL, the bad cholesterol that increases the risk for a heart attack. This is consistent with my low levels of LDL. Two good effects from one allele!\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>But there are no free lunches in genetics. For example, having two copies of the delta32 version of the CCR5 gene makes you \u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/ask.php?id=336\">pretty resistant to HIV infection\u003c/a>. But it makes you more susceptible to the West Nile Virus. Having one copy of the sickle cell version of the hemoglobin gene makes you \u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/ask.php?id=271\">resistant to malaria\u003c/a>. But your kids might end up with full blown sickle cell anemia. And so on.\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 e2 version of the APOE gene is no different. It makes me less likely to get Alzheimer’s and, most of the time, to have a heart attack. But it means that I can end up with higher triglycerides from what I eat. This is consistent with what I have seen at the doctor’s. \u003c/p>\n\u003cp>Triglycerides are actually an independent predictor of heart attack risk. So even though my LDL is low, I need to watch my diet to keep the triglycerides down. If I am not careful, my increased triglycerides might cancel out my decreased LDL and so change my reduced heart attack risk to an increased one. \u003c/p>\n\u003cp>Being e2/e2 also puts me at risk for a relatively rare disease called \u003ca href=\"http://www.kimballgenetics.com/tests-apo_e.html\">hyperlipoproteinemia type III\u003c/a> (HLP type 3). One reason this disease is rare is because being e2/e2 is rare. For example, only around 0.4% of people of European background have this genetic combination.\u003c/p>\n\u003cp>But HLP type 3 is obviously more common for me since I am in that 0.4% group already. Still, only 2% of e2/e2 people end up with HLP type 3 so it is a low risk for me. I decided to look into it anyway.\u003c/p>\n\u003cp>This disease has various symptoms but the most worrisome ones for me are increased risk of heart attack and abnormal glucose tolerance. My fasting glucose levels are stubbornly high whenever I take my yearly blood test. Which makes me wonder if this genetic difference is affecting my glucose tolerance and I am on my way to HLP type 3.\u003c/p>\n\u003cp>Of course, lots of genetic differences are involved in establishing someone’s glucose tolerance. And the environment plays a role too. So my glucose tolerance might have nothing to do with me starting to get HLP type 3.\u003c/p>\n\u003cp>Still, I am definitely going to ask my doctor about it at my next visit. It is rare but there are specific blood tests I can ask for that can tell me if I have this condition. Who’d have thought that a lowered risk of Alzheimer’s would only be a silver lining…\u003c/p>\n\u003cp>*\u003cem>Well, more of a measured giddiness. I know this is just one of the many genes involved in Alzheimer’s but still, it was good news\u003c/em>.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.3393857 -121.8949555\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/19244/the-cloud-in-the-silver-lining","authors":["6177"],"categories":["quest_4"],"tags":["quest_134","quest_135","quest_3458","quest_3546","quest_3553","quest_3555","quest_1192","quest_1197","quest_1332","quest_3610","quest_2162","quest_3804"],"featImg":"quest_15236","label":"quest"},"quest_14601":{"type":"posts","id":"quest_14601","meta":{"index":"posts_1591205157","site":"quest","id":"14601","score":null,"sort":[1306166662000]},"guestAuthors":[],"slug":"uncovering-risk-one-gene-at-a-time","title":"Uncovering Risk One Gene at a Time","publishDate":1306166662,"format":"standard","headTitle":"QUEST | KQED Science","labelTerm":{"site":"quest"},"content":"\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/05/MathFormula2.jpg\" alt=\"\">\u003c/a>\u003cem>Many genetic tests just uncover one small bit of\u003cbr>your disease risk formula.\u003cbr>Image courtesy of \u003ca href=\"http://en.wikipedia.org/wiki/File:Math_lecture_at_TKK.JPG\">Tungsten\u003c/a>\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Since 23andMe is offering data on Alzheimer’s risk but only with an upgrade, I decided to get that upgrade. I got the new results last week and opened it right up. There was a new Alzheimer’s link with a little lock on it.\u003c/p>\n\u003cp>The lock is to keep me out until I feel ready to deal with the news. Well, I’m ready…\u003c/p>\n\u003cp>When I opened the lock, I was given information about one gene, APOE. This was pretty disappointing. In my case, I was able to guess my APOE status with the old information. \u003c/p>\n\u003cp>I understand that for people who couldn’t guess their APOE status before that these new results might be useful. But I expected more. Lots of genes all impact our risk of getting Alzheimer’s and scientists are making real progress figuring these out.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>What I was hoping to see was a compilation of all the information out there. See, my APOE data suggests that I am at a lower risk. But what if all my other genes are of the wrong type and put me at a higher risk? Then I might be at a higher risk than I think I am.\u003c/p>\n\u003cp>And my situation is better than people who have APOE gene versions that put them at a higher risk. What if all of their other genes put them at a lower risk? Now they are worried for no reason.\u003c/p>\n\u003cp>This points to one of the big issues with genetic tests and complex genetic diseases. Right now we know a bit about some of the genes involved but we don’t yet know the whole story. \u003c/p>\n\u003cp>It is kind of like having a whiteboard with a vast, awful, Jimmy Neutronesque formula scrawled across it. This is our genetic risk for getting something like Alzheimer’s. \u003c/p>\n\u003cp>Unfortunately, a blanket of ignorance hides most of the formula from us. We can only get a glimpse of one small part of it. What we then try to do is figure out our risk from that glimpse.\u003c/p>\n\u003cp>So let’s say we manage to uncover a bit of the blanket in the corner and we see a 0.5X. Does that mean that I am half as likely to get Alzheimer’s? Hardly. We have managed to see a piece of the whole formula but the rest remains hidden.