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Prior to KQED, she was an editor with \u003cem>Crosscurrents\u003c/em> at KALW Radio in San Francisco. As a freelance reporter, she has filed stories for \u003cem>The California Report, Marketplace, Nautilus\u003c/em> and \u003cem>The New York Times Magazine.\u003c/em>\r\n\r\nPrior to her work in radio, Julia was an environmental reporter for the \u003cem>San Jose Mercury News\u003c/em> and Bay Area News Group, where her work was recognized with awards from the California Newspaper Publishers Association and the Society of Professional Journalists. Her radio honors include awards and citations from the Sony Radio Academy Awards and the National Lesbian and Gay Journalists Association.\r\n\r\nJulia hails from Montreal, Canada and lives in Oakland. She is the editor of the humor collection\u003cem> DRIVEL: Deliciously Bad Writing by Your Favorite Authors.\u003c/em>","avatar":"https://secure.gravatar.com/avatar/7fe25e0cf81dec2d4f74f1d4737a2871?s=600&d=blank&r=g","twitter":"juliascribe","facebook":null,"instagram":null,"linkedin":null,"sites":[{"site":"","roles":["editor"]},{"site":"arts","roles":["administrator"]},{"site":"news","roles":["subscriber"]},{"site":"futureofyou","roles":["editor"]},{"site":"science","roles":["administrator"]}],"headData":{"title":"Julia Scott | KQED","description":"KQED Contributor","ogImgSrc":"https://secure.gravatar.com/avatar/7fe25e0cf81dec2d4f74f1d4737a2871?s=600&d=blank&r=g","twImgSrc":"https://secure.gravatar.com/avatar/7fe25e0cf81dec2d4f74f1d4737a2871?s=600&d=blank&r=g"},"isLoading":false,"link":"/author/jscott"}},"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":"/"}},"futureofyou_440218":{"type":"posts","id":"futureofyou_440218","meta":{"index":"posts_1591205157","site":"futureofyou","id":"440218","score":null,"sort":[1521156163000]},"guestAuthors":[],"slug":"biologists-trace-genetic-roots-of-evolution-one-cell-at-a-time","title":"Biologists Trace Genetic Roots Of Evolution, One Cell at a Time","publishDate":1521156163,"format":"standard","headTitle":"Future of You | KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>Genetic mutations are the driving force of evolution, and now scientists have managed to study the effect of mutations in exquisite detail by watching what happens as they pop up in single cells.\u003c/p>\n\u003cp>Only about one percent of mutations were bad enough to kill off the cell, according to a \u003ca href=\"http://science.sciencemag.org/cgi/doi/10.1126/science.aan0797\" target=\"_blank\" rel=\"noopener\">report\u003c/a> published Thursday in \u003cem>Science\u003c/em>. Most of the time, these small changes in its DNA appeared to have no effect at all.[contextly_sidebar id=\"kvnKbnjyKwJnWuLsgRUewEIFcd5eTbqG\"]\u003c/p>\n\u003cp>Mutations have been studied for centuries, says \u003ca href=\"https://www.micalis.fr/micalis_eng/Poles-and-teams/Pole-Biosys/AJ-Aymerich-Jules/SyBER-group-Jules/SyBER-members/Lydia-Robert\" target=\"_blank\" rel=\"noopener\">Lydia Robert\u003c/a>, a researcher at INRA, an agricultural research institute in Paris, France, who notes that they can have medical impacts ranging from antibiotic resistance to cancer.\u003c/p>\n\u003cp>But research on mutations basically has focused on large-scale effects in populations.\u003c/p>\n\u003cp>\"You have a test tube with millions of bacteria, for instance, and you try to measure some property which is an average of all the cells in the population,\" says Robert.[contextly_sidebar id=\"B1EJ5qXFqZz59odJ0F4Nzqz7Z0w5fjPW\"]\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>In contrast, she and her colleagues wanted to study mutations in single cells.\u003c/p>\n\u003cp>So they turned to a so-called \"mother machine\" — a microfluidics device equipped with hundreds of tiny tubes, each no wider than a single E. coli bacterium.\u003c/p>\n\u003cp>\u003cstrong>'Mother Machine'\u003c/strong>\u003cbr>\nThey trapped a single bacterial cell in each tube, and spied on them with a microscope. Every time the bacterial cell divided into two, to reproduce itself, its genetic material got copied. If that copying process went awry and made a mistake, producing a mutation, this error got flagged by a fluorescent tag. The research team tracked about 20,000 mutations over hundreds of generations.\u003c/p>\n\u003cp>The researchers first checked to see if some cells might have an increased mutation rate compared to others.\u003c/p>\n\u003cp>\"We were surprised that in fact it was not the case,\" says Robert, explaining that, under their experimental conditions, all the cells seemed to share the same probability of acquiring mutations, and these genetic changes seemed to occur at a steady rate.\u003c/p>\n\u003cp>\"Many, many of them had no effect at all. This was a bit of a surprise to me,\" Robert says. \"I would have expected a lot of mutations to be slightly bad, and they are not even bad at all.\"\u003c/p>\n\u003cp>Just one percent of the time, a mutation killed the cell outright. And a mutation was very harmful to a cell (but not lethal) about 0.2 percent of the time.\u003c/p>\n\u003cp>\"Most of the time it's really neutral. The cell gets a mutation but it does nothing to the cell,\" says Robert.\u003c/p>\n\u003cp>\u003cstrong>Study Conditions\u003c/strong>\u003cbr>\nIn this study, the bacteria in the little tubes were living under good conditions and weren't exposed to any natural selection or competition—so the researchers could not determine how often mutations produced a beneficial effect that enhanced the bacterial cells' growth and survival.\u003c/p>\n\u003cp>Future studies could start to explore that. \"We're going to change, basically, the environment and see what it changes,\" Robert says. \"What happens if the environment is harsher? Is it going to change the way mutations occur, or are they going to kill more of the cells or less of the cells?\"\u003c/p>\n\u003cp>Already, what the researchers have observed so far confirms a lot of the core thinking that goes into evolutionary biology, says \u003ca href=\"http://myxo.css.msu.edu/\">Richard Lenski\u003c/a>, a biologist at Michigan State University who has spent the last three decades following the evolution of bacteria populations living in flasks in his lab.\u003c/p>\n\u003cp>\"What's exciting about this paper is the technical elegance of it, the rigorous quantification,\" says Lenski, \"This is another nice demonstration that random mutation really has this kind of clock-like dynamic, and that, absent natural selection, populations will, in fact, not only not be able to hold their own, but will tend to decay over time,\" because most mutations are either neutral or deleterious.[contextly_sidebar id=\"KsUxGvhivFMcATApHvyB6fQZaguGW0J5\"]\u003c/p>\n\u003cp>Looking at mutations without any natural selection is very artificial, Lenski says, \"but that allows them to really focus on the underlying process of mutation.\"\u003c/p>\n\u003cp>Some people study evolution in the real world, in all its gory detail, he says. But there's also value in studying genetic changes in this kind of controlled setting that can give a cleaner answers.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"Fitting those two together is always a challenge,\" says Lenski, \"but that's the way science works.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Biologists+Trace+Genetic+Roots+Of+Evolution%2C+One+Cell+At+A+Time&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n","blocks":[],"excerpt":"\u003cem>E.coli\u003c/em> bacteria are giving researchers the chance to study single genetic mutations. ","status":"publish","parent":0,"modified":1524871150,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":22,"wordCount":725},"headData":{"title":"Biologists Trace Genetic Roots Of Evolution, One Cell at a Time | KQED","description":"E.coli bacteria are giving researchers the chance to study single genetic mutations. ","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"Biologists Trace Genetic Roots Of Evolution, One Cell at a Time","datePublished":"2018-03-15T23:22:43.000Z","dateModified":"2018-04-27T23:19:10.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"disqusIdentifier":"440218 https://ww2.kqed.org/futureofyou/?p=440218","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/03/15/biologists-trace-genetic-roots-of-evolution-one-cell-at-a-time/","disqusTitle":"Biologists Trace Genetic Roots Of Evolution, One Cell at a Time","source":"Your Genes","nprImageCredit":"Kwangshin Kim","nprByline":"Nell Greenfieldboyce\u003cbr />NPR Shots","nprImageAgency":"Science Source","nprStoryId":"593918690","nprApiLink":"http://api.npr.org/query?id=593918690&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2018/03/15/593918690/biologists-trace-genetic-roots-of-evolution-one-cell-at-a-time?ft=nprml&f=593918690","nprRetrievedStory":"1","nprPubDate":"Thu, 15 Mar 2018 14:29:00 -0400","nprStoryDate":"Thu, 15 Mar 2018 14:01:00 -0400","nprLastModifiedDate":"Thu, 15 Mar 2018 14:29:20 -0400","path":"/futureofyou/440218/biologists-trace-genetic-roots-of-evolution-one-cell-at-a-time","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Genetic mutations are the driving force of evolution, and now scientists have managed to study the effect of mutations in exquisite detail by watching what happens as they pop up in single cells.