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"content": "\u003cp>By now you have heard about \u003ca href=\"https://ww2.kqed.org/futureofyou/2017/11/15/explainer-the-new-gene-editing-tool-significantly-more-precise-than-crispr/\">CRISPR/Cas9\u003c/a>. This is the revolutionary new way to fix genes in most any living thing, including people. It has already transformed biological research and is poised to do the same in curing genetic disease.\u003c/p>\n\u003cp>And now you can see a part of the process actually happening in living color, in a direct observation of the enzyme Cas9 cutting a strand of DNA.\u003c/p>\n\u003cp>https://twitter.com/hnisimasu/status/928933260159197184\u003c/p>\n\u003cp>The yellow blob is Cas9, which gets the ball rolling on editing a gene, and the long strands of orange are the DNA. Here, Cas9 scans for the right spot on the DNA to make an incision, then around 30 seconds in makes the cut, creating “cleaved DNA.” The next step for a successful edit would be for the cell’s internal machinery, in the process of mending the cut, to replace the surrounding DNA, hopefully correcting a disease-causing genetic mutation.\u003c/p>\n\u003cp>Researcher Osamu Nureki “filmed” this action by moving a tiny needle back and forth across Cas9. This imaging process is called\u003ca href=\"https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-16712-6_478\" target=\"_blank\" rel=\"noopener\"> high‐speed atomic‐force microscopy\u003c/a>.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>What makes it especially satisfying as a scientist is to see the CRISPR/Cas9 system work its magic, with my own eyes. How processes like gene editing work are, for the most part, inferred indirectly from experiments. To actually see Cas9 do its job is a bit mind-blowing.\u003c/p>\n\u003cp>As a scientist, I find this video unbearably cool.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>\u003cspan style=\"font-weight: 400\">Dr. Barry Starr is a scientist in the\u003c/span>\u003ca href=\"https://med.stanford.edu/genetics.html\"> \u003cspan style=\"font-weight: 400\">Department of Genetics\u003c/span>\u003c/a>\u003cspan style=\"font-weight: 400\"> at Stanford University who runs the\u003c/span>\u003ca href=\"https://med.stanford.edu/genetics/tech.html\"> \u003cspan style=\"font-weight: 400\">Stanford at The Tech\u003c/span>\u003c/a>\u003cspan style=\"font-weight: 400\"> program and the\u003c/span>\u003ca href=\"http://genetics.thetech.org/\"> \u003cspan style=\"font-weight: 400\">Understanding Genetics\u003c/span>\u003c/a>\u003cspan style=\"font-weight: 400\"> website with\u003c/span>\u003ca href=\"https://www.thetech.org/\"> \u003cspan style=\"font-weight: 400\">The Tech Museum of Innovation\u003c/span>\u003c/a>\u003cspan style=\"font-weight: 400\"> in San Jose CA. Before running the program, he worked as a research scientist in the biotechnology field. \u003c/span>\u003c/em>\u003c/p>\n\n",
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"content": "\u003cp>Scientists have created a stable organism containing DNA most likely never seen before on Earth\u003cb>.\u003c/b>\u003c/p>\n\u003cp>The intention was to create \"organisms with wholly unnatural attributes and traits not found elsewhere in nature,” as one of the researchers put it. With more advances, these organisms could potentially be used in the creation of medicines and industrial biologicals.\u003c/p>\n\u003cp>The development is described in a \u003ca href=\"http://www.pnas.org/content/early/2017/01/17/1616443114\" target=\"_blank\">new study\u003c/a> published in Proceedings of the National Academy of Sciences.\u003c/p>\n\u003cp>\u003cstrong>Synthetic DNA\u003c/strong>\u003c/p>\n\u003cp>The building blocks of DNA, and thus of all life on Earth, are represented by a four-letter \"alphabet.\" Each letter represents one of the compounds that form DNA. The letters—A, T, C and G—are used in different combinations to encode the instructions that govern the development and traits of living organisms.\u003c/p>\n\u003caside class=\"pullquote alignright\">'We can now get the light of life to stay on. That suggests that all of life's processes can be subject to manipulation.'\u003c/aside>\n\u003cp>Just as scrawled graffiti, a Harlequin romance and a Shakespeare play are written using the same alphabet, so too are a virus, a pig and a human being written with the same set of four bases.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>That started to change \u003ca href=\"https://ww2.kqed.org/science/2014/05/19/dna-adding-two-letters-to-lifes-alphabet/\" target=\"_blank\">back in 2014\u003c/a>, when a group of researchers at The Scripps Research Institute synthesized two new letters, then managed to coax E.coli bacteria into accepting them\u003cstrong>. \u003c/strong>While that was a significant achievement, the bacteria was not ideal and suffered from multiple problems including a tendency not to pass the new letters on to the next generation. Since the artificial bases were not stable in the DNA, they were lost over time.\u003c/p>\n\u003cp>\u003cstrong>Back to the Beginning for CRISPR\u003c/strong>\u003c/p>\n\u003cfigure id=\"attachment_325792\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg class=\"size-medium wp-image-325792\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2017/01/CRISPR800a-800x533.jpg\" alt=\"Back to basics for CRISPR/Cas9.\" width=\"800\" height=\"533\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a.jpg 800w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a-160x107.jpg 160w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a-768x512.jpg 768w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a-240x160.jpg 240w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a-375x250.jpg 375w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a-520x346.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">Back to basics for CRISPR/Cas9. \u003ccite>(Wikipedia)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>One of the ways these researchers managed to get the bacteria to hold on to these new letters was by using one of the biggest things to hit biology in the last few years—the \u003ca href=\"http://genetics.thetech.org/ask-a-geneticist/why-crispr-revolutionary-and-how-it-works\">gene-editing system CRISPR/Cas9\u003c/a>. This tool provides a way to precisely change the DNA of a living thing. It has already revolutionized science in the lab and may one day revolutionize human health as well.\u003c/p>\n\u003cp>CRISPR/Cas9 has a very humble origin—it works as an immune system for bacteria. It essentially looks for a certain set of bases found in an invading virus's DNA and cuts the viral DNA at that spot. This destroys the virus.\u003c/p>\n\u003cp>In creating their new organism, the researchers have taken CRISPR/Cas9 back to its original use. But instead of cutting the DNA of invading viruses, CRISPR/Cas9 now cuts the bacterial DNA, which kills the bacteria. Sounds self-defeating, except that it only does this if the bacteria has lost its new letters.