\u003c/p>\n\u003cp>My APOE status is really just a bit of the formula for my Alzheimer’s risk peeking out from under the blanket. I don’t know the rest of the formula and so don’t know the rest of the risk.\u003c/p>\n\u003cp>APOE status is a well-studied risk that we know a lot about. We have completely uncovered it on our whiteboard. Some studies are staring to reveal other parts of the board but they aren’t completely clear yet. This is probably why 23andMe left them out.\u003c/p>\n\u003cp>I decided to look at the hazy parts of my equation using good old \u003ca href=\"http://www.snpedia.com/index.php/SNPedia\">SNPedia\u003c/a>. Remember, they have lots of information about DNA variants and disease that isn’t as filtered as is 23andMe’s. \u003c/p>\n\u003cp>Here is what I found when I put my data from 23andMe through SNPedia. I have listed the SNP, what I have at the SNP (the allele), and my risk for Alzheimer’s for those that give me a higher or lower chance for Alzheimer’s. I haven’t put in the ones that have normal risk.\u003c/p>\n\u003cp>\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/05/AlzTable2.jpg\">\u003c/p>\n\u003cp>I came out very well here. I am at a much lower risk for getting Alzheimer’s when I look at these SNPs. Yay! \u003c/p>\n\u003cp>But what if I just had s4934 data? I would come out thinking I was at a higher risk when I am actually at a lower one. Lots of needless worry over nothing…\u003c/p>\n\u003cp>Now I shouldn’t get complacent, this is still only a bit of my risk for Alzheimer’s. There may be some killer SNP lurking in my DNA, ready to spring Alzheimer’s on me. Or a long list of small, not-yet-discovered SNPs that will eat away at my supposed lower risk for Alzheimer’s. We just don’t know yet.\u003c/p>\n\u003cp>And I haven’t even begun to talk about environmental impacts. We know so little about that one with Alzheimer’s that we haven’t even found the whiteboard yet!\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n","blocks":[],"excerpt":"Genetic tests for complex diseases just tell you part of your genetic risk and nothing about your environmental risks.","status":"publish","parent":0,"modified":1306166662,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":24,"wordCount":774},"headData":{"title":"Uncovering Risk One Gene at a Time | KQED","description":"Genetic tests for complex diseases just tell you part of your genetic risk and nothing about your environmental risks.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"14601 http://www.kqed.org/quest/blog/2011/05/23/uncovering-risk-one-gene-at-a-time/","disqusUrl":"https://ww2.kqed.org/quest/2011/05/23/uncovering-risk-one-gene-at-a-time/","disqusTitle":"Uncovering Risk One Gene at a Time","path":"/quest/14601/uncovering-risk-one-gene-at-a-time","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/05/MathFormula2.jpg\" alt=\"\">\u003c/a>\u003cem>Many genetic tests just uncover one small bit of\u003cbr>your disease risk formula.\u003cbr>Image courtesy of \u003ca href=\"http://en.wikipedia.org/wiki/File:Math_lecture_at_TKK.JPG\">Tungsten\u003c/a>\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Since 23andMe is offering data on Alzheimer’s risk but only with an upgrade, I decided to get that upgrade. I got the new results last week and opened it right up. There was a new Alzheimer’s link with a little lock on it.\u003c/p>\n\u003cp>The lock is to keep me out until I feel ready to deal with the news. Well, I’m ready…\u003c/p>\n\u003cp>When I opened the lock, I was given information about one gene, APOE. This was pretty disappointing. In my case, I was able to guess my APOE status with the old information. \u003c/p>\n\u003cp>I understand that for people who couldn’t guess their APOE status before that these new results might be useful. But I expected more. Lots of genes all impact our risk of getting Alzheimer’s and scientists are making real progress figuring these out.\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>\u003c!--more-->\u003c/p>\n\u003cp>What I was hoping to see was a compilation of all the information out there. See, my APOE data suggests that I am at a lower risk. But what if all my other genes are of the wrong type and put me at a higher risk? Then I might be at a higher risk than I think I am.\u003c/p>\n\u003cp>And my situation is better than people who have APOE gene versions that put them at a higher risk. What if all of their other genes put them at a lower risk? Now they are worried for no reason.\u003c/p>\n\u003cp>This points to one of the big issues with genetic tests and complex genetic diseases. Right now we know a bit about some of the genes involved but we don’t yet know the whole story. \u003c/p>\n\u003cp>It is kind of like having a whiteboard with a vast, awful, Jimmy Neutronesque formula scrawled across it. This is our genetic risk for getting something like Alzheimer’s. \u003c/p>\n\u003cp>Unfortunately, a blanket of ignorance hides most of the formula from us. We can only get a glimpse of one small part of it. What we then try to do is figure out our risk from that glimpse.\u003c/p>\n\u003cp>So let’s say we manage to uncover a bit of the blanket in the corner and we see a 0.5X. Does that mean that I am half as likely to get Alzheimer’s? Hardly. We have managed to see a piece of the whole formula but the rest remains hidden.\u003c/p>\n\u003cp>My APOE status is really just a bit of the formula for my Alzheimer’s risk peeking out from under the blanket. I don’t know the rest of the formula and so don’t know the rest of the risk.\u003c/p>\n\u003cp>APOE status is a well-studied risk that we know a lot about. We have completely uncovered it on our whiteboard. Some studies are staring to reveal other parts of the board but they aren’t completely clear yet. This is probably why 23andMe left them out.\u003c/p>\n\u003cp>I decided to look at the hazy parts of my equation using good old \u003ca href=\"http://www.snpedia.com/index.php/SNPedia\">SNPedia\u003c/a>. Remember, they have lots of information about DNA variants and disease that isn’t as filtered as is 23andMe’s. \u003c/p>\n\u003cp>Here is what I found when I put my data from 23andMe through SNPedia. I have listed the SNP, what I have at the SNP (the allele), and my risk for Alzheimer’s for those that give me a higher or lower chance for Alzheimer’s. I haven’t put in the ones that have normal risk.