\u003c/p>\n\u003cp>Only about one percent of mutations were bad enough to kill off the cell, according to a \u003ca href=\"http://science.sciencemag.org/cgi/doi/10.1126/science.aan0797\" target=\"_blank\" rel=\"noopener\">report\u003c/a> published Thursday in \u003cem>Science\u003c/em>. Most of the time, these small changes in its DNA appeared to have no effect at all.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Mutations have been studied for centuries, says \u003ca href=\"https://www.micalis.fr/micalis_eng/Poles-and-teams/Pole-Biosys/AJ-Aymerich-Jules/SyBER-group-Jules/SyBER-members/Lydia-Robert\" target=\"_blank\" rel=\"noopener\">Lydia Robert\u003c/a>, a researcher at INRA, an agricultural research institute in Paris, France, who notes that they can have medical impacts ranging from antibiotic resistance to cancer.\u003c/p>\n\u003cp>But research on mutations basically has focused on large-scale effects in populations.\u003c/p>\n\u003cp>\"You have a test tube with millions of bacteria, for instance, and you try to measure some property which is an average of all the cells in the population,\" says Robert.\u003c/p>\u003cp>\u003c/p>\u003cp>\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 contrast, she and her colleagues wanted to study mutations in single cells.\u003c/p>\n\u003cp>So they turned to a so-called \"mother machine\" — a microfluidics device equipped with hundreds of tiny tubes, each no wider than a single E. coli bacterium.\u003c/p>\n\u003cp>\u003cstrong>'Mother Machine'\u003c/strong>\u003cbr>\nThey trapped a single bacterial cell in each tube, and spied on them with a microscope. Every time the bacterial cell divided into two, to reproduce itself, its genetic material got copied. If that copying process went awry and made a mistake, producing a mutation, this error got flagged by a fluorescent tag. The research team tracked about 20,000 mutations over hundreds of generations.\u003c/p>\n\u003cp>The researchers first checked to see if some cells might have an increased mutation rate compared to others.\u003c/p>\n\u003cp>\"We were surprised that in fact it was not the case,\" says Robert, explaining that, under their experimental conditions, all the cells seemed to share the same probability of acquiring mutations, and these genetic changes seemed to occur at a steady rate.\u003c/p>\n\u003cp>\"Many, many of them had no effect at all. This was a bit of a surprise to me,\" Robert says. \"I would have expected a lot of mutations to be slightly bad, and they are not even bad at all.\"\u003c/p>\n\u003cp>Just one percent of the time, a mutation killed the cell outright. And a mutation was very harmful to a cell (but not lethal) about 0.2 percent of the time.\u003c/p>\n\u003cp>\"Most of the time it's really neutral. The cell gets a mutation but it does nothing to the cell,\" says Robert.\u003c/p>\n\u003cp>\u003cstrong>Study Conditions\u003c/strong>\u003cbr>\nIn this study, the bacteria in the little tubes were living under good conditions and weren't exposed to any natural selection or competition—so the researchers could not determine how often mutations produced a beneficial effect that enhanced the bacterial cells' growth and survival.\u003c/p>\n\u003cp>Future studies could start to explore that. \"We're going to change, basically, the environment and see what it changes,\" Robert says. \"What happens if the environment is harsher? Is it going to change the way mutations occur, or are they going to kill more of the cells or less of the cells?\"\u003c/p>\n\u003cp>Already, what the researchers have observed so far confirms a lot of the core thinking that goes into evolutionary biology, says \u003ca href=\"http://myxo.css.msu.edu/\">Richard Lenski\u003c/a>, a biologist at Michigan State University who has spent the last three decades following the evolution of bacteria populations living in flasks in his lab.\u003c/p>\n\u003cp>\"What's exciting about this paper is the technical elegance of it, the rigorous quantification,\" says Lenski, \"This is another nice demonstration that random mutation really has this kind of clock-like dynamic, and that, absent natural selection, populations will, in fact, not only not be able to hold their own, but will tend to decay over time,\" because most mutations are either neutral or deleterious.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Looking at mutations without any natural selection is very artificial, Lenski says, \"but that allows them to really focus on the underlying process of mutation.\"\u003c/p>\n\u003cp>Some people study evolution in the real world, in all its gory detail, he says. But there's also value in studying genetic changes in this kind of controlled setting that can give a cleaner answers.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"Fitting those two together is always a challenge,\" says Lenski, \"but that's the way science works.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Biologists+Trace+Genetic+Roots+Of+Evolution%2C+One+Cell+At+A+Time&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/440218/biologists-trace-genetic-roots-of-evolution-one-cell-at-a-time","authors":["byline_futureofyou_440218"],"programs":["futureofyou_54"],"categories":["futureofyou_1","futureofyou_1064"],"tags":["futureofyou_830","futureofyou_916","futureofyou_967"],"collections":["futureofyou_1094"],"featImg":"futureofyou_440219","label":"source_futureofyou_440218"},"futureofyou_435077":{"type":"posts","id":"futureofyou_435077","meta":{"index":"posts_1591205157","site":"futureofyou","id":"435077","score":null,"sort":[1504107174000]},"guestAuthors":[],"slug":"the-american-dad-is-getting-older-study","title":"The American Dad is Getting Older, Says Comprehensive Study","publishDate":1504107174,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{"site":"futureofyou"},"content":"\u003cp>More American men are waiting to start a family until after the age of 40, according to a\u003cstrong> \u003c/strong>\u003ca href=\"https://academic.oup.com/humrep/article-abstract/doi/10.1093/humrep/dex267/4096427/The-age-of-fathers-in-the-USA-is-rising-an?redirectedFrom=fulltext\" target=\"_blank\" rel=\"noopener noreferrer\">study\u003c/a> published Wednesday in \u003cem>Human Reproduction\u003c/em>.\u003c/p>\n\u003caside class=\"pullquote alignright\">The oldest father recorded in the past 44 years was 88. The youngest was 11.\u003c/aside>\n\u003cp>Using the Centers for Disease Control's National Vital Statistics System, the first-ever comprehensive analysis of all reported births from 1975 to 2015 -- all 168,867,480 of them -- showed that mean average paternal age increased three years from 27.4 to 30.9.\u003c/p>\n\u003cp>Overall, the percentage of fathers over the age of 40 increased from four percent in 1975 to nearly nine percent in 2015. And one percent of all babies are now born to fathers over 50.\u003c/p>\n\u003cp>The oldest father recorded in the past 44 years was 88. The youngest was 11.\u003c/p>\n\u003cp>Dr. Michael Eisenberg, an assistant professor of urology at Stanford University School of Medicine, is senior author of the study. He was inspired to undertake the data analysis after becoming frustrated that all the birth-age demographic analyses track mothers, not fathers. The study took over a year to complete.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>It can be challenging to characterize paternity trends because slightly over 10 percent of U.S. birth records are missing the father's information.\u003c/p>\n\u003cp>\"Urologists are kind of gatekeepers for men’s reproductive health. This gives us a glimpse into the basic demographics of paternal populations, and that's important,\" says Eisenberg.\u003c/p>\n\u003cp>\u003cstrong>A Shifting Norm\u003c/strong>\u003c/p>\n\u003cp>Women have been waiting \u003ca href=\"http://time.com/4181151/first-time-moms-average-age/\" target=\"_blank\" rel=\"noopener noreferrer\">longer and longer\u003c/a> to enter motherhood, though fathers and mothers are both stretching out their prefamily years. The average age gap between first-time mothers and fathers is now 2.3 years.\u003c/p>\n\u003cp>\"The gap between the father's age and mother's age has declined, suggesting that maybe there’s a bit more parity now between parents,\" says Eisenberg. \"I think that's a good thing.