\u003c/p>\n\u003cp>That means the bacteria that pass on the new letters thrive and continue to divide, while the letter-losing bacteria are wiped out. Now, generation after generation, only bacteria with the new bases are produced.\u003c/p>\n\u003cp>Of course this wouldn’t be all that efficient if the majority of bacteria lost the artificial bases and so died--there wouldn't be enough bacteria to do anything with.\u003c/p>\n\u003cfigure id=\"attachment_325790\" class=\"wp-caption alignright\" style=\"max-width: 400px\">\u003cimg class=\"size-full wp-image-325790\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2017/01/DNaM-skeletal.png\" alt=\"Say hello to dNaM, one of DNA's first new letters in 3.5 billion years or so. \" width=\"400\" height=\"436\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2017/01/DNaM-skeletal.png 400w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/DNaM-skeletal-160x174.png 160w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/DNaM-skeletal-240x262.png 240w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/DNaM-skeletal-375x409.png 375w\" sizes=\"(max-width: 400px) 100vw, 400px\">\u003cfigcaption class=\"wp-caption-text\">Say hello to dNaM, one of DNA's first new letters in 3.5 billion years or so. \u003ccite>(Wikipedia)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>To make it more likely that the bacteria hold onto their new bases, these researchers also chemically modified one of the bases to something the bacteria liked better. Now the bacteria are more likely to keep these bases, but if they do lose them, they are eliminated from the population. Such an elegant solution!\u003c/p>\n\u003cp>Though the bacteria has successfully incorporated the new letters, it is not actually using them, because the cellular machinery can’t decipher what the letters mean.\u003c/p>\n\u003cp>Scientists hope that won't always be the case. They intend on tweaking the bacteria so they can make sense of the new letters. Then the new organisms could be crafted into something useful. Down the line, researchers could also figure out how to expand the alphabet of more complex organisms.\u003c/p>\n\u003cp>Even if the bacteria the researchers experimented on isn’t yet ready for primetime, it is very cool in that it probably does things that life on Earth has never done before. Which is still a marvel for all science lovers out there.\u003c/p>\n\u003cp>Said one of the scientists, in a statement:\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"We can now get the light of life to stay on. That suggests that all of life's processes can be subject to manipulation.\"\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Scientists have created a stable organism containing DNA most likely never seen before on Earth\u003cb>.\u003c/b>\u003c/p>\n\u003cp>The intention was to create \"organisms with wholly unnatural attributes and traits not found elsewhere in nature,” as one of the researchers put it. With more advances, these organisms could potentially be used in the creation of medicines and industrial biologicals.\u003c/p>\n\u003cp>The development is described in a \u003ca href=\"http://www.pnas.org/content/early/2017/01/17/1616443114\" target=\"_blank\">new study\u003c/a> published in Proceedings of the National Academy of Sciences.\u003c/p>\n\u003cp>\u003cstrong>Synthetic DNA\u003c/strong>\u003c/p>\n\u003cp>The building blocks of DNA, and thus of all life on Earth, are represented by a four-letter \"alphabet.\" Each letter represents one of the compounds that form DNA. The letters—A, T, C and G—are used in different combinations to encode the instructions that govern the development and traits of living organisms.\u003c/p>\n\u003caside class=\"pullquote alignright\">'We can now get the light of life to stay on. That suggests that all of life's processes can be subject to manipulation.'\u003c/aside>\n\u003cp>Just as scrawled graffiti, a Harlequin romance and a Shakespeare play are written using the same alphabet, so too are a virus, a pig and a human being written with the same set of four bases.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>That started to change \u003ca href=\"https://ww2.kqed.org/science/2014/05/19/dna-adding-two-letters-to-lifes-alphabet/\" target=\"_blank\">back in 2014\u003c/a>, when a group of researchers at The Scripps Research Institute synthesized two new letters, then managed to coax E.coli bacteria into accepting them\u003cstrong>. \u003c/strong>While that was a significant achievement, the bacteria was not ideal and suffered from multiple problems including a tendency not to pass the new letters on to the next generation. Since the artificial bases were not stable in the DNA, they were lost over time.\u003c/p>\n\u003cp>\u003cstrong>Back to the Beginning for CRISPR\u003c/strong>\u003c/p>\n\u003cfigure id=\"attachment_325792\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg class=\"size-medium wp-image-325792\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2017/01/CRISPR800a-800x533.jpg\" alt=\"Back to basics for CRISPR/Cas9.\" width=\"800\" height=\"533\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a.jpg 800w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a-160x107.jpg 160w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a-768x512.jpg 768w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a-240x160.jpg 240w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a-375x250.jpg 375w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/CRISPR800a-520x346.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">Back to basics for CRISPR/Cas9. \u003ccite>(Wikipedia)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>One of the ways these researchers managed to get the bacteria to hold on to these new letters was by using one of the biggest things to hit biology in the last few years—the \u003ca href=\"http://genetics.thetech.org/ask-a-geneticist/why-crispr-revolutionary-and-how-it-works\">gene-editing system CRISPR/Cas9\u003c/a>. This tool provides a way to precisely change the DNA of a living thing. It has already revolutionized science in the lab and may one day revolutionize human health as well.\u003c/p>\n\u003cp>CRISPR/Cas9 has a very humble origin—it works as an immune system for bacteria. It essentially looks for a certain set of bases found in an invading virus's DNA and cuts the viral DNA at that spot. This destroys the virus.\u003c/p>\n\u003cp>In creating their new organism, the researchers have taken CRISPR/Cas9 back to its original use. But instead of cutting the DNA of invading viruses, CRISPR/Cas9 now cuts the bacterial DNA, which kills the bacteria. Sounds self-defeating, except that it only does this if the bacteria has lost its new letters.\u003c/p>\n\u003cp>That means the bacteria that pass on the new letters thrive and continue to divide, while the letter-losing bacteria are wiped out. Now, generation after generation, only bacteria with the new bases are produced.