\u003c/p>\n\u003cp>\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/05/AlzTable2.jpg\">\u003c/p>\n\u003cp>I came out very well here. I am at a much lower risk for getting Alzheimer’s when I look at these SNPs. Yay! \u003c/p>\n\u003cp>But what if I just had s4934 data? I would come out thinking I was at a higher risk when I am actually at a lower one. Lots of needless worry over nothing…\u003c/p>\n\u003cp>Now I shouldn’t get complacent, this is still only a bit of my risk for Alzheimer’s. There may be some killer SNP lurking in my DNA, ready to spring Alzheimer’s on me. Or a long list of small, not-yet-discovered SNPs that will eat away at my supposed lower risk for Alzheimer’s. We just don’t know yet.\u003c/p>\n\u003cp>And I haven’t even begun to talk about environmental impacts. We know so little about that one with Alzheimer’s that we haven’t even found the whiteboard yet!\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/14601/uncovering-risk-one-gene-at-a-time","authors":["6177"],"categories":["quest_4"],"tags":["quest_43","quest_134","quest_135","quest_3458","quest_3530","quest_3545","quest_3546","quest_3552","quest_1195","quest_2436","quest_3768"],"label":"quest"},"quest_14037":{"type":"posts","id":"quest_14037","meta":{"index":"posts_1591205157","site":"quest","id":"14037","score":null,"sort":[1303749791000]},"guestAuthors":[],"slug":"better-left-unknown","title":"Better Left Unknown?","publishDate":1303749791,"format":"standard","headTitle":"QUEST | KQED Science","labelTerm":{"site":"quest"},"content":"\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/Redact2.jpg\" alt=\"\">\u003c/a>\u003cem>I might be better off NOT knowing some things about my genes.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Last \u003ca href=\"http://ww2.kqed.org/quest/2011/04/11/dna-diving-for-alzheimer%E2%80%99s/\">blog \u003c/a>I talked about how I was able to wrest information about my APOE gene from my 23andMe data. I wanted to know because of this gene’s link to late onset Alzheimer’s disease.\u003c/p>\n\u003cp>APOE comes in three versions: e2, e3, and e4. People with two e4 versions are around 15 times more likely to end up with Alzheimer’s than are people with two e3 versions. And if these e4 folks do get the disease, it tends to come at an earlier age. \u003c/p>\n\u003cp>I found out that I actually have two e2 versions which protects me somewhat from getting late onset Alzheimer’s. Good news? I guess…\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>In all of this, I didn’t ask whether this information is worth knowing. Being e2/e2 doesn’t mean I won’t get Alzheimer’s…it just means I am at a lower risk. But at least I didn’t find out I was e4/e4. Then I’d know I was more likely to get Alzheimer’s but not be able to do anything medically useful with that information. \u003c/p>\n\u003cp>Being e4/e4 would not have meant that I would for sure end up with Alzheimer’s. So it wouldn’t be like having two copies of the \u003ca href=\"http://www.ornl.gov/sci/techresources/Human_Genome/posters/chromosome/cftr.shtml\">delta-508\u003c/a> marker of the CFTR gene. In that case, I would almost certainly have developed cystic fibrosis. No, two copies of e4 would just mean that I was at a higher risk.\u003c/p>\n\u003cp>And knowing this wouldn’t be able to help me medically at all. There aren’t any good preventative measures I could take to stave off Alzheimer’s. \u003c/p>\n\u003cp>Now this isn’t always true with these kinds of increased risk genetic markers—some are definitely worth knowing. Women who have certain \u003ca href=\"http://www.cancer.gov/cancertopics/factsheet/Risk/BRCA\">BRCA1/BRCA2\u003c/a> markers are at an increased risk for getting breast or ovarian cancer. They can choose to screen early (and often) in the hope of catching the cancer early when it is more treatable. Or, more drastically, they can choose to have their breasts and/or ovaries removed. Neither is really an option for Alzheimer’s.\u003c/p>\n\u003cp>So knowing my APOE status isn’t really that useful medically (at least not yet). I can’t do anything useful with the information other than wait and see if I end up with Alzheimer’s. Which is pretty much what I would have done without the test.\u003c/p>\n\u003cp>I’m bringing all of this up because 23andMe is now offering people their APOE information (with an upgrade to their new chip, of course). People can now find out their particular combination of e2, e3, and e4 markers*. \u003c/p>\n\u003cp>In the past, the question was whether or not direct to consumer (DTC) genetic testing companies should offer such a test. That ship has either sailed or is getting ready to leave the harbor. The test will be made available to people who really want the information.\u003c/p>\n\u003cp>So now the key question is whether knowing your APOE status is worth it. The answer to this question will be different for different people. Given this, the most important thing is for people to have the information they need to make the right choice about whether they want to know their APOE status or not.\u003c/p>\n\u003cp>One way to figure this out is with a genetic counselor but most DTC tests don’t mandate that you need to talk to one before you are tested. This means it is absolutely critical that the online information provided by DTC companies are presented in an easy to understand way that does not oversell the genetic test. The DTC companies need to be upfront in the fact that this test is not predictive and that there are no proven preventative measures that can keep Alzheimer’s at bay.\u003c/p>\n\u003cp>I’ll let you all judge how well 23andMe has done at letting people know about what you can learn from the APOE test and what you can do with that knowledge. Click \u003ca href=\"https://www.23andme.com/health/alzheimers/\">here \u003c/a>to read what they have to say.\u003c/p>\n\u003cp>* \u003cem>You have always been able to get your APOE status with a more expensive genetic test from \u003ca href=\"http://www.decodeme.com/\">deCODEme\u003c/a>.\u003c/em>\u003c/p>\n\u003cp>\u003ca href=\"http://www.thetech.org/genetics/ask.php?id=405\">Learn more about how genes and the environment work together to cause Alzheimer's.