\"\u003c/p>\n\u003cp>In May, the CDC \u003ca href=\"http://www.slate.com/blogs/xx_factor/2017/05/17/cdc_data_says_women_in_their_thirties_are_having_more_babies_than_women.html\">released data \u003c/a>that marked an important milestone in modern U.S. society: For the first time, more women are entering motherhood in their 30s than their 20s. In 2016, the birth rate among women ages 30 to 34 narrowly surpassed that of women 25 to 29.\u003c/p>\n\u003cp>The Stanford University analysis reported variations by race, education and even geography. While mean paternal age has increased across all races and ethnicities, Asian-Americans were the oldest dads, while African- and Hispanic-Americans were on the younger side of the spectrum. In 1972, the mean age of Japanese-American fathers was 30.7 on average. In 2015, it was just over 36 -- the steepest increase of all.\u003c/p>\n\u003cp>Fathers with college degrees are waiting the longest to have kids. Men who live in the Northeast are the oldest overall.\u003c/p>\n\u003cp>\u003cstrong>Reproductive Risks From Waiting For Fatherhood\u003c/strong>\u003c/p>\n\u003cp>It can be difficult to characterize who an \"older\" father is. Some studies include men over 35, others start the clock at age 40.\u003c/p>\n\u003cp>But a preponderance of studies do agree that the longer a man waits to have children, the higher the risk of his offspring developing \u003ca href=\"http://www.jaacap.org/article/S0890-8567(17)30070-9/fulltext\">autism or schizophrenia\u003c/a>, or being born with a birth defect.\u003c/p>\n\u003cp>\"Men who are 55 have a higher risk than those who are 35. The incidence is two to three times in men who are over 40 years old -- this seems to be the consensus right now,\" says Dr. Magdalena Janecka, who studies genetic and developmental psychiatry at the Icahn School of Medicine at Mount Sinai, in New York.\u003c/p>\n\u003cp>There are two widely studied, perhaps overlapping, hypotheses for this. One is that as men age, their sperm develop genetic mutations. \u003ca href=\"http://www.nature.com/nature/journal/v432/n7013/full/432048a.html?foxtrotcallback=true\">A 2004 study \u003c/a>published in \u003cem>Nature \u003c/em>found that the number of DNA mutations in sperm is three times higher in men aged 36–57 than in men under age 35. (The study is behind a paywall but the results are summarized \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2566050/\">here\u003c/a>).\u003c/p>\n\u003cp>The second hypothesis, which Janecka says has stronger grounding in research, is that men who get started as fathers later in life are a self-selecting group who may have their \u003ca href=\"http://www.jaacap.org/article/S0890-8567(17)30070-9/pdf\">own social development challenges\u003c/a>. Those traits then get passed on to their offspring.\u003c/p>\n\u003cp>\"They themselves may suffer from some autism traits; they may be more withdrawn, for instance,\" says Janecka. \"Those men would be more likely to have a child with autism at any time in life.\"\u003c/p>\n\u003cp>Both Janecka and Eisenberg point out that the autism risk, though well-documented, is still very small and statistically rare.\u003c/p>\n\u003cp>\"People do ask me about risk to offspring, being an older father. I tell them the risks are at a population level, not at an individual level,\" says Eisenberg.\u003c/p>\n\u003cp>But the numbers, now that he has them, do speak for themselves.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"When we’re talking about four million births a year, and one percent of them is to men over 50, that is potentially something you would see,\" he adds.\u003c/p>\n\n","blocks":[],"excerpt":"More American men are waiting to start a family until after the age of 40, according to a study published Wednesday.","status":"publish","parent":0,"modified":1504122470,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":26,"wordCount":817},"headData":{"title":"The American Dad is Getting Older, Says Comprehensive Study | KQED","description":"More American men are waiting to start a family until after the age of 40, according to a study published Wednesday.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"The American Dad is Getting Older, Says Comprehensive Study","datePublished":"2017-08-30T15:32:54.000Z","dateModified":"2017-08-30T19:47:50.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"disqusIdentifier":"435077 https://ww2.kqed.org/futureofyou/?p=435077","disqusUrl":"https://ww2.kqed.org/futureofyou/2017/08/30/the-american-dad-is-getting-older-study/","disqusTitle":"The American Dad is Getting Older, Says Comprehensive Study","path":"/futureofyou/435077/the-american-dad-is-getting-older-study","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>More American men are waiting to start a family until after the age of 40, according to a\u003cstrong> \u003c/strong>\u003ca href=\"https://academic.oup.com/humrep/article-abstract/doi/10.1093/humrep/dex267/4096427/The-age-of-fathers-in-the-USA-is-rising-an?redirectedFrom=fulltext\" target=\"_blank\" rel=\"noopener noreferrer\">study\u003c/a> published Wednesday in \u003cem>Human Reproduction\u003c/em>.\u003c/p>\n\u003caside class=\"pullquote alignright\">The oldest father recorded in the past 44 years was 88. The youngest was 11.\u003c/aside>\n\u003cp>Using the Centers for Disease Control's National Vital Statistics System, the first-ever comprehensive analysis of all reported births from 1975 to 2015 -- all 168,867,480 of them -- showed that mean average paternal age increased three years from 27.4 to 30.9.\u003c/p>\n\u003cp>Overall, the percentage of fathers over the age of 40 increased from four percent in 1975 to nearly nine percent in 2015. And one percent of all babies are now born to fathers over 50.\u003c/p>\n\u003cp>The oldest father recorded in the past 44 years was 88. The youngest was 11.\u003c/p>\n\u003cp>Dr. Michael Eisenberg, an assistant professor of urology at Stanford University School of Medicine, is senior author of the study. He was inspired to undertake the data analysis after becoming frustrated that all the birth-age demographic analyses track mothers, not fathers. The study took over a year to complete.\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 can be challenging to characterize paternity trends because slightly over 10 percent of U.S. birth records are missing the father's information.\u003c/p>\n\u003cp>\"Urologists are kind of gatekeepers for men’s reproductive health. This gives us a glimpse into the basic demographics of paternal populations, and that's important,\" says Eisenberg.\u003c/p>\n\u003cp>\u003cstrong>A Shifting Norm\u003c/strong>\u003c/p>\n\u003cp>Women have been waiting \u003ca href=\"http://time.com/4181151/first-time-moms-average-age/\" target=\"_blank\" rel=\"noopener noreferrer\">longer and longer\u003c/a> to enter motherhood, though fathers and mothers are both stretching out their prefamily years. The average age gap between first-time mothers and fathers is now 2.3 years.\u003c/p>\n\u003cp>\"The gap between the father's age and mother's age has declined, suggesting that maybe there’s a bit more parity now between parents,\" says Eisenberg. \"I think that's a good thing.\"\u003c/p>\n\u003cp>In May, the CDC \u003ca href=\"http://www.slate.com/blogs/xx_factor/2017/05/17/cdc_data_says_women_in_their_thirties_are_having_more_babies_than_women.html\">released data \u003c/a>that marked an important milestone in modern U.S. society: For the first time, more women are entering motherhood in their 30s than their 20s. In 2016, the birth rate among women ages 30 to 34 narrowly surpassed that of women 25 to 29.\u003c/p>\n\u003cp>The Stanford University analysis reported variations by race, education and even geography. While mean paternal age has increased across all races and ethnicities, Asian-Americans were the oldest dads, while African- and Hispanic-Americans were on the younger side of the spectrum. In 1972, the mean age of Japanese-American fathers was 30.7 on average. In 2015, it was just over 36 -- the steepest increase of all.\u003c/p>\n\u003cp>Fathers with college degrees are waiting the longest to have kids. Men who live in the Northeast are the oldest overall.\u003c/p>\n\u003cp>\u003cstrong>Reproductive Risks From Waiting For Fatherhood\u003c/strong>\u003c/p>\n\u003cp>It can be difficult to characterize who an \"older\" father is. Some studies include men over 35, others start the clock at age 40.\u003c/p>\n\u003cp>But a preponderance of studies do agree that the longer a man waits to have children, the higher the risk of his offspring developing \u003ca href=\"http://www.jaacap.org/article/S0890-8567(17)30070-9/fulltext\">autism or schizophrenia\u003c/a>, or being born with a birth defect.