\u003c/p>\n\u003cp>Of course this wouldn’t be all that efficient if the majority of bacteria lost the artificial bases and so died--there wouldn't be enough bacteria to do anything with.\u003c/p>\n\u003cfigure id=\"attachment_325790\" class=\"wp-caption alignright\" style=\"max-width: 400px\">\u003cimg class=\"size-full wp-image-325790\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2017/01/DNaM-skeletal.png\" alt=\"Say hello to dNaM, one of DNA's first new letters in 3.5 billion years or so. \" width=\"400\" height=\"436\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2017/01/DNaM-skeletal.png 400w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/DNaM-skeletal-160x174.png 160w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/DNaM-skeletal-240x262.png 240w, https://ww2.kqed.org/app/uploads/sites/13/2017/01/DNaM-skeletal-375x409.png 375w\" sizes=\"(max-width: 400px) 100vw, 400px\">\u003cfigcaption class=\"wp-caption-text\">Say hello to dNaM, one of DNA's first new letters in 3.5 billion years or so. \u003ccite>(Wikipedia)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>To make it more likely that the bacteria hold onto their new bases, these researchers also chemically modified one of the bases to something the bacteria liked better. Now the bacteria are more likely to keep these bases, but if they do lose them, they are eliminated from the population. Such an elegant solution!\u003c/p>\n\u003cp>Though the bacteria has successfully incorporated the new letters, it is not actually using them, because the cellular machinery can’t decipher what the letters mean.\u003c/p>\n\u003cp>Scientists hope that won't always be the case. They intend on tweaking the bacteria so they can make sense of the new letters. Then the new organisms could be crafted into something useful. Down the line, researchers could also figure out how to expand the alphabet of more complex organisms.\u003c/p>\n\u003cp>Even if the bacteria the researchers experimented on isn’t yet ready for primetime, it is very cool in that it probably does things that life on Earth has never done before. Which is still a marvel for all science lovers out there.\u003c/p>\n\u003cp>Said one of the scientists, in a statement:\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"We can now get the light of life to stay on. That suggests that all of life's processes can be subject to manipulation.\"\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>Have pity on those poor parents desperately trying to coax a protesting toddler to eat something she has pushed away in disgust. While moms and dads may fault themselves for an inability to evoke the magic words that will open-sesame their offspring's mouth, it turns out there's a good chance some of that child's -- er, shall we say \"discretion\" -- is innate.\u003c/p>\n\u003caside class=\"pullquote alignright\">Parents who model good eating habits and avoid conflict at the table do better at getting their kids to eat foods they find unappealing. Two weeks of exposure to vegetables -- with a reward -- has also been shown to work.\u003c/aside>\n\u003cp>Once again, it's in the genes.\u003c/p>\n\u003cp>A new \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/27739065\" target=\"_blank\">study \u003c/a>concludes that around half of toddlers' fussiness probably is genetically determined. Researchers at University College London looked at 1,932 Welsh and English twin pairs and their families. When the children were 16 months old, the parents were given the 35-item \u003ca href=\"https://www.ucl.ac.uk/hbrc/resources/resources_eb/CEBQwithscores.pdf\">Child Eating Behaviour Questionnaire\u003c/a> as a gauge of how fussy each child was about food.\u003c/p>\n\u003cp>To figure out how much of this behavior was genetic, the researchers looked at 626 identical twin pairs to see how often both children scored similarly on the questionnaire. Since identical twins essentially have the same DNA, both children will exhibit a purely genetic trait -- every time.\u003c/p>\n\u003cp>This is not what the researchers found. While the identical twins often shared the same level of food fussiness, it did not occur 100 percent of the time.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>So genetics appears not to be the whole story: It could be the twins’ shared environment accounts for their similar but not identical eating habits.\u003c/p>\n\u003cp>To test the role of environment in shaping the toddlers' pickiness, the study also\u003cstrong> \u003c/strong>looked at\u003cstrong> \u003c/strong>1,306 pairs of fraternal twins, who share the same amount of DNA as any two siblings—around 50 percent on average.\u003c/p>\n\u003cp>If something is purely environmental, two twins in a fraternal pair should share the same trait as often as two twins in an identical pair. The researchers found that this was not the case. The fraternal twins were actually less likely to share the same eating behavior compared to identical twins.\u003c/p>\n\u003cp>This study suggests that both genetics \u003cem>and\u003c/em> the environment play a role in food fussiness. After crunching the data, the researchers conclude that each accounts for somewhere between 41 and 52 percent of the behavior.\u003c/p>\n\u003cp>\u003cstrong>Getting Your Toddler to Eat\u003c/strong>\u003c/p>\n\u003cp>But enough with the numbers. The takeaway for parents: Don't give up hope that you can have an influence on what your fussy children are willing to eat. Skillful parenting can make a difference if you start early, and the sooner the better.\u003c/p>\n\u003cp>For example, a \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2530930/\">study \u003c/a>from 2005 suggested that parents could best affect their children's eating habits by eating well themselves and avoiding conflicts at the dinner table.\u003c/p>\n\u003caside class=\"alignright\">\u003cspan style=\"font-weight: normal\">\u003cstrong>A note about twin studies\u003c/strong>\u003cbr>\nThere is some \u003ca href=\"https://www.madinamerica.com/2013/03/the-trouble-with-twin-studies/\" target=\"_blank\">debate\u003c/a> about how well studies of identical versus fraternal twins determine the level of genetic influence in a particular trait. These comparisons rely on the assumption that the shared environment of fraternal twins is the same as the shared environment of identical twins. The potential flaw is that identical twins may be treated more alike than fraternal twins. If that is true, twin studies would \u003cem>overestimate\u003c/em> the role of genetics, as environmental factors could be the real reason for greater levels of similarity in identical twins.\u003c/span>\u003c/aside>\n\u003cp>These researchers examined the eating habits of 173 girls, once when they were 7 years old and again when they were 9. At both junctures, the parents were interviewed to understand both their eating habits and how they tried to encourage their daughters to eat healthier foods.