\u003c/a> \u003c/p>\n\u003cp>\u003cem>I put this video in the last blog but it probably should have gone in this one. It shows the unintended consequences of finding out you are e4/e4.\u003c/em>\u003c/p>\n\u003cp style=\"text-align: center\">\n\u003ciframe width=\"425\" height=\"349\" src=\"http://www.youtube.com/embed/oGuvzlD7Yx8\" frameborder=\"0\">\u003c/iframe>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n","blocks":[],"excerpt":"Just because we can find out about some of our genetic information, should we? Even though the results are often not very useful or even very informative, they can sometimes be a real burden.","status":"publish","parent":0,"modified":1303749791,"stats":{"hasAudio":false,"hasVideo":true,"hasChartOrMap":true,"iframeSrcs":["http://www.youtube.com/embed/oGuvzlD7Yx8"],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":21,"wordCount":777},"headData":{"title":"Better Left Unknown? | KQED","description":"Just because we can find out about some of our genetic information, should we? Even though the results are often not very useful or even very informative, they can sometimes be a real burden.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"14037 http://www.kqed.org/quest/blog/2011/04/25/better-left-unknown/","disqusUrl":"https://ww2.kqed.org/quest/2011/04/25/better-left-unknown/","disqusTitle":"Better Left Unknown?","path":"/quest/14037/better-left-unknown","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/Redact2.jpg\" alt=\"\">\u003c/a>\u003cem>I might be better off NOT knowing some things about my genes.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Last \u003ca href=\"http://ww2.kqed.org/quest/2011/04/11/dna-diving-for-alzheimer%E2%80%99s/\">blog \u003c/a>I talked about how I was able to wrest information about my APOE gene from my 23andMe data. I wanted to know because of this gene’s link to late onset Alzheimer’s disease.\u003c/p>\n\u003cp>APOE comes in three versions: e2, e3, and e4. People with two e4 versions are around 15 times more likely to end up with Alzheimer’s than are people with two e3 versions. And if these e4 folks do get the disease, it tends to come at an earlier age. \u003c/p>\n\u003cp>I found out that I actually have two e2 versions which protects me somewhat from getting late onset Alzheimer’s. Good news? I guess…\u003c/p>\n\u003cp>\u003c!--more-->\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 all of this, I didn’t ask whether this information is worth knowing. Being e2/e2 doesn’t mean I won’t get Alzheimer’s…it just means I am at a lower risk. But at least I didn’t find out I was e4/e4. Then I’d know I was more likely to get Alzheimer’s but not be able to do anything medically useful with that information. \u003c/p>\n\u003cp>Being e4/e4 would not have meant that I would for sure end up with Alzheimer’s. So it wouldn’t be like having two copies of the \u003ca href=\"http://www.ornl.gov/sci/techresources/Human_Genome/posters/chromosome/cftr.shtml\">delta-508\u003c/a> marker of the CFTR gene. In that case, I would almost certainly have developed cystic fibrosis. No, two copies of e4 would just mean that I was at a higher risk.\u003c/p>\n\u003cp>And knowing this wouldn’t be able to help me medically at all. There aren’t any good preventative measures I could take to stave off Alzheimer’s. \u003c/p>\n\u003cp>Now this isn’t always true with these kinds of increased risk genetic markers—some are definitely worth knowing. Women who have certain \u003ca href=\"http://www.cancer.gov/cancertopics/factsheet/Risk/BRCA\">BRCA1/BRCA2\u003c/a> markers are at an increased risk for getting breast or ovarian cancer. They can choose to screen early (and often) in the hope of catching the cancer early when it is more treatable. Or, more drastically, they can choose to have their breasts and/or ovaries removed. Neither is really an option for Alzheimer’s.\u003c/p>\n\u003cp>So knowing my APOE status isn’t really that useful medically (at least not yet). I can’t do anything useful with the information other than wait and see if I end up with Alzheimer’s. Which is pretty much what I would have done without the test.\u003c/p>\n\u003cp>I’m bringing all of this up because 23andMe is now offering people their APOE information (with an upgrade to their new chip, of course). People can now find out their particular combination of e2, e3, and e4 markers*. \u003c/p>\n\u003cp>In the past, the question was whether or not direct to consumer (DTC) genetic testing companies should offer such a test. That ship has either sailed or is getting ready to leave the harbor. The test will be made available to people who really want the information.\u003c/p>\n\u003cp>So now the key question is whether knowing your APOE status is worth it. The answer to this question will be different for different people. Given this, the most important thing is for people to have the information they need to make the right choice about whether they want to know their APOE status or not.\u003c/p>\n\u003cp>One way to figure this out is with a genetic counselor but most DTC tests don’t mandate that you need to talk to one before you are tested. This means it is absolutely critical that the online information provided by DTC companies are presented in an easy to understand way that does not oversell the genetic test. The DTC companies need to be upfront in the fact that this test is not predictive and that there are no proven preventative measures that can keep Alzheimer’s at bay.\u003c/p>\n\u003cp>I’ll let you all judge how well 23andMe has done at letting people know about what you can learn from the APOE test and what you can do with that knowledge. Click \u003ca href=\"https://www.23andme.com/health/alzheimers/\">here \u003c/a>to read what they have to say.\u003c/p>\n\u003cp>* \u003cem>You have always been able to get your APOE status with a more expensive genetic test from \u003ca href=\"http://www.decodeme.com/\">deCODEme\u003c/a>.\u003c/em>\u003c/p>\n\u003cp>\u003ca href=\"http://www.thetech.org/genetics/ask.php?id=405\">Learn more about how genes and the environment work together to cause Alzheimer's.\u003c/a> \u003c/p>\n\u003cp>\u003cem>I put this video in the last blog but it probably should have gone in this one. It shows the unintended consequences of finding out you are e4/e4.