\u003c/p>\n\u003cp>\"Men who are 55 have a higher risk than those who are 35. The incidence is two to three times in men who are over 40 years old -- this seems to be the consensus right now,\" says Dr. Magdalena Janecka, who studies genetic and developmental psychiatry at the Icahn School of Medicine at Mount Sinai, in New York.\u003c/p>\n\u003cp>There are two widely studied, perhaps overlapping, hypotheses for this. One is that as men age, their sperm develop genetic mutations. \u003ca href=\"http://www.nature.com/nature/journal/v432/n7013/full/432048a.html?foxtrotcallback=true\">A 2004 study \u003c/a>published in \u003cem>Nature \u003c/em>found that the number of DNA mutations in sperm is three times higher in men aged 36–57 than in men under age 35. (The study is behind a paywall but the results are summarized \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2566050/\">here\u003c/a>).\u003c/p>\n\u003cp>The second hypothesis, which Janecka says has stronger grounding in research, is that men who get started as fathers later in life are a self-selecting group who may have their \u003ca href=\"http://www.jaacap.org/article/S0890-8567(17)30070-9/pdf\">own social development challenges\u003c/a>. Those traits then get passed on to their offspring.\u003c/p>\n\u003cp>\"They themselves may suffer from some autism traits; they may be more withdrawn, for instance,\" says Janecka. \"Those men would be more likely to have a child with autism at any time in life.\"\u003c/p>\n\u003cp>Both Janecka and Eisenberg point out that the autism risk, though well-documented, is still very small and statistically rare.\u003c/p>\n\u003cp>\"People do ask me about risk to offspring, being an older father. I tell them the risks are at a population level, not at an individual level,\" says Eisenberg.\u003c/p>\n\u003cp>But the numbers, now that he has them, do speak for themselves.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"When we’re talking about four million births a year, and one percent of them is to men over 50, that is potentially something you would see,\" he adds.\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/435077/the-american-dad-is-getting-older-study","authors":["8664"],"categories":["futureofyou_1"],"tags":["futureofyou_555","futureofyou_1347","futureofyou_1275","futureofyou_916","futureofyou_1348"],"featImg":"futureofyou_435104","label":"futureofyou"},"futureofyou_178320":{"type":"posts","id":"futureofyou_178320","meta":{"index":"posts_1591205157","site":"futureofyou","id":"178320","score":null,"sort":[1465398047000]},"guestAuthors":[],"slug":"genetic-cause-found-for-progressive-multiple-sclerosis","title":"One Genetic Cause Found for Progressive Multiple Sclerosis","publishDate":1465398047,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{"site":"futureofyou"},"content":"\u003cp>One of the most severe form of multiple sclerosis (MS) is \u003ca href=\"http://www.newswise.com/articles/scientists-find-genetic-cause-of-multiple-sclerosis\" target=\"_blank\">sometimes caused\u003c/a> by the malfunction of a single gene, NR1H3, a group of researchers from the University of British Columbia \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/27253448\" target=\"_blank\">reports\u003c/a> in the journal \u003ca href=\"http://www.cell.com/neuron/home\" target=\"_blank\">Neuron\u003c/a>. Some 60-70% of people with a certain type of mutation in this gene will end up with primary-progressive MS (PPMS), a particularly nasty form of the disease.\u003c/p>\n\u003cp>This is by far the strongest connection ever found between any single genetic mutation and MS.\u003c/p>\n\u003cp>Fortunately, mutations in this gene are very rare, meaning that only something on the order of 1 in 1,000 cases of MS can be directly linked to them. But this discovery is a bigger deal than these numbers make it sound.\u003c/p>\n\u003cp>Identifying NR1H3 uncovers a new pathway in the cell to explore to find new treatments for PPMS. This will obviously help the 15% of MS patients suffering from PPMS but it may also help even more patients than this. Since many cases of MS eventually progress to PPMS, these new treatments could help many MS patients in the later stages of their disease.\u003c/p>\n\u003cp>https://www.youtube.com/watch?v=Naecv3h868c\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003cstrong>Short-Circuited Nervous System\u003c/strong>\u003c/p>\n\u003cp>Multiple sclerosis (MS) is a disease in which a person's immune system attacks the outer covering of nerve cells. The slow loss of this myelin sheath causes nerves to short-circuit, which can cause problems ranging from vision loss, fatigue, loss of coordination, and trouble walking, to paralysis and even death for the 400,000 or so Americans who have the disease.\u003c/p>\n\u003cp>The wide range of symptoms comes about because what happens to a particular patient depends on which nerves happen to have been attacked.\u003c/p>\n\u003cp>The most common form of MS is relapsing-remitting MS (RRMS). With this form, disease progression comes in spurts. There are periods where the symptoms become more severe and periods where symptoms lessen or even disappear.\u003c/p>\n\u003cp>PPMS is the more disabling form, where the disease progresses without periods of remission. The gene these researchers identified helps to explain this second form of the disease.\u003c/p>\n\u003cfigure id=\"attachment_179207\" class=\"wp-caption alignright\" style=\"max-width: 504px\">\u003ca href=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/06/MSdiagram_lg.jpg\">\u003cimg class=\"size-full wp-image-179207\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/06/MSdiagram_lg.jpg\" alt=\"In multiple sclerosis, the myelin that covers nerve cells becomes inflamed, swollen, and detached. It is then destroyed, forming a scar over the axons (nerve fibers). Sclerosis means scar.\" width=\"504\" height=\"198\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/06/MSdiagram_lg.jpg 504w, https://ww2.kqed.org/app/uploads/sites/13/2016/06/MSdiagram_lg-400x157.jpg 400w\" sizes=\"(max-width: 504px) 100vw, 504px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">In multiple sclerosis, the myelin that covers nerve cells becomes inflamed, swollen, and detached. It is then destroyed, forming a scar over the axons (nerve fibers). Sclerosis means scar. \u003ccite>(NIH/Patient Education Institute)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>It makes sense that the NR1H3 gene might be involved in PPMS, because this gene plays a role in both the immune system and in repairing the myelin sheath around nerve cells. The study suggests that when this gene isn’t working right, the immune system sometimes overreacts to something in the environment, causing it to attack the myelin sheath. The sheath can’t then be repaired once the attack happens. Symptoms continue to get worse as the immune system attacks again, and again.\u003c/p>\n\u003cp>Now that scientists know NR1H3 plays a role in MS, they can focus their energies on finding treatments that balance the gene's malfunction.\u003c/p>\n\u003cp>\u003cstrong>Finding a Disease-Causing Variant\u003c/strong>\u003c/p>\n\u003cp>The researchers discovered this gene was involved in MS by studying two Canadian families who had many members with the disease. Even so, the gene was not easy to find.\u003c/p>\n\u003cp>The first step was to sequence and compare every gene in two first cousins, both of whom had the PPMS form of the disease. Researchers were looking for genetic differences the two shared that might explain why they both had MS.\u003c/p>\n\u003cp>This type of sequencing is called “\u003ca href=\"http://ww2.kqed.org/futureofyou/2016/05/10/social-media-uncovers-rare-diagnosis-after-years-of-frustration/\" target=\"_blank\">exome sequencing\u003c/a>,” and it looks only at the 2% of our DNA that is genes. The reports for the two cousins found 48,333 variants in one cousin and 47,681 variants in the other.\u003c/p>\n\u003cp>[contextly_sidebar id=\"tNU4KtLSa2o4yP3TV2RNkJ4Yge6g2UpT\"]A variant is simply a difference from the DNA scientists use as a reference, called the\u003ca href=\"https://en.wikipedia.org/wiki/Reference_genome\" target=\"_blank\"> reference genome\u003c/a>. It is simply a set of DNA that scientists have agreed that they will compare the DNA they are studying to.\u003c/p>\n\u003cp>Most of these tens of thousands of variants are silent and have little or no effect, while others might give us traits that make us unique, such as eye color or the shape of our toes.\u003c/p>\n\u003cp>Researchers winnowed down the number of variants that might be responsible for the MS that ran in this family to 37, by looking for variants that the two cousins shared, that were rare (if a disease causing variant is common then lots of people would have the disease), and that might be predicted to affect how a gene works.