\u003c/p>\n\u003cp>The results showed that modeling food behaviors worked far better than trying to force a child to eat better. In other words: Don't preach broccoli when you're sneaking hot dogs yourself.\u003c/p>\n\u003cp>Another \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4037818/\">study \u003c/a>from University College London, this one from 2014, suggests an alternative to pitched battles at the dinner table. Try repeatedly exposing your children to a food they dislike and reward offer a reward when they venture a bite.\u003c/p>\n\u003cp>This approach can pay off big. The researchers had parents offer a small bite of a \"target vegetable\" that their three-year-olds didn’t like each day for 14 days. If the children ate it, they were rewarded with a sticker.\u003c/p>\n\u003cp>After two weeks of repeated exposure and reward, only around 13 percent of these kids still said they disliked the food.\u003c/p>\n\u003cp>That's a big contrast to the control group, for which no instructions were issued. A whopping 90 percent of these kids still would not unclamp their jaws and eat the yucky food at the end of the trial period.\u003c/p>\n\u003cp>So a little bit of parental effort and some stickers can go a long way. Genetics plays a big role in kids' fussiness but it isn't the only factor. If parents eat a wide variety of food and patiently keep offering new foods to their kids, these parents may end up with less fussy kids.\u003c/p>\n\u003cp>Or ... you could do it this way:\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>https://www.youtube.com/watch?v=KNNpydUfduo\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Have pity on those poor parents desperately trying to coax a protesting toddler to eat something she has pushed away in disgust. While moms and dads may fault themselves for an inability to evoke the magic words that will open-sesame their offspring's mouth, it turns out there's a good chance some of that child's -- er, shall we say \"discretion\" -- is innate.\u003c/p>\n\u003caside class=\"pullquote alignright\">Parents who model good eating habits and avoid conflict at the table do better at getting their kids to eat foods they find unappealing. Two weeks of exposure to vegetables -- with a reward -- has also been shown to work.\u003c/aside>\n\u003cp>Once again, it's in the genes.\u003c/p>\n\u003cp>A new \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/27739065\" target=\"_blank\">study \u003c/a>concludes that around half of toddlers' fussiness probably is genetically determined. Researchers at University College London looked at 1,932 Welsh and English twin pairs and their families. When the children were 16 months old, the parents were given the 35-item \u003ca href=\"https://www.ucl.ac.uk/hbrc/resources/resources_eb/CEBQwithscores.pdf\">Child Eating Behaviour Questionnaire\u003c/a> as a gauge of how fussy each child was about food.\u003c/p>\n\u003cp>To figure out how much of this behavior was genetic, the researchers looked at 626 identical twin pairs to see how often both children scored similarly on the questionnaire. Since identical twins essentially have the same DNA, both children will exhibit a purely genetic trait -- every time.\u003c/p>\n\u003cp>This is not what the researchers found. While the identical twins often shared the same level of food fussiness, it did not occur 100 percent of the time.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>So genetics appears not to be the whole story: It could be the twins’ shared environment accounts for their similar but not identical eating habits.\u003c/p>\n\u003cp>To test the role of environment in shaping the toddlers' pickiness, the study also\u003cstrong> \u003c/strong>looked at\u003cstrong> \u003c/strong>1,306 pairs of fraternal twins, who share the same amount of DNA as any two siblings—around 50 percent on average.\u003c/p>\n\u003cp>If something is purely environmental, two twins in a fraternal pair should share the same trait as often as two twins in an identical pair. The researchers found that this was not the case. The fraternal twins were actually less likely to share the same eating behavior compared to identical twins.\u003c/p>\n\u003cp>This study suggests that both genetics \u003cem>and\u003c/em> the environment play a role in food fussiness. After crunching the data, the researchers conclude that each accounts for somewhere between 41 and 52 percent of the behavior.\u003c/p>\n\u003cp>\u003cstrong>Getting Your Toddler to Eat\u003c/strong>\u003c/p>\n\u003cp>But enough with the numbers. The takeaway for parents: Don't give up hope that you can have an influence on what your fussy children are willing to eat. Skillful parenting can make a difference if you start early, and the sooner the better.\u003c/p>\n\u003cp>For example, a \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2530930/\">study \u003c/a>from 2005 suggested that parents could best affect their children's eating habits by eating well themselves and avoiding conflicts at the dinner table.\u003c/p>\n\u003caside class=\"alignright\">\u003cspan style=\"font-weight: normal\">\u003cstrong>A note about twin studies\u003c/strong>\u003cbr>\nThere is some \u003ca href=\"https://www.madinamerica.com/2013/03/the-trouble-with-twin-studies/\" target=\"_blank\">debate\u003c/a> about how well studies of identical versus fraternal twins determine the level of genetic influence in a particular trait. These comparisons rely on the assumption that the shared environment of fraternal twins is the same as the shared environment of identical twins. The potential flaw is that identical twins may be treated more alike than fraternal twins. If that is true, twin studies would \u003cem>overestimate\u003c/em> the role of genetics, as environmental factors could be the real reason for greater levels of similarity in identical twins.\u003c/span>\u003c/aside>\n\u003cp>These researchers examined the eating habits of 173 girls, once when they were 7 years old and again when they were 9. At both junctures, the parents were interviewed to understand both their eating habits and how they tried to encourage their daughters to eat healthier foods.\u003c/p>\n\u003cp>The results showed that modeling food behaviors worked far better than trying to force a child to eat better. In other words: Don't preach broccoli when you're sneaking hot dogs yourself.\u003c/p>\n\u003cp>Another \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4037818/\">study \u003c/a>from University College London, this one from 2014, suggests an alternative to pitched battles at the dinner table. Try repeatedly exposing your children to a food they dislike and reward offer a reward when they venture a bite.\u003c/p>\n\u003cp>This approach can pay off big. The researchers had parents offer a small bite of a \"target vegetable\" that their three-year-olds didn’t like each day for 14 days. If the children ate it, they were rewarded with a sticker.\u003c/p>\n\u003cp>After two weeks of repeated exposure and reward, only around 13 percent of these kids still said they disliked the food.\u003c/p>\n\u003cp>That's a big contrast to the control group, for which no instructions were issued. A whopping 90 percent of these kids still would not unclamp their jaws and eat the yucky food at the end of the trial period.\u003c/p>\n\u003cp>So a little bit of parental effort and some stickers can go a long way. Genetics plays a big role in kids' fussiness but it isn't the only factor. If parents eat a wide variety of food and patiently keep offering new foods to their kids, these parents may end up with less fussy kids.\u003c/p>\n\u003cp>Or ... you could do it this way:\u003c/p>\n\u003cp>\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/KNNpydUfduo'\n title='//www.youtube.com/embed/KNNpydUfduo'\n allowfullscreen='true'\n style='border:0;'>\u003c/iframe>\n \u003c/span>\n \u003c/span>\u003c/p>\u003cp>\n\u003c/div>\u003c/p>",