\u003c/em>\u003c/p>\n\u003cp style=\"text-align: center\">\n\u003ciframe width=\"425\" height=\"349\" src=\"http://www.youtube.com/embed/oGuvzlD7Yx8\" frameborder=\"0\">\u003c/iframe>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/14037/better-left-unknown","authors":["6177"],"categories":["quest_4"],"tags":["quest_43","quest_134","quest_135","quest_3458","quest_377","quest_3530","quest_3553","quest_3554","quest_3555","quest_3587","quest_1195","quest_1197","quest_3652","quest_2161"],"featImg":"quest_13535","label":"quest"},"quest_13504":{"type":"posts","id":"quest_13504","meta":{"index":"posts_1591205157","site":"quest","id":"13504","score":null,"sort":[1302537708000]},"guestAuthors":[],"slug":"dna-diving-for-alzheimer%e2%80%99s","title":"DNA Diving for Alzheimer’s","publishDate":1302537708,"format":"standard","headTitle":"DNA Diving for Alzheimer’s | KQED","labelTerm":{"site":"quest"},"content":"\u003ctable align=\"left\">\n\u003ctbody>\n\u003ctr>\n\u003ctd>\u003cimg decoding=\"async\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/AlzPetScan22.gif\" alt=\"\">\u003cbr>\n\u003cspan style=\"color: #999999\">My 23andMe test tells me I am less likely to end up\u003cbr>\nwith the brain on the left.\u003cbr>\nImage courtesy of \u003ca href=\"http://commons.wikimedia.org/wiki/File:PiB_PET_Images_AD.jpg\">Klunkwe\u003c/a>.\u003c/span>\u003c/td>\n\u003c/tr>\n\u003c/tbody>\n\u003c/table>\n\u003cp>I was having lunch with a colleague the other day and we got to talking about genetic testing (yes, we are that geeky). I told him about how my 23andMe test had missed my being prediabetic. This says a lot about what 23andMe’s test can tell me about my risk for diabetes. Not much.\u003c/p>\n\u003cp>Now as I have \u003ca href=\"http://ww2.kqed.org/quest/2009/10/12/do-these-genes-make-me-look-diabetic/\">said before\u003c/a>, the fact that 23andMe can’t tell me that I’m likely to become diabetic from their DNA test isn’t their fault (other than, perhaps, some overselling on their part). Diabetes research just isn’t far enough along to be able to accurately predict whether someone will get diabetes or not. Or to make any really meaningful prediction about diabetes at all.\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>We then got to talking about Alzheimer’s. Turns out his family tree is littered with Alzheimer’s on both his mother’s and father’s side. He ran into a similar problem–23andMe doesn’t report anything for Alzheimer’s.\u003c/p>\n\u003cp>But here the situation is a bit different than for diabetes. There are a couple of DNA markers that can tell us a lot about our future risk for late onset Alzheimer’s. It just so happens that 23andMe doesn’t report on them.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>These markers deal with the APOE gene. This gene comes in three common versions: e2, e3, and e4. People with two copies of the e4 version are 15 times more likely to develop Alzheimer’s and if they do end up with the disease, it tends to come earlier. (One copy of e4 increases your risk about 3 times.)\u003c/p>\n\u003cp>With a little help from my colleague, I decided to dig a bit deeper into Alzheimer’s and see what I could figure out from what 23andMe did provide. Turns out I can figure out a whole lot about my APOE status. And that I can help other people figure out more from their results too.\u003c/p>\n\u003cp>The two markers (also called \u003ca href=\"http://www.ncbi.nlm.nih.gov/About/primer/snps.html\">SNP\u003c/a>s) that deal with APOE and Alzheimer’s are rs429358 and rs7412. Here, according to \u003ca href=\"http://www.snpedia.com/index.php/ApoE\">SNPedia\u003c/a>, are the combinations of these markers that tell you your APOE status:\u003c/p>\n\u003cp style=\"text-align: center\">\u003cimg decoding=\"async\" class=\"alignnone\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/APOEtable2.jpg\" alt=\"\">\u003c/p>\n\u003cp>To my surprise, 23andMe gives information on one of them, rs7412. Even though this isn’t usually enough to tell whether you have the dreaded e4 version or not, in my case it was. I almost certainly do not have any versions of e4 (yay!).\u003c/p>\n\u003cp>See, my results at rs7412 are TT*. If I am interpreting these results correctly, this means I almost certainly have two copies of the e2 version of the APOE gene. In terms of my Alzheimer’s risk this is great news as being e2/e2 actually lowers your risk for getting the disease. (There is a chance I could be e1 but this doesn’t seem to be a very common version at all.)\u003c/p>\n\u003cp>Of course this doesn’t mean I won’t get Alzheimer’s…I still might. After all, the \u003ca href=\"http://www.alz.org/alzheimers_disease_causes_risk_factors.asp#familyhistory\">risk \u003c/a>for someone over 85 getting Alzheimer’s is almost 50%. Even though this number lumps e4 and e2 folks together, e2 people do not have a 0% risk for Alzheimer’s nor do e4 people have a 100% chance. People with e4 are just more likely to have Alzheimer’s than e2 people.\u003c/p>\n\u003cp>It might help to think about getting Alzheimer’s like drawing an inside straight in poker. Everyone might do it but people who are playing with wildcards are more likely to get it. These are the e4 folks. But it isn’t a for sure thing…you still may not draw the straight even with deuces wild.\u003c/p>\n\u003cp>Same thing with not having e4. Now I am less likely to draw that inside straight because there are no wild cards but it can still happen.\u003c/p>\n\u003cp>Because I was TT at rs7412, my case was pretty easy to figure out. Next blog I’ll try to help people out who are TC or CC at rs7412.\u003c/p>\n\u003cp>*\u003cem>Remember, we have two copies of each of our genes. So I have a T at rs7412 in one copy and a T at rs7412 in my other copy.\u003c/em>\u003c/p>\n\u003cp>\u003cem>A video showing why knowing your APOE status isn’t necessarily a good thing.