\u003c/p>\n\u003cp>The team next compared 185 people without the disease to all nine family members with the disease, to find which of these 37 was in the MS patients but not the group without MS. This eliminated another 33 variants.\u003c/p>\n\u003cp>Researchers then took the remaining four and looked for them in 2,053 MS patients and 799 people without MS. This eliminated three more, leaving a single variant in the NR1H3 gene as the only candidate left.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>This approach of comparing people with and without a disease is a common way to \u003ca href=\"http://ww2.kqed.org/futureofyou/2016/05/10/social-media-uncovers-rare-diagnosis-after-years-of-frustration/\" target=\"_blank\">find DNA differences\u003c/a> that can lead to a certain disease. What made it work in this case was that lots of people in a single family had the disease, and it has become much less expensive to look at every gene a person has.\u003c/p>\n\n","blocks":[],"excerpt":"The genetic mutation causes a small percentage of MS cases, but the discovery could lead to treatments that benefit many more.","status":"publish","parent":0,"modified":1475120906,"stats":{"hasAudio":false,"hasVideo":true,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":23,"wordCount":898},"headData":{"title":"One Genetic Cause Found for Progressive Multiple Sclerosis | KQED","description":"The genetic mutation causes a small percentage of MS cases, but the discovery could lead to treatments that benefit many more.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"One Genetic Cause Found for Progressive Multiple Sclerosis","datePublished":"2016-06-08T15:00:47.000Z","dateModified":"2016-09-29T03:48:26.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"disqusIdentifier":"178320 http://ww2.kqed.org/futureofyou/?p=178320","disqusUrl":"https://ww2.kqed.org/futureofyou/2016/06/08/genetic-cause-found-for-progressive-multiple-sclerosis/","disqusTitle":"One Genetic Cause Found for Progressive Multiple Sclerosis","nprByline":"Barry Starr","path":"/futureofyou/178320/genetic-cause-found-for-progressive-multiple-sclerosis","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>One of the most severe form of multiple sclerosis (MS) is \u003ca href=\"http://www.newswise.com/articles/scientists-find-genetic-cause-of-multiple-sclerosis\" target=\"_blank\">sometimes caused\u003c/a> by the malfunction of a single gene, NR1H3, a group of researchers from the University of British Columbia \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/27253448\" target=\"_blank\">reports\u003c/a> in the journal \u003ca href=\"http://www.cell.com/neuron/home\" target=\"_blank\">Neuron\u003c/a>. Some 60-70% of people with a certain type of mutation in this gene will end up with primary-progressive MS (PPMS), a particularly nasty form of the disease.\u003c/p>\n\u003cp>This is by far the strongest connection ever found between any single genetic mutation and MS.\u003c/p>\n\u003cp>Fortunately, mutations in this gene are very rare, meaning that only something on the order of 1 in 1,000 cases of MS can be directly linked to them. But this discovery is a bigger deal than these numbers make it sound.\u003c/p>\n\u003cp>Identifying NR1H3 uncovers a new pathway in the cell to explore to find new treatments for PPMS. This will obviously help the 15% of MS patients suffering from PPMS but it may also help even more patients than this. Since many cases of MS eventually progress to PPMS, these new treatments could help many MS patients in the later stages of their disease.\u003c/p>\u003c/p>\u003cp>\u003cspan class='utils-parseShortcode-shortcodes-__youtubeShortcode__embedYoutube'>\n \u003cspan class='utils-parseShortcode-shortcodes-__youtubeShortcode__embedYoutubeInside'>\n \u003ciframe\n loading='lazy'\n class='utils-parseShortcode-shortcodes-__youtubeShortcode__youtubePlayer'\n type='text/html'\n src='//www.youtube.com/embed/Naecv3h868c'\n title='//www.youtube.com/embed/Naecv3h868c'\n allowfullscreen='true'\n style='border:0;'>\u003c/iframe>\n \u003c/span>\n \u003c/span>\u003c/p>\u003cp>\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>\u003cstrong>Short-Circuited Nervous System\u003c/strong>\u003c/p>\n\u003cp>Multiple sclerosis (MS) is a disease in which a person's immune system attacks the outer covering of nerve cells. The slow loss of this myelin sheath causes nerves to short-circuit, which can cause problems ranging from vision loss, fatigue, loss of coordination, and trouble walking, to paralysis and even death for the 400,000 or so Americans who have the disease.\u003c/p>\n\u003cp>The wide range of symptoms comes about because what happens to a particular patient depends on which nerves happen to have been attacked.\u003c/p>\n\u003cp>The most common form of MS is relapsing-remitting MS (RRMS). With this form, disease progression comes in spurts. There are periods where the symptoms become more severe and periods where symptoms lessen or even disappear.\u003c/p>\n\u003cp>PPMS is the more disabling form, where the disease progresses without periods of remission. The gene these researchers identified helps to explain this second form of the disease.\u003c/p>\n\u003cfigure id=\"attachment_179207\" class=\"wp-caption alignright\" style=\"max-width: 504px\">\u003ca href=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/06/MSdiagram_lg.jpg\">\u003cimg class=\"size-full wp-image-179207\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/06/MSdiagram_lg.jpg\" alt=\"In multiple sclerosis, the myelin that covers nerve cells becomes inflamed, swollen, and detached. It is then destroyed, forming a scar over the axons (nerve fibers). Sclerosis means scar.\" width=\"504\" height=\"198\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/06/MSdiagram_lg.jpg 504w, https://ww2.kqed.org/app/uploads/sites/13/2016/06/MSdiagram_lg-400x157.jpg 400w\" sizes=\"(max-width: 504px) 100vw, 504px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">In multiple sclerosis, the myelin that covers nerve cells becomes inflamed, swollen, and detached. It is then destroyed, forming a scar over the axons (nerve fibers). Sclerosis means scar. \u003ccite>(NIH/Patient Education Institute)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>It makes sense that the NR1H3 gene might be involved in PPMS, because this gene plays a role in both the immune system and in repairing the myelin sheath around nerve cells. The study suggests that when this gene isn’t working right, the immune system sometimes overreacts to something in the environment, causing it to attack the myelin sheath. The sheath can’t then be repaired once the attack happens. Symptoms continue to get worse as the immune system attacks again, and again.\u003c/p>\n\u003cp>Now that scientists know NR1H3 plays a role in MS, they can focus their energies on finding treatments that balance the gene's malfunction.\u003c/p>\n\u003cp>\u003cstrong>Finding a Disease-Causing Variant\u003c/strong>\u003c/p>\n\u003cp>The researchers discovered this gene was involved in MS by studying two Canadian families who had many members with the disease. Even so, the gene was not easy to find.\u003c/p>\n\u003cp>The first step was to sequence and compare every gene in two first cousins, both of whom had the PPMS form of the disease. Researchers were looking for genetic differences the two shared that might explain why they both had MS.\u003c/p>\n\u003cp>This type of sequencing is called “\u003ca href=\"http://ww2.kqed.org/futureofyou/2016/05/10/social-media-uncovers-rare-diagnosis-after-years-of-frustration/\" target=\"_blank\">exome sequencing\u003c/a>,” and it looks only at the 2% of our DNA that is genes. The reports for the two cousins found 48,333 variants in one cousin and 47,681 variants in the other.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>A variant is simply a difference from the DNA scientists use as a reference, called the\u003ca href=\"https://en.wikipedia.org/wiki/Reference_genome\" target=\"_blank\"> reference genome\u003c/a>. It is simply a set of DNA that scientists have agreed that they will compare the DNA they are studying to.\u003c/p>\n\u003cp>Most of these tens of thousands of variants are silent and have little or no effect, while others might give us traits that make us unique, such as eye color or the shape of our toes.\u003c/p>\n\u003cp>Researchers winnowed down the number of variants that might be responsible for the MS that ran in this family to 37, by looking for variants that the two cousins shared, that were rare (if a disease causing variant is common then lots of people would have the disease), and that might be predicted to affect how a gene works.\u003c/p>\n\u003cp>The team next compared 185 people without the disease to all nine family members with the disease, to find which of these 37 was in the MS patients but not the group without MS. This eliminated another 33 variants.