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"content": "\u003cp>A recent study making \u003ca href=\"https://ww2.kqed.org/futureofyou/2016/08/24/with-gene-test-some-breast-cancer-patients-can-skip-chemo-study/\" target=\"_blank\">headlines\u003c/a> around the world found that some early-stage breast cancer patients could avoid chemotherapy with only a slightly higher risk of the cancer recurring and spreading than those who underwent the treatment.\u003c/p>\n\u003caside class=\"pullquote alignright\">There is often potential variation in study numbers that make the headlines.\u003c/aside>\n\u003cp>The study found that after five years, women with a particular genetic profile--uncovered in a genetic test--fared hardly any better after chemo than woman who skipped the treatment.\u003c/p>\n\u003cp>The cancer failed to spread in 95.9 percent of the women who received chemotherapy, compared to 94.5 percent of those who went without it.\u003c/p>\n\u003cp>This appears to mean that if you have the right genetic profile, you would be taking on only a 1.5 percent greater risk by avoiding a costly treatment known for side effects such as hair loss, mouth sores, diarrhea and, in rare cases, leukemia or other diseases.\u003c/p>\n\u003cp>[contextly_sidebar id=\"umpVHsLRM86oNnIerZgYm9lySd4eYGjp\"]Deanna Attai, assistant clinical professor of surgery at the David Geffen School of Medicine at the University of California, Los Angeles, told Health News Review that one of her takeaways from the study was that it is \"very clear that not all patients benefit from chemotherapy. Our old habit of recommending chemotherapy 'just to be sure' is not appropriate.\"\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>While that may be true for some clinicians and patients, a close look at the study results shows there is more potential variation in the risk rates than the headline number of 1.5 percent suggests.\u003c/p>\n\u003cp>That's because the narrow, 1.5 percent difference between the two groups could be just \u003ca href=\"http://www.wisegeek.com/what-is-statistical-noise.htm\" target=\"_blank\">statistical noise\u003c/a>--a random variation that would not be duplicated if the experiment were run again. If and when someone replicates this study, it could turn out that women who get chemo might do a bit worse or might do a bit better. And the same is true for women who don't get chemo.\u003c/p>\n\u003cp>How would you know that?\u003c/p>\n\u003cp>You'd have to look for two numbers that are sometimes deep in the data. These numbers are really different sides of the same coin and are related to each other. These two measures can often give you some idea about how significant a result really is.\u003c/p>\n\u003cp>\u003cstrong>Are the Results Significant?\u003c/strong>\u003c/p>\n\u003cp>One way to tell if a result is significant--meaning not due to chance-- is by looking for the number that tells you how likely it is the result is random. That number is called the p-value.\u003c/p>\n\u003cfigure id=\"attachment_234680\" class=\"wp-caption alignright\" style=\"max-width: 800px\">\u003ca href=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/08/ChemoNCI.jpg\">\u003cimg class=\"wp-image-234680 size-medium\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/08/ChemoNCI-800x475.jpg\" alt=\"Woman receiving chemotherapy.\" width=\"800\" height=\"475\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Woman receiving chemotherapy.\u003c/figcaption>\u003c/figure>\n\u003cp>A p-value of 0.1 means there is a 10 percent chance the result happened randomly. A 0.2 translates into a 20 percent chance the result is random, and so on. Scientists have decided that in most experiments, a result is significant if the p-value is less than 0.05. (Though this threshold of validity is not without \u003ca href=\"http://amstat.tandfonline.com/doi/abs/10.1080/00031305.2016.1154108\" target=\"_blank\">controversy\u003c/a>.)\u003c/p>\n\u003cp>So when trying to determine the significance of a particular result, you should look for the p-value that's associated with it. Ideally you want this number to be lower than 0.05. Anything much higher could be a red flag.\u003c/p>\n\u003cp>In the breast cancer study, it turns out that the p-value for the 1.5 percent lower risk offered by chemotherapy is 0.27. That is very high for a scientific study. It means there is a 27 percent chance the result was random.\u003c/p>\n\u003cp>\"That is pretty highly insignificant,\" Susan Wei, an assistant professor in the Division of Biostatistics at the University of Minnesota, told \u003ca href=\"http://www.healthnewsreview.org/2016/08/much-significance-health-news-give-statistically-nonsignificant-results-case-study-stories-skipping-breast-cancer-chemo/\" target=\"_blank\">Health News Review\u003c/a>.\u003c/p>\n\u003cp>In other words, the study can’t say with certainty that a woman who chooses not to have chemo actually takes on only a 1.5 percent higher risk. The risk could be somewhat higher or lower, and this may or may not make a difference in someone's treatment decisions.\u003c/p>\n\u003cp>\u003cstrong>How Confident Can You Be in the Results?\u003c/strong>\u003c/p>\n\u003cp>Another way to evaluate a result involves looking at how confident researchers are that they would get the same result if they repeated the experiment. This is another way of asking whether or not the study is relevant for a broader population.\u003c/p>\n\u003cp>This measure is called the \"95 percent confidence interval,\" or CI.\u003c/p>\n\u003cp>The CI tells you that 95 percent of the time, when the experiment is repeated, the result will fall between a specific range of numbers. Ideally, you want this range to be small. The wider the range of possible results, the less confidence the researcher can have in the particular result they got.\u003c/p>\n\u003cp>It's something like the margin of error in a poll: If it's too great, it will put the outcome in doubt.\u003c/p>\n\u003cp>Let's take a made-up poll that shows Hillary Clinton beating Donald Trump 40-33. That sounds very good for Clinton supporters. But if the margin of error were 10 percent, that would mean the poll results could actually be 50-23 in favor of Clinton or 30-43 in favor of Trump. When the margin of error is so large it can swing the outcome in the opposite direction, that means the poll results are statistically in question.