\u003c/em>\u003c/p>\n\u003cp style=\"text-align: center\">\n\u003ciframe loading=\"lazy\" width=\"425\" height=\"349\" src=\"http://www.youtube.com/embed/oGuvzlD7Yx8\" frameborder=\"0\">\u003c/iframe>\u003c/p>\n\u003cp>Learn more about current Bay Area genetic research from \u003ca href=\"http://www.kqed.org/a/forum/R201104050900\">KQED’s Forum. \u003c/a>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n","blocks":[],"excerpt":"I was able to figure out my APOE status and so one of my key risk factors for developing late onset Alzheimer's from my 23andMe test even though 23andMe doesn't officially report any results for Alzheimer's.","status":"publish","parent":0,"modified":1684974330,"stats":{"hasAudio":false,"hasVideo":true,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":20,"wordCount":777},"headData":{"title":"DNA Diving for Alzheimer’s | KQED","description":"I was able to figure out my APOE status and so one of my key risk factors for developing late onset Alzheimer's from my 23andMe test even though 23andMe doesn't officially report any results for Alzheimer's.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"templateType":"standard","featuredImageType":"standard","excludeFromSiteSearch":"Include","articleAge":"0","path":"/quest/13504/dna-diving-for-alzheimer%e2%80%99s","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003ctable align=\"left\">\n\u003ctbody>\n\u003ctr>\n\u003ctd>\u003cimg decoding=\"async\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/AlzPetScan22.gif\" alt=\"\">\u003cbr>\n\u003cspan style=\"color: #999999\">My 23andMe test tells me I am less likely to end up\u003cbr>\nwith the brain on the left.\u003cbr>\nImage courtesy of \u003ca href=\"http://commons.wikimedia.org/wiki/File:PiB_PET_Images_AD.jpg\">Klunkwe\u003c/a>.\u003c/span>\u003c/td>\n\u003c/tr>\n\u003c/tbody>\n\u003c/table>\n\u003cp>I was having lunch with a colleague the other day and we got to talking about genetic testing (yes, we are that geeky). I told him about how my 23andMe test had missed my being prediabetic. This says a lot about what 23andMe’s test can tell me about my risk for diabetes. Not much.\u003c/p>\n\u003cp>Now as I have \u003ca href=\"http://ww2.kqed.org/quest/2009/10/12/do-these-genes-make-me-look-diabetic/\">said before\u003c/a>, the fact that 23andMe can’t tell me that I’m likely to become diabetic from their DNA test isn’t their fault (other than, perhaps, some overselling on their part). Diabetes research just isn’t far enough along to be able to accurately predict whether someone will get diabetes or not. Or to make any really meaningful prediction about diabetes at all.\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>We then got to talking about Alzheimer’s. Turns out his family tree is littered with Alzheimer’s on both his mother’s and father’s side. He ran into a similar problem–23andMe doesn’t report anything for Alzheimer’s.\u003c/p>\n\u003cp>But here the situation is a bit different than for diabetes. There are a couple of DNA markers that can tell us a lot about our future risk for late onset Alzheimer’s. It just so happens that 23andMe doesn’t report on them.\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>These markers deal with the APOE gene. This gene comes in three common versions: e2, e3, and e4. People with two copies of the e4 version are 15 times more likely to develop Alzheimer’s and if they do end up with the disease, it tends to come earlier. (One copy of e4 increases your risk about 3 times.)\u003c/p>\n\u003cp>With a little help from my colleague, I decided to dig a bit deeper into Alzheimer’s and see what I could figure out from what 23andMe did provide. Turns out I can figure out a whole lot about my APOE status. And that I can help other people figure out more from their results too.\u003c/p>\n\u003cp>The two markers (also called \u003ca href=\"http://www.ncbi.nlm.nih.gov/About/primer/snps.html\">SNP\u003c/a>s) that deal with APOE and Alzheimer’s are rs429358 and rs7412. Here, according to \u003ca href=\"http://www.snpedia.com/index.php/ApoE\">SNPedia\u003c/a>, are the combinations of these markers that tell you your APOE status:\u003c/p>\n\u003cp style=\"text-align: center\">\u003cimg decoding=\"async\" class=\"alignnone\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/APOEtable2.jpg\" alt=\"\">\u003c/p>\n\u003cp>To my surprise, 23andMe gives information on one of them, rs7412. Even though this isn’t usually enough to tell whether you have the dreaded e4 version or not, in my case it was. I almost certainly do not have any versions of e4 (yay!).\u003c/p>\n\u003cp>See, my results at rs7412 are TT*. If I am interpreting these results correctly, this means I almost certainly have two copies of the e2 version of the APOE gene. In terms of my Alzheimer’s risk this is great news as being e2/e2 actually lowers your risk for getting the disease. (There is a chance I could be e1 but this doesn’t seem to be a very common version at all.)\u003c/p>\n\u003cp>Of course this doesn’t mean I won’t get Alzheimer’s…I still might. After all, the \u003ca href=\"http://www.alz.org/alzheimers_disease_causes_risk_factors.asp#familyhistory\">risk \u003c/a>for someone over 85 getting Alzheimer’s is almost 50%. Even though this number lumps e4 and e2 folks together, e2 people do not have a 0% risk for Alzheimer’s nor do e4 people have a 100% chance. People with e4 are just more likely to have Alzheimer’s than e2 people.\u003c/p>\n\u003cp>It might help to think about getting Alzheimer’s like drawing an inside straight in poker. Everyone might do it but people who are playing with wildcards are more likely to get it. These are the e4 folks. But it isn’t a for sure thing…you still may not draw the straight even with deuces wild.\u003c/p>\n\u003cp>Same thing with not having e4. Now I am less likely to draw that inside straight because there are no wild cards but it can still happen.\u003c/p>\n\u003cp>Because I was TT at rs7412, my case was pretty easy to figure out. Next blog I’ll try to help people out who are TC or CC at rs7412.\u003c/p>\n\u003cp>*\u003cem>Remember, we have two copies of each of our genes. So I have a T at rs7412 in one copy and a T at rs7412 in my other copy.\u003c/em>\u003c/p>\n\u003cp>\u003cem>A video showing why knowing your APOE status isn’t necessarily a good thing.