\u003c/p>\n\u003cp>Researchers then took the remaining four and looked for them in 2,053 MS patients and 799 people without MS. This eliminated three more, leaving a single variant in the NR1H3 gene as the only candidate left.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>This approach of comparing people with and without a disease is a common way to \u003ca href=\"http://ww2.kqed.org/futureofyou/2016/05/10/social-media-uncovers-rare-diagnosis-after-years-of-frustration/\" target=\"_blank\">find DNA differences\u003c/a> that can lead to a certain disease. What made it work in this case was that lots of people in a single family had the disease, and it has become much less expensive to look at every gene a person has.\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/178320/genetic-cause-found-for-progressive-multiple-sclerosis","authors":["byline_futureofyou_178320"],"categories":["futureofyou_1064"],"tags":["futureofyou_324","futureofyou_916","futureofyou_949"],"featImg":"futureofyou_178350","label":"futureofyou"},"futureofyou_160842":{"type":"posts","id":"futureofyou_160842","meta":{"index":"posts_1591205157","site":"futureofyou","id":"160842","score":null,"sort":[1462916001000]},"guestAuthors":[],"slug":"social-media-uncovers-rare-diagnosis-after-years-of-frustration","title":"Through Social Media, Family Connects to Rare Diagnosis – And Hope","publishDate":1462916001,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{"site":"futureofyou"},"content":"\u003cp>If you are suffering from an illness fewer than a dozen people in the world are known to have, getting a proper diagnosis can start to feel like a hunt for something that doesn't exist.\u003c/p>\n\u003cp>That's the position one family found themselves in before they turned to social media in search of an answer, managing to discover in one day an answer that had eluded doctors for years.\u003c/p>\n\u003caside class=\"pullquote alignright\">'These days there are ribbons and awareness weeks for so many diseases, but when yours is ultra-rare, you feel completely isolated. You feel like you’re never going to hear another person say, ‘Us too!’ And being connected to other families changes all that.' \u003ccite>Bo Bigelow\u003c/cite>\u003c/aside>\n\u003cp>It's a story that illustrates the power of crowdsourcing. Tess Bigelow, six years old, became the eighth person in the world known to have a mutation of the gene called USP7. This defective gene could be the reason she functions at the level of an 18-month-old child, with developmental delays in basic functions such as walking and talking.\u003c/p>\n\u003cp>Last August, Bo Bigelow, Tess' father, put up \u003ca href=\"http://www.portlandrootsmedia.com/tess-genetic-mystery\" target=\"_blank\">a website\u003c/a> about his daughter's genetic mutation then posted it to Facebook and Twitter. From a \u003ca href=\"https://www.bcm.edu/news/genetics/diagnostic-discovery-through-social-media\" target=\"_blank\">press release\u003c/a> about the case sent out last September by Baylor College of Medicine in Houston:\u003c/p>\n\u003cblockquote>\u003cp>\"Help us find others like Tess.\" Bo Bigelow's plea jumps off the page of his blog, echoing across the continent from his leafy green home city of Portland, Maine.\u003c/p>\n\u003cp>When he posted his call to action, all he knew was that his young daughter has a mutation in her USP7 gene and that she has global developmental delay, hip dysplasia and visual impairment caused by her brain (not a problem in her eyes themselves) among other health issues.\u003c/p>\u003c/blockquote>\n\u003cp>Bo and his wife, Kate, who live in Maine, hoped to find other families affected by the same mutation.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\"We thought we were embarking on this months- or years-long odyssey to find at least one other person,\" says Bo Bigelow. \"And instead, by that evening we were on the horn with Baylor. They found us in less than 24 hours, and it’s from people being so great about spreading it and having their friends spread it.\"\u003c/p>\n\u003cp>It was a friend of Bigelow's brother-in-law who \u003ca href=\"https://www.reddit.com/r/genetics/comments/3gr6a8/hi_rgenetics_need_your_help_i_have_a_little/\" target=\"_blank\">posted\u003c/a> Tess' case on Reddit. That's where a worker at a Baylor lab spotted it -- a lab that is one of the few in the world studying USP7.\u003c/p>\n\u003cfigure id=\"attachment_161424\" class=\"wp-caption aligncenter\" style=\"max-width: 720px\">\u003ca href=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/05/special-olympics-e1462926780310.jpg\">\u003cimg class=\"size-full wp-image-161424\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/05/special-olympics-e1462926780310.jpg\" alt=\"Tess walked 100 meters this spring in the Special Olympics. She needed some help staying in her lane, and had to stop to gather her stamina, but crossed the finish line to the cheers of her family. Her father did a podcast episode about the event.\" width=\"720\" height=\"592\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/05/special-olympics-e1462926780310.jpg 720w, https://ww2.kqed.org/app/uploads/sites/13/2016/05/special-olympics-e1462926780310-400x329.jpg 400w\" sizes=\"(max-width: 720px) 100vw, 720px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Tess walked 100 meters this spring in the Special Olympics. She needed some help staying in her lane, and had to stop to gather her stamina, but crossed the finish line to the cheers of her family. Her father did a \u003ca href=\"http://www.portlandrootsmedia.com/strongerpodcast/2016/5/4/68-special-is-an-understatement\" target=\"_blank\">podcast episode\u003c/a> about the event. \u003ccite>(Bo Bigelow/Facebook)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Most striking of all, Bigelow says, that first email from Mike Fountain, a predoctoral fellow in the lab, said the Baylor team had identified other families who had children affected by the same genetic mutation. Just connecting with them has eased Bo and Kate's worries.\u003c/p>\n\u003cp>\"These days there are ribbons and awareness-weeks for so many diseases,\" Bigelow says, \"but when yours is ultra-rare, you feel completely isolated. You feel like you're never going to hear another person say, 'Us too!' And being connected to other families changes all that.\"\u003c/p>\n\u003cp>Fountain's colleague, researcher and Baylor genetics professor Christian Schaaf, had already found seven children around the world with USP7 mutations and symptoms similar to Tess'. Schaaf and 18 of his colleagues were getting ready to publish \u003ca href=\"http://www.cell.com/molecular-cell/abstract/S1097-2765(15)00617-6?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1097276515006176%3Fshowall%3Dtrue\">research\u003c/a> in the journal \u003cem>Molecular Cell \u003c/em>describing how USP7 becomes a \"disease gene.\"\u003c/p>\n\u003cp>USP7 and two other genes are critical in the process of recycling and breaking down the proteins in a cell that are no longer of use. This process keeps all the work of our cells in balance; when it's out of whack, it can lead to cancers, neurodegenerative diseases or genetic disorders.\u003c/p>\n\u003cp>https://youtu.be/TF7zOV0KT0s\u003c/p>\n\u003cp>Bigelow says the family doesn't yet have official confirmation that Tess' symptoms are caused by her genetic mutation. Baylor researchers are examining that now and he expects to hear soon whether the lab will accept her for inclusion in potential treatments, now in development. Meanwhile, he says, Baylor asked him to use his website and social media skills to search out other families, and he's found two more who have children with a USP7 mutation.\u003c/p>\n\u003cp>\u003cstrong>Crowdsourcing Diagnoses Takes Hold\u003c/strong>\u003c/p>\n\u003cp>Patients or parents like Tess' who are seeking answers to seemingly unsolvable medical mysteries have new tools to reach out, not only on social media, but in crowdsourcing websites like \u003ca href=\"https://www.crowdmed.com/\" target=\"_blank\">CrowdMed\u003c/a>, a subscription service for people seeking answers to medical conundrums.\u003c/p>\n\u003cp>At CrowdMed, people who have symptoms but have yet to find a diagnosis seek opinions from the site's \"medical detectives,\" only some of whom are medical professionals.\u003c/p>\n\u003cp>The process involves patients posting their symptoms and other relevant data, opening their case up to the site's diagnostic community. When a diagnosis is offered, the other \"detectives\" vote on it, and that opinion moves up or down according to those votes and the weight assigned to each diagnostician, which is determined by their past accuracy.\u003c/p>\n\u003cp>\"We call it a stock market for diagnoses,\" CrowdMed co-founder Jessica Greenwalt told Future of You editor Jon Brooks at a University of San Francisco medical technology conference in March.