\u003c/p>\n\u003cp>If the margin of error were only, say, three percent, the narrowest lead Clinton could have would be 37 to 36; there is no potential change in the outcome -- she still wins.\u003c/p>\n\u003cp>Now let's look at the breast cancer study.\u003c/p>\n\u003cp>Of the women who received chemo, 95.9 percent of them made it to the 5-year mark with no breast cancer spreading.\u003c/p>\n\u003cp>But a more complete reporting of the results shows the CI for that group of women is a range between 94 and 97.2 percent. That means if someone repeats the experiment, the number of women who receive chemo and make it five years with no cancer spreading could be anywhere between 94 and 97.2 percent. So the benefit of getting chemo could be higher or lower than the study suggests.\u003c/p>\n\u003cp>For the women who didn't get chemo, the CI is between 92.3 and 95.9 percent.\u003c/p>\n\u003cp>Chemo: 94 to 97.2 percent\u003c/p>\n\u003cp>No Chemo: 92.3 to 95.9 percent\u003c/p>\n\u003cp>It means the study isn't able to say that if you have a particular genetic profile, you can avoid chemotherapy and do just as well after five years as women who get chemo. You can't know the answer to that because the possible results have such a wide range and overlap that they can even swing the outcome in the opposite direction:\u003c/p>\n\u003cp>\u003c!-- iframe plugin v.4.3 wordpress.org/plugins/iframe/ -->\u003cbr>\n\u003ciframe id=\"datawrapper-chart-eJ9aC\" src=\"//datawrapper.dwcdn.net/eJ9aC/3/\" frameborder=\"0\" allowtransparency=\"true\" allowfullscreen=\"allowfullscreen\" webkitallowfullscreen=\"webkitallowfullscreen\" mozallowfullscreen=\"mozallowfullscreen\" oallowfullscreen=\"oallowfullscreen\" msallowfullscreen=\"msallowfullscreen\" width=\"100%\" height=\"230\" scrolling=\"yes\" class=\"iframe-class\">\u003c/iframe>\u003c/p>\n\u003cp>Bottom line, the CI tells you the study can't say whether or not women with this particular genetic profile can safely avoid chemo and do almost as well five years later as those who got chemo. Researchers would need to repeat the experiment, maybe several times, maybe with a larger group or by making other changes, to get a more confident answer.\u003c/p>\n\u003cp>That doesn't make this a bad study; it still showed that a lot of women with a certain genetic profile did not have their cancer spread despite foregoing chemo. However, the results still need to be more firmly proved.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>Attai, the UCLA surgery professor, told Health News Review: \"Studies like these often raise more questions and prompt discussion. It is important to note that we do not yet have the 'crystal ball' that will tell an individual patient with absolute certainty that their cancer will recur or not. We are closer than we’ve ever been, but we do not have a test that will predict the outcome with 100 percent certainty.\"\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>A recent study making \u003ca href=\"https://ww2.kqed.org/futureofyou/2016/08/24/with-gene-test-some-breast-cancer-patients-can-skip-chemo-study/\" target=\"_blank\">headlines\u003c/a> around the world found that some early-stage breast cancer patients could avoid chemotherapy with only a slightly higher risk of the cancer recurring and spreading than those who underwent the treatment.\u003c/p>\n\u003caside class=\"pullquote alignright\">There is often potential variation in study numbers that make the headlines.\u003c/aside>\n\u003cp>The study found that after five years, women with a particular genetic profile--uncovered in a genetic test--fared hardly any better after chemo than woman who skipped the treatment.\u003c/p>\n\u003cp>The cancer failed to spread in 95.9 percent of the women who received chemotherapy, compared to 94.5 percent of those who went without it.\u003c/p>\n\u003cp>This appears to mean that if you have the right genetic profile, you would be taking on only a 1.5 percent greater risk by avoiding a costly treatment known for side effects such as hair loss, mouth sores, diarrhea and, in rare cases, leukemia or other diseases.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>Deanna Attai, assistant clinical professor of surgery at the David Geffen School of Medicine at the University of California, Los Angeles, told Health News Review that one of her takeaways from the study was that it is \"very clear that not all patients benefit from chemotherapy. Our old habit of recommending chemotherapy 'just to be sure' is not appropriate.\"\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>While that may be true for some clinicians and patients, a close look at the study results shows there is more potential variation in the risk rates than the headline number of 1.5 percent suggests.\u003c/p>\n\u003cp>That's because the narrow, 1.5 percent difference between the two groups could be just \u003ca href=\"http://www.wisegeek.com/what-is-statistical-noise.htm\" target=\"_blank\">statistical noise\u003c/a>--a random variation that would not be duplicated if the experiment were run again. If and when someone replicates this study, it could turn out that women who get chemo might do a bit worse or might do a bit better. And the same is true for women who don't get chemo.\u003c/p>\n\u003cp>How would you know that?\u003c/p>\n\u003cp>You'd have to look for two numbers that are sometimes deep in the data. These numbers are really different sides of the same coin and are related to each other. These two measures can often give you some idea about how significant a result really is.\u003c/p>\n\u003cp>\u003cstrong>Are the Results Significant?\u003c/strong>\u003c/p>\n\u003cp>One way to tell if a result is significant--meaning not due to chance-- is by looking for the number that tells you how likely it is the result is random. That number is called the p-value.\u003c/p>\n\u003cfigure id=\"attachment_234680\" class=\"wp-caption alignright\" style=\"max-width: 800px\">\u003ca href=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/08/ChemoNCI.jpg\">\u003cimg class=\"wp-image-234680 size-medium\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/08/ChemoNCI-800x475.jpg\" alt=\"Woman receiving chemotherapy.\" width=\"800\" height=\"475\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Woman receiving chemotherapy.\u003c/figcaption>\u003c/figure>\n\u003cp>A p-value of 0.1 means there is a 10 percent chance the result happened randomly. A 0.2 translates into a 20 percent chance the result is random, and so on. Scientists have decided that in most experiments, a result is significant if the p-value is less than 0.05. (Though this threshold of validity is not without \u003ca href=\"http://amstat.tandfonline.com/doi/abs/10.1080/00031305.2016.1154108\" target=\"_blank\">controversy\u003c/a>.)