\u003c/em>\u003c/p>\n\u003cp style=\"text-align: center\">\n\u003ciframe loading=\"lazy\" width=\"425\" height=\"349\" src=\"http://www.youtube.com/embed/oGuvzlD7Yx8\" frameborder=\"0\">\u003c/iframe>\u003c/p>\n\u003cp>Learn more about current Bay Area genetic research from \u003ca href=\"http://www.kqed.org/a/forum/R201104050900\">KQED’s Forum. \u003c/a>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/13504/dna-diving-for-alzheimer%e2%80%99s","authors":["6177"],"categories":["quest_4"],"tags":["quest_43","quest_134","quest_135","quest_3457","quest_3458","quest_377","quest_3530","quest_3553","quest_3554","quest_3555","quest_1195","quest_1197","quest_3652","quest_2161"],"featImg":"quest_13535","label":"quest"},"quest_11083":{"type":"posts","id":"quest_11083","meta":{"index":"posts_1591205157","site":"quest","id":"11083","score":null,"sort":[1292007667000]},"guestAuthors":[],"slug":"doh-dha-supplements-dont-reduce-alzheimers-risks","title":"D'OH! DHA Supplements Don't Reduce Alzheimer's Risks","publishDate":1292007667,"format":"standard","headTitle":"QUEST | KQED Science","labelTerm":{"site":"quest"},"content":"\u003cp>\u003cspan class=\"left\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/old-woman1.jpg\" alt=\"\">\u003cem>Another promising dietary supplement fails to deliver protection against a target disease, this time Alzheimer's. Image courtesy of \u003ca href=\"http://www.flickr.com/photos/outcast104/1428795376/\">outcast104\u003c/a>.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Another promising dietary supplement fails to deliver protection against a target disease, this time Alzheimer's.\u003c/p>\n\u003cp>\u003ca href=\"http://en.wikipedia.org/wiki/Docosahexaenoic_acid\">DHA\u003c/a> (or docosahexaenoic acid for the geekier among you) is an omega-3 fatty acid that is abundant in the brain. Epidemiological studies have suggested that people who consume more DHA from fish have a lower incidence of Alzheimer's disease. Further, DHA supplementation has improved markers of cognitive impairment in mouse models of Alzheimer's disease.\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>Scientists speculated that DHA supplementation may be beneficial in treating cognitive decline because previous research has suggested that among all omega-3 fatty acids, DHA was the only one associated with a reduced incidence of impairment. Also, the other major omega-3 fatty acid found in fish, eicosapentaenoic acid (EPA), is not present in the human brain, whereas DHA is abundant.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The study, published in \u003cem>\u003ca href=\"http://jama.ama-assn.org/content/304/17/1903.short?rss=1&;ssource=mfc\">JAMA\u003c/a>\u003c/em>, was a collaborative effort by scientists from the Oregon Health and Science University, UC San Diego, Yale, UC San Francisco, NYU and others. It was a randomized, double-blind, placebo-controlled trial of DHA supplementation in patients with mild to moderate Alzheimer's disease.\u003c/p>\n\u003cp>The researchers found no benefit of 2 g/day DHA supplementation on cognitive performance on the Alzheimer's Disease Assessment Scale (ADAS) or Clinical Dementia Rating (CDR) compared to placebo. There was also no measurable benefit of DHA on brain volume, which typically declines with Alzheimer's progression.\u003c/p>\n\u003cp>Though this research does not rule out a benefit of DHA on cognitive health, it does not bode well for regular supplementation. The treatment lasted for 18 months and cognitive changes were detected in both groups. So if DHA had any effect on the rate of cognitive decline it should have been apparent.\u003c/p>\n\u003cp>It is possible that beginning DHA treatment after early signs of Alzheimer's have already been detected is too late for any meaningful protection offered by DHA. Maybe some benefit would have been found if the treatment began in healthy adults before symptoms of cognitive decline developed.\u003c/p>\n\u003cp>It may also be that DHA is beneficial, but is not effective in supplement form. DHA is very vulnerable to oxidative damage, and some research has shown that it provides more cognitive benefit when co-administered with an antioxidant (lutein) to protect it. DHA ingested in the form of food (fish) would not be subject to the same level of oxidative degradation, which may explain the results seen in epidemiological data.\u003c/p>\n\u003cp>It is not uncommon for supplements to fail to replicate epidemiological benefits seem from foods, and more careful studies are needed to determine the nutritional benefit, if any, of DHA on cognitive aging.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.76355 -122.458\u003c/p>\n\n","blocks":[],"excerpt":"Another promising dietary supplement fails to deliver protection against a target disease, this time Alzheimer's.","status":"publish","parent":0,"modified":1292007667,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":14,"wordCount":461},"headData":{"title":"D'OH! DHA Supplements Don't Reduce Alzheimer's Risks | KQED","description":"Another promising dietary supplement fails to deliver protection against a target disease, this time Alzheimer's.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"11083 http://www.kqed.org/quest/blog/?p=11083","disqusUrl":"https://ww2.kqed.org/quest/2010/12/10/doh-dha-supplements-dont-reduce-alzheimers-risks/","disqusTitle":"D'OH! DHA Supplements Don't Reduce Alzheimer's Risks","path":"/quest/11083/doh-dha-supplements-dont-reduce-alzheimers-risks","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"left\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2010/12/old-woman1.jpg\" alt=\"\">\u003cem>Another promising dietary supplement fails to deliver protection against a target disease, this time Alzheimer's. Image courtesy of \u003ca href=\"http://www.flickr.com/photos/outcast104/1428795376/\">outcast104\u003c/a>.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Another promising dietary supplement fails to deliver protection against a target disease, this time Alzheimer's.\u003c/p>\n\u003cp>\u003ca href=\"http://en.wikipedia.org/wiki/Docosahexaenoic_acid\">DHA\u003c/a> (or docosahexaenoic acid for the geekier among you) is an omega-3 fatty acid that is abundant in the brain. Epidemiological studies have suggested that people who consume more DHA from fish have a lower incidence of Alzheimer's disease. Further, DHA supplementation has improved markers of cognitive impairment in mouse models of Alzheimer's disease.\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>Scientists speculated that DHA supplementation may be beneficial in treating cognitive decline because previous research has suggested that among all omega-3 fatty acids, DHA was the only one associated with a reduced incidence of impairment. Also, the other major omega-3 fatty acid found in fish, eicosapentaenoic acid (EPA), is not present in the human brain, whereas DHA is abundant.\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 study, published in \u003cem>\u003ca href=\"http://jama.ama-assn.org/content/304/17/1903.short?rss=1&;ssource=mfc\">JAMA\u003c/a>\u003c/em>, was a collaborative effort by scientists from the Oregon Health and Science University, UC San Diego, Yale, UC San Francisco, NYU and others. It was a randomized, double-blind, placebo-controlled trial of DHA supplementation in patients with mild to moderate Alzheimer's disease.\u003c/p>\n\u003cp>The researchers found no benefit of 2 g/day DHA supplementation on cognitive performance on the Alzheimer's Disease Assessment Scale (ADAS) or Clinical Dementia Rating (CDR) compared to placebo. There was also no measurable benefit of DHA on brain volume, which typically declines with Alzheimer's progression.\u003c/p>\n\u003cp>Though this research does not rule out a benefit of DHA on cognitive health, it does not bode well for regular supplementation. The treatment lasted for 18 months and cognitive changes were detected in both groups. So if DHA had any effect on the rate of cognitive decline it should have been apparent.\u003c/p>\n\u003cp>It is possible that beginning DHA treatment after early signs of Alzheimer's have already been detected is too late for any meaningful protection offered by DHA. Maybe some benefit would have been found if the treatment began in healthy adults before symptoms of cognitive decline developed.\u003c/p>\n\u003cp>It may also be that DHA is beneficial, but is not effective in supplement form. DHA is very vulnerable to oxidative damage, and some research has shown that it provides more cognitive benefit when co-administered with an antioxidant (lutein) to protect it. DHA ingested in the form of food (fish) would not be subject to the same level of oxidative degradation, which may explain the results seen in epidemiological data.\u003c/p>\n\u003cp>It is not uncommon for supplements to fail to replicate epidemiological benefits seem from foods, and more careful studies are needed to determine the nutritional benefit, if any, of DHA on cognitive aging.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.76355 -122.458\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/11083/doh-dha-supplements-dont-reduce-alzheimers-risks","authors":["10218"],"categories":["quest_12"],"tags":["quest_83","quest_135","quest_645","quest_820","quest_1009","quest_1079","quest_2022","quest_2065","quest_2839"],"featImg":"quest_11174","label":"quest"}},"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/2023/08/possible-5gxfizEbKOJ-pbF5ASgxrs_.1400x1400.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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We cover topics like how fed-up administrators are developing surprising tactics to deal with classroom disruptions; how listening to podcasts are helping kids develop reading skills; the consequences of overparenting; and why interdisciplinary learning can engage students on all ends of the traditional achievement spectrum. This podcast is part of the MindShift education site, a division of KQED News. KQED is an NPR/PBS member station based in San Francisco. You can also visit the MindShift website for episodes and supplemental blog posts or tweet us \u003ca href=\"https://twitter.com/MindShiftKQED\">@MindShiftKQED\u003c/a> or visit us at \u003ca href=\"/mindshift\">MindShift.KQED.org\u003c/a>","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2022/02/mindshift2021-tile-3000x3000-1-scaled-1.jpg","imageAlt":"KQED MindShift: How We Will Learn","officialWebsiteLink":"/mindshift/","meta":{"site":"news","source":"kqed","order":"2"},"link":"/podcasts/mindshift","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/mindshift-podcast/id1078765985","google":"https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM1NzY0NjAwNDI5","npr":"https://www.npr.org/podcasts/464615685/mind-shift-podcast","stitcher":"https://www.stitcher.com/podcast/kqed/stories-teachers-share","spotify":"https://open.spotify.com/show/0MxSpNYZKNprFLCl7eEtyx"}},"morning-edition":{"id":"morning-edition","title":"Morning Edition","info":"\u003cem>Morning Edition\u003c/em> takes listeners around the country and the world with multi-faceted stories and commentaries every weekday. Hosts Steve Inskeep, David Greene and Rachel Martin bring you the latest breaking news and features to prepare you for the day.","airtime":"MON-FRI 3am-9am","imageSrc":"https://ww2.kqed.org/app/uploads/2021/10/ME_1400.jpg","officialWebsiteLink":"https://www.npr.org/programs/morning-edition/","meta":{"site":"news","source":"npr"},"link":"/radio/program/morning-edition"},"onourwatch":{"id":"onourwatch","title":"On Our Watch","tagline":"Police secrets, unsealed","info":"For decades, the process for how police police themselves has been inconsistent – if not opaque. In some states, like California, these proceedings were completely hidden. After a new police transparency law unsealed scores of internal affairs files, our reporters set out to examine these cases and the shadow world of police discipline. 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. Is it the officers, or the public they've sworn to serve?","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/01/OOW_Tile_Final.png","imageAlt":"On Our Watch from NPR and KQED","officialWebsiteLink":"/podcasts/onourwatch","meta":{"site":"news","source":"kqed","order":"1"},"link":"/podcasts/onourwatch","subscribe":{"apple":"https://podcasts.apple.com/podcast/id1567098962","google":"https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5ucHIub3JnLzUxMDM2MC9wb2RjYXN0LnhtbD9zYz1nb29nbGVwb2RjYXN0cw","npr":"https://rpb3r.app.goo.gl/onourwatch","spotify":"https://open.spotify.com/show/0OLWoyizopu6tY1XiuX70x","tuneIn":"https://tunein.com/radio/On-Our-Watch-p1436229/","stitcher":"https://www.stitcher.com/show/on-our-watch","rss":"https://feeds.npr.org/510360/podcast.xml"}},"on-the-media":{"id":"on-the-media","title":"On The Media","info":"Our weekly podcast explores how the media 'sausage' is made, casts an incisive eye on fluctuations in the marketplace of ideas, and examines threats to the freedom of information and expression in America and abroad. 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