\u003c/p>\n\u003cp>She said the site had resolved close to 800 cases in which the patient has reported the CrowdMed diagnosis was correct.\u003c/p>\n\u003cp>\"The nice thing about not limiting it to physicians,\" Greenwalt said, \"is we get people who are not stuck in the same method of thought training. Or they're not afraid to suggest the rare diagnosis. We see this a lot, where doctors are afraid to say it might be this rare condition.\"\u003c/p>\n\u003cp>A writer who \u003ca href=\"http://www.elle.com/culture/news/a28783/the-crowd-will-see-you-now/\" target=\"_blank\">reviewed C\u003c/a>rowdMed for Elle discovered one of the common pitfalls of self-diagnosis: worrying about a range of diseases she'd never heard of. But she also wrote she felt encouraged to do research about her health and supported by the care people offered in listening to and responding to her case.\u003c/p>\n\u003cp>\"While reporting this piece,\" wrote Molly Langmuir, \"I vacillated between viewing CrowdMed as a dire indictment of our medical system—things are so bad we've had to turn to a bunch of strangers who may or may not have had medical training—and a heartening sign of progress, a surprisingly effective way of putting the 'care' back into health\u003c/p>\n\u003cp>\u003ca href=\"https://www.mygene2.org/MyGene2/\" target=\"_blank\">MyGene2\u003c/a> is another crowdsourcing site. It serves as an information hub where those with rare genetic disorders can share information, and researchers and clinicians working with a particular condition or gene can contact people who may benefit from new treatments or ideas.\u003c/p>\n\u003cp>The site just went live this spring and already features more than 100 families and 87 different problematic genes.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>Jon Brooks contributed to this post.\u003c/em>\u003c/p>\n\n","blocks":[],"excerpt":"Only after turning to social media did six-year-old Tess Bigelow's parents learn of a lab researching her rare genetic mutation.","status":"publish","parent":0,"modified":1476850729,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":28,"wordCount":1210},"headData":{"title":"Through Social Media, Family Connects to Rare Diagnosis – And Hope | KQED","description":"Only after turning to social media did six-year-old Tess Bigelow's parents learn of a lab researching her rare genetic mutation.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"Through Social Media, Family Connects to Rare Diagnosis – And Hope","datePublished":"2016-05-10T21:33:21.000Z","dateModified":"2016-10-19T04:18:49.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"disqusIdentifier":"160842 http://ww2.kqed.org/futureofyou/?p=160842","disqusUrl":"https://ww2.kqed.org/futureofyou/2016/05/10/social-media-uncovers-rare-diagnosis-after-years-of-frustration/","disqusTitle":"Through Social Media, Family Connects to Rare Diagnosis – And Hope","path":"/futureofyou/160842/social-media-uncovers-rare-diagnosis-after-years-of-frustration","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>If you are suffering from an illness fewer than a dozen people in the world are known to have, getting a proper diagnosis can start to feel like a hunt for something that doesn't exist.\u003c/p>\n\u003cp>That's the position one family found themselves in before they turned to social media in search of an answer, managing to discover in one day an answer that had eluded doctors for years.\u003c/p>\n\u003caside class=\"pullquote alignright\">'These days there are ribbons and awareness weeks for so many diseases, but when yours is ultra-rare, you feel completely isolated. You feel like you’re never going to hear another person say, ‘Us too!’ And being connected to other families changes all that.' \u003ccite>Bo Bigelow\u003c/cite>\u003c/aside>\n\u003cp>It's a story that illustrates the power of crowdsourcing. Tess Bigelow, six years old, became the eighth person in the world known to have a mutation of the gene called USP7. This defective gene could be the reason she functions at the level of an 18-month-old child, with developmental delays in basic functions such as walking and talking.\u003c/p>\n\u003cp>Last August, Bo Bigelow, Tess' father, put up \u003ca href=\"http://www.portlandrootsmedia.com/tess-genetic-mystery\" target=\"_blank\">a website\u003c/a> about his daughter's genetic mutation then posted it to Facebook and Twitter. From a \u003ca href=\"https://www.bcm.edu/news/genetics/diagnostic-discovery-through-social-media\" target=\"_blank\">press release\u003c/a> about the case sent out last September by Baylor College of Medicine in Houston:\u003c/p>\n\u003cblockquote>\u003cp>\"Help us find others like Tess.\" Bo Bigelow's plea jumps off the page of his blog, echoing across the continent from his leafy green home city of Portland, Maine.\u003c/p>\n\u003cp>When he posted his call to action, all he knew was that his young daughter has a mutation in her USP7 gene and that she has global developmental delay, hip dysplasia and visual impairment caused by her brain (not a problem in her eyes themselves) among other health issues.\u003c/p>\u003c/blockquote>\n\u003cp>Bo and his wife, Kate, who live in Maine, hoped to find other families affected by the same mutation.\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>\"We thought we were embarking on this months- or years-long odyssey to find at least one other person,\" says Bo Bigelow. \"And instead, by that evening we were on the horn with Baylor. They found us in less than 24 hours, and it’s from people being so great about spreading it and having their friends spread it.\"\u003c/p>\n\u003cp>It was a friend of Bigelow's brother-in-law who \u003ca href=\"https://www.reddit.com/r/genetics/comments/3gr6a8/hi_rgenetics_need_your_help_i_have_a_little/\" target=\"_blank\">posted\u003c/a> Tess' case on Reddit. That's where a worker at a Baylor lab spotted it -- a lab that is one of the few in the world studying USP7.\u003c/p>\n\u003cfigure id=\"attachment_161424\" class=\"wp-caption aligncenter\" style=\"max-width: 720px\">\u003ca href=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/05/special-olympics-e1462926780310.jpg\">\u003cimg class=\"size-full wp-image-161424\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/05/special-olympics-e1462926780310.jpg\" alt=\"Tess walked 100 meters this spring in the Special Olympics. She needed some help staying in her lane, and had to stop to gather her stamina, but crossed the finish line to the cheers of her family. Her father did a podcast episode about the event.\" width=\"720\" height=\"592\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/05/special-olympics-e1462926780310.jpg 720w, https://ww2.kqed.org/app/uploads/sites/13/2016/05/special-olympics-e1462926780310-400x329.jpg 400w\" sizes=\"(max-width: 720px) 100vw, 720px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Tess walked 100 meters this spring in the Special Olympics. She needed some help staying in her lane, and had to stop to gather her stamina, but crossed the finish line to the cheers of her family. Her father did a \u003ca href=\"http://www.portlandrootsmedia.com/strongerpodcast/2016/5/4/68-special-is-an-understatement\" target=\"_blank\">podcast episode\u003c/a> about the event. \u003ccite>(Bo Bigelow/Facebook)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Most striking of all, Bigelow says, that first email from Mike Fountain, a predoctoral fellow in the lab, said the Baylor team had identified other families who had children affected by the same genetic mutation. Just connecting with them has eased Bo and Kate's worries.\u003c/p>\n\u003cp>\"These days there are ribbons and awareness-weeks for so many diseases,\" Bigelow says, \"but when yours is ultra-rare, you feel completely isolated. You feel like you're never going to hear another person say, 'Us too!' And being connected to other families changes all that.\"\u003c/p>\n\u003cp>Fountain's colleague, researcher and Baylor genetics professor Christian Schaaf, had already found seven children around the world with USP7 mutations and symptoms similar to Tess'. Schaaf and 18 of his colleagues were getting ready to publish \u003ca href=\"http://www.cell.com/molecular-cell/abstract/S1097-2765(15)00617-6?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1097276515006176%3Fshowall%3Dtrue\">research\u003c/a> in the journal \u003cem>Molecular Cell \u003c/em>describing how USP7 becomes a \"disease gene.\"\u003c/p>\n\u003cp>USP7 and two other genes are critical in the process of recycling and breaking down the proteins in a cell that are no longer of use. This process keeps all the work of our cells in balance; when it's out of whack, it can lead to cancers, neurodegenerative diseases or genetic disorders.\u003c/p>\u003c/p>\u003cp>\u003cspan class='utils-parseShortcode-shortcodes-__youtubeShortcode__embedYoutube'>\n \u003cspan class='utils-parseShortcode-shortcodes-__youtubeShortcode__embedYoutubeInside'>\n \u003ciframe\n loading='lazy'\n class='utils-parseShortcode-shortcodes-__youtubeShortcode__youtubePlayer'\n type='text/html'\n src='//www.youtube.com/embed/TF7zOV0KT0s'\n title='//www.youtube.com/embed/TF7zOV0KT0s'\n allowfullscreen='true'\n style='border:0;'>\u003c/iframe>\n \u003c/span>\n \u003c/span>\u003c/p>\u003cp>\u003cp>Bigelow says the family doesn't yet have official confirmation that Tess' symptoms are caused by her genetic mutation. Baylor researchers are examining that now and he expects to hear soon whether the lab will accept her for inclusion in potential treatments, now in development. Meanwhile, he says, Baylor asked him to use his website and social media skills to search out other families, and he's found two more who have children with a USP7 mutation.\u003c/p>\n\u003cp>\u003cstrong>Crowdsourcing Diagnoses Takes Hold\u003c/strong>\u003c/p>\n\u003cp>Patients or parents like Tess' who are seeking answers to seemingly unsolvable medical mysteries have new tools to reach out, not only on social media, but in crowdsourcing websites like \u003ca href=\"https://www.crowdmed.com/\" target=\"_blank\">CrowdMed\u003c/a>, a subscription service for people seeking answers to medical conundrums.\u003c/p>\n\u003cp>At CrowdMed, people who have symptoms but have yet to find a diagnosis seek opinions from the site's \"medical detectives,\" only some of whom are medical professionals.\u003c/p>\n\u003cp>The process involves patients posting their symptoms and other relevant data, opening their case up to the site's diagnostic community. When a diagnosis is offered, the other \"detectives\" vote on it, and that opinion moves up or down according to those votes and the weight assigned to each diagnostician, which is determined by their past accuracy.\u003c/p>\n\u003cp>\"We call it a stock market for diagnoses,\" CrowdMed co-founder Jessica Greenwalt told Future of You editor Jon Brooks at a University of San Francisco medical technology conference in March.\u003c/p>\n\u003cp>She said the site had resolved close to 800 cases in which the patient has reported the CrowdMed diagnosis was correct.\u003c/p>\n\u003cp>\"The nice thing about not limiting it to physicians,\" Greenwalt said, \"is we get people who are not stuck in the same method of thought training. Or they're not afraid to suggest the rare diagnosis. We see this a lot, where doctors are afraid to say it might be this rare condition.\"\u003c/p>\n\u003cp>A writer who \u003ca href=\"http://www.elle.com/culture/news/a28783/the-crowd-will-see-you-now/\" target=\"_blank\">reviewed C\u003c/a>rowdMed for Elle discovered one of the common pitfalls of self-diagnosis: worrying about a range of diseases she'd never heard of. But she also wrote she felt encouraged to do research about her health and supported by the care people offered in listening to and responding to her case.\u003c/p>\n\u003cp>\"While reporting this piece,\" wrote Molly Langmuir, \"I vacillated between viewing CrowdMed as a dire indictment of our medical system—things are so bad we've had to turn to a bunch of strangers who may or may not have had medical training—and a heartening sign of progress, a surprisingly effective way of putting the 'care' back into health\u003c/p>\n\u003cp>\u003ca href=\"https://www.mygene2.org/MyGene2/\" target=\"_blank\">MyGene2\u003c/a> is another crowdsourcing site. It serves as an information hub where those with rare genetic disorders can share information, and researchers and clinicians working with a particular condition or gene can contact people who may benefit from new treatments or ideas.\u003c/p>\n\u003cp>The site just went live this spring and already features more than 100 families and 87 different problematic genes.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"floatright"},"numeric":["floatright"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>Jon Brooks contributed to this post.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/160842/social-media-uncovers-rare-diagnosis-after-years-of-frustration","authors":["235"],"categories":["futureofyou_1060"],"tags":["futureofyou_914","futureofyou_124","futureofyou_915","futureofyou_916"],"featImg":"futureofyou_161306","label":"futureofyou"}},"programsReducer":{"possible":{"id":"possible","title":"Possible","info":"Possible is hosted by entrepreneur Reid Hoffman and writer Aria Finger. Together in Possible, Hoffman and Finger lead enlightening discussions about building a brighter collective future. The show features interviews with visionary guests like Trevor Noah, Sam Altman and Janette Sadik-Khan. Possible paints an optimistic portrait of the world we can create through science, policy, business, art and our shared humanity. It asks: What if everything goes right for once? How can we get there? Each episode also includes a short fiction story generated by advanced AI GPT-4, serving as a thought-provoking springboard to speculate how humanity could leverage technology for good.","airtime":"SUN 2pm","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/Possible-Podcast-Tile-360x360-1.jpg","officialWebsiteLink":"https://www.possible.fm/","meta":{"site":"news","source":"Possible"},"link":"/radio/program/possible","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/possible/id1677184070","spotify":"https://open.spotify.com/show/730YpdUSNlMyPQwNnyjp4k"}},"1a":{"id":"1a","title":"1A","info":"1A is home to the national conversation. 1A brings on great guests and frames the best debate in ways that make you think, share and engage.","airtime":"MON-THU 11pm-12am","imageSrc":"https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/1a.jpg","officialWebsiteLink":"https://the1a.org/","meta":{"site":"news","source":"npr"},"link":"/radio/program/1a","subscribe":{"npr":"https://rpb3r.app.goo.gl/RBrW","apple":"https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?s=143441&mt=2&id=1188724250&at=11l79Y&ct=nprdirectory","tuneIn":"https://tunein.com/radio/1A-p947376/","rss":"https://feeds.npr.org/510316/podcast.xml"}},"all-things-considered":{"id":"all-things-considered","title":"All Things Considered","info":"Every weekday, \u003cem>All Things Considered\u003c/em> hosts Robert Siegel, Audie Cornish, Ari Shapiro, and Kelly McEvers present the program's trademark mix of news, interviews, commentaries, reviews, and offbeat features. Michel Martin hosts on the weekends.","airtime":"MON-FRI 1pm-2pm, 4:30pm-6:30pm\u003cbr />SAT-SUN 5pm-6pm","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/All-Things-Considered-Podcast-Tile-360x360-1.jpg","officialWebsiteLink":"https://www.npr.org/programs/all-things-considered/","meta":{"site":"news","source":"npr"},"link":"/radio/program/all-things-considered"},"american-suburb-podcast":{"id":"american-suburb-podcast","title":"American Suburb: The Podcast","tagline":"The flip side of gentrification, told through one town","info":"Gentrification is changing cities across America, forcing people from neighborhoods they have long called home. Call them the displaced. Now those priced out of the Bay Area are looking for a better life in an unlikely place. American Suburb follows this migration to one California town along the Delta, 45 miles from San Francisco. But is this once sleepy suburb ready for them?","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/American-Suburb-Podcast-Tile-703x703-1.jpg","officialWebsiteLink":"/news/series/american-suburb-podcast","meta":{"site":"news","source":"kqed","order":"13"},"link":"/news/series/american-suburb-podcast/","subscribe":{"npr":"https://rpb3r.app.goo.gl/RBrW","apple":"https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?mt=2&id=1287748328","tuneIn":"https://tunein.com/radio/American-Suburb-p1086805/","rss":"https://ww2.kqed.org/news/series/american-suburb-podcast/feed/podcast","google":"https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkMzMDExODgxNjA5"}},"baycurious":{"id":"baycurious","title":"Bay Curious","tagline":"Exploring the Bay Area, one question at a time","info":"KQED’s new podcast, Bay Curious, gets to the bottom of the mysteries — both profound and peculiar — that give the Bay Area its unique identity. And we’ll do it with your help! You ask the questions. You decide what Bay Curious investigates. 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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/2024/04/Mindshift-Podcast-Tile-703x703-1.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. 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On Our Watch brings listeners into the rooms where officers are questioned and witnesses are interrogated to find out who this system is really protecting. 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