\u003c/p>\n\u003cp>So when trying to determine the significance of a particular result, you should look for the p-value that's associated with it. Ideally you want this number to be lower than 0.05. Anything much higher could be a red flag.\u003c/p>\n\u003cp>In the breast cancer study, it turns out that the p-value for the 1.5 percent lower risk offered by chemotherapy is 0.27. That is very high for a scientific study. It means there is a 27 percent chance the result was random.\u003c/p>\n\u003cp>\"That is pretty highly insignificant,\" Susan Wei, an assistant professor in the Division of Biostatistics at the University of Minnesota, told \u003ca href=\"http://www.healthnewsreview.org/2016/08/much-significance-health-news-give-statistically-nonsignificant-results-case-study-stories-skipping-breast-cancer-chemo/\" target=\"_blank\">Health News Review\u003c/a>.\u003c/p>\n\u003cp>In other words, the study can’t say with certainty that a woman who chooses not to have chemo actually takes on only a 1.5 percent higher risk. The risk could be somewhat higher or lower, and this may or may not make a difference in someone's treatment decisions.\u003c/p>\n\u003cp>\u003cstrong>How Confident Can You Be in the Results?\u003c/strong>\u003c/p>\n\u003cp>Another way to evaluate a result involves looking at how confident researchers are that they would get the same result if they repeated the experiment. This is another way of asking whether or not the study is relevant for a broader population.\u003c/p>\n\u003cp>This measure is called the \"95 percent confidence interval,\" or CI.\u003c/p>\n\u003cp>The CI tells you that 95 percent of the time, when the experiment is repeated, the result will fall between a specific range of numbers. Ideally, you want this range to be small. The wider the range of possible results, the less confidence the researcher can have in the particular result they got.\u003c/p>\n\u003cp>It's something like the margin of error in a poll: If it's too great, it will put the outcome in doubt.\u003c/p>\n\u003cp>Let's take a made-up poll that shows Hillary Clinton beating Donald Trump 40-33. That sounds very good for Clinton supporters. But if the margin of error were 10 percent, that would mean the poll results could actually be 50-23 in favor of Clinton or 30-43 in favor of Trump. When the margin of error is so large it can swing the outcome in the opposite direction, that means the poll results are statistically in question.\u003c/p>\n\u003cp>If the margin of error were only, say, three percent, the narrowest lead Clinton could have would be 37 to 36; there is no potential change in the outcome -- she still wins.\u003c/p>\n\u003cp>Now let's look at the breast cancer study.\u003c/p>\n\u003cp>Of the women who received chemo, 95.9 percent of them made it to the 5-year mark with no breast cancer spreading.\u003c/p>\n\u003cp>But a more complete reporting of the results shows the CI for that group of women is a range between 94 and 97.2 percent. That means if someone repeats the experiment, the number of women who receive chemo and make it five years with no cancer spreading could be anywhere between 94 and 97.2 percent. So the benefit of getting chemo could be higher or lower than the study suggests.\u003c/p>\n\u003cp>For the women who didn't get chemo, the CI is between 92.3 and 95.9 percent.\u003c/p>\n\u003cp>Chemo: 94 to 97.2 percent\u003c/p>\n\u003cp>No Chemo: 92.3 to 95.9 percent\u003c/p>\n\u003cp>It means the study isn't able to say that if you have a particular genetic profile, you can avoid chemotherapy and do just as well after five years as women who get chemo. You can't know the answer to that because the possible results have such a wide range and overlap that they can even swing the outcome in the opposite direction:\u003c/p>\n\u003cp>\u003c!-- iframe plugin v.4.3 wordpress.org/plugins/iframe/ -->\u003cbr>\n\u003ciframe id=\"datawrapper-chart-eJ9aC\" src=\"//datawrapper.dwcdn.net/eJ9aC/3/\" frameborder=\"0\" allowtransparency=\"true\" allowfullscreen=\"allowfullscreen\" webkitallowfullscreen=\"webkitallowfullscreen\" mozallowfullscreen=\"mozallowfullscreen\" oallowfullscreen=\"oallowfullscreen\" msallowfullscreen=\"msallowfullscreen\" width=\"100%\" height=\"230\" scrolling=\"yes\" class=\"iframe-class\">\u003c/iframe>\u003c/p>\n\u003cp>Bottom line, the CI tells you the study can't say whether or not women with this particular genetic profile can safely avoid chemo and do almost as well five years later as those who got chemo. Researchers would need to repeat the experiment, maybe several times, maybe with a larger group or by making other changes, to get a more confident answer.\u003c/p>\n\u003cp>That doesn't make this a bad study; it still showed that a lot of women with a certain genetic profile did not have their cancer spread despite foregoing chemo. However, the results still need to be more firmly proved.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Attai, the UCLA surgery professor, told Health News Review: \"Studies like these often raise more questions and prompt discussion. It is important to note that we do not yet have the 'crystal ball' that will tell an individual patient with absolute certainty that their cancer will recur or not. We are closer than we’ve ever been, but we do not have a test that will predict the outcome with 100 percent certainty.\"\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>People are social animals. And, of course, some people are more social than others. Think Penny and Sheldon from The Big Bang Theory to get a feel for the range.\u003c/p>\n\u003cp>A new \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/27325757\" target=\"_blank\">study \u003c/a>has found a genetic difference that might explain at least part of this spectrum of sociability. It might even help us understand how someone can go from being shy as a child to outgoing as an adult or vice versa.\u003c/p>\n\u003cp>The gene involved, the oxytocin gene, makes perfect sense as it is intimately involved in sociability. It has the instructions for making the hormone oxytocin and this hormone forges bonds when \u003ca href=\"http://examinedexistence.com/why-we-fall-in-love-the-science-of-love/\" target=\"_blank\">falling in love\u003c/a>, plays a critical role in \u003ca href=\"http://www.livescience.com/42198-what-is-oxytocin.html\" target=\"_blank\">mother-child bonding\u003c/a> and improves people's ability to\u003ca href=\"http://blog.oup.com/2014/10/oxytocin-social-emotion-recognition/\" target=\"_blank\"> read emotions\u003c/a> accurately in the face of another person. Oxytocin isn’t the whole story, but it is almost certainly a piece in these puzzles.\u003c/p>\n\u003cfigure id=\"attachment_194618\" class=\"wp-caption alignright\" style=\"max-width: 449px\">\u003ca href=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/06/DNAmet.jpg\">\u003cimg class=\"size-full wp-image-194618\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/06/DNAmet.jpg\" alt=\"Adding methyl groups (bright spots) can change how a gene works. (Wikimedia Commons)\" width=\"449\" height=\"375\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/06/DNAmet.jpg 449w, https://ww2.kqed.org/app/uploads/sites/13/2016/06/DNAmet-400x334.jpg 400w\" sizes=\"(max-width: 449px) 100vw, 449px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Adding methyl groups (bright spots) can change how a gene works. (Wikimedia Commons)\u003c/figcaption>\u003c/figure>\n\u003cp>In this new study, the researchers collected the spit of 121 healthy volunteers and looked at their oxytocin gene. But the team wasn't looking at the A’s, G’s, C’s and T’s that have the genetic instructions for \u003cem>making\u003c/em> oxytocin. Instead, they were looking at something that decorates the gene and affects \u003cem>how much\u003c/em> oxytocin the gene says to make. That something is called methyl groups.\u003c/p>\n\u003cp>In general, the more \u003ca href=\"http://www.nature.com/scitable/topicpage/the-role-of-methylation-in-gene-expression-1070\" target=\"_blank\">methylation \u003c/a>a gene has, the less active it is. And the less active it is, the less product it makes. So an oxytocin gene with a lot of methylation will make less oxytocin. And an oxytocin gene with just a little methylation will make more of it.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Methylation is not, in and of itself, a negative thing. It's a process that helps regulate gene expression so the body gets the right amount of hormones and other critical molecules in the cell. But it can go awry in ways that result in physical or mental disease.\u003c/p>\n\u003cp>What we do and how we live our life can affect the level of methylation on our DNA. We know that enzymes in the cells trigger methylation or demethylation, but we aren't always sure how our experiences causes those enzymes to start working in a specific way\u003cstrong>.\u003c/strong>\u003c/p>\n\u003cp>The researchers in the oxytocin study found that, most of the time, a more methylated oxytocin gene translated to less sociability in these healthy volunteers. They used a variety of tests to look at this.\u003c/p>\n\u003cp>[contextly_sidebar id=\"zH8cDFgkmXKDcG64eHDHwF24kcSN55Jk\"]The first test was a self-reported survey. The more anxious people said they were about their relationships, the more likely they were to have more methyl groups on the oxytocin gene in their DNA.\u003c/p>\n\u003cp>The second test checked how well people can read emotions on a person’s face. They were shown images of people becoming happy, sad, angry or fearful over a 10-second span of time and were asked to identify the emotion as soon as they were confident in the answer. More methylation meant longer times to tell when someone was getting angry.\u003c/p>\n\u003cp>The last tests looked directly at the brain. In one, researchers studied participants' brains in a couple of different ways while the participants thought about how other people might be feeling or what their point of view might be. Researchers found that, during this test, the parts of the brain involved in sociability were less active in people whose oxytocin genes were more methylated.\u003c/p>\n\u003cp>Taken together, this research points toward the idea that people with a more methylated oxytocin gene are less sociable. Which, if true, is something that can change over our lifetimes. And just might point to a way to treat people who are severely affected by their lack of sociability (think of people toward one end of the autism spectrum).\u003c/p>\n\u003cp>\u003cstrong>Sounds Good But…\u003c/strong>\u003c/p>\n\u003cfigure id=\"attachment_194621\" class=\"wp-caption alignright\" style=\"max-width: 500px\">\u003cimg class=\"size-full wp-image-194621\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/06/GrainOfSalt.jpg\" alt=\"The study is a preliminary one and the results should be taken with a grain of salt. (Flickr)\" width=\"500\" height=\"340\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/06/GrainOfSalt.jpg 500w, https://ww2.kqed.org/app/uploads/sites/13/2016/06/GrainOfSalt-400x272.jpg 400w\" sizes=\"(max-width: 500px) 100vw, 500px\">\u003cfigcaption class=\"wp-caption-text\">The study is a preliminary one and the results should be taken with a grain of salt. (\u003ca href=\"https://c1.staticflickr.com/3/2414/1580792921_f8abfbc901_z.jpg?zz=1\" target=\"_blank\">Flickr\u003c/a>)\u003c/figcaption>\u003c/figure>\n\u003cp>This is all very exciting, but there are a few things to keep in mind.\u003c/p>\n\u003cp>First off, this was a small study: only 121 people. Scientific literature is littered with claims that didn’t hold up when applied to larger groups.\u003c/p>\n\u003cp>Secondly, researchers looked at the DNA in the participants’ spit. Genes often have different levels of methylation in different parts of the body (this is part of the reason a muscle cell is different from a brain cell, even though they have the same DNA). So what is true in spit may not be true in the brain. A \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/25355443\" target=\"_blank\">study\u003c/a> showed that DNA methylation in spit is closer to what's in the brain than is DNA in the blood, but it is still not the same.\u003c/p>\n\u003cp>Third, they didn’t directly look at the levels of oxytocin in the participants. Methylation usually weakens a gene, but not always.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Still, it is an interesting study, giving the first indication that methylation of the oxytocin gene plays a role in sociability. We’ll have to see if it pans out in a larger study. If it does, it might make for an interesting new target to go after for conditions where lack of sociability characterizes the illness.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>People are social animals. And, of course, some people are more social than others. Think Penny and Sheldon from The Big Bang Theory to get a feel for the range.\u003c/p>\n\u003cp>A new \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/27325757\" target=\"_blank\">study \u003c/a>has found a genetic difference that might explain at least part of this spectrum of sociability. It might even help us understand how someone can go from being shy as a child to outgoing as an adult or vice versa.\u003c/p>\n\u003cp>The gene involved, the oxytocin gene, makes perfect sense as it is intimately involved in sociability. It has the instructions for making the hormone oxytocin and this hormone forges bonds when \u003ca href=\"http://examinedexistence.com/why-we-fall-in-love-the-science-of-love/\" target=\"_blank\">falling in love\u003c/a>, plays a critical role in \u003ca href=\"http://www.livescience.com/42198-what-is-oxytocin.html\" target=\"_blank\">mother-child bonding\u003c/a> and improves people's ability to\u003ca href=\"http://blog.oup.com/2014/10/oxytocin-social-emotion-recognition/\" target=\"_blank\"> read emotions\u003c/a> accurately in the face of another person. Oxytocin isn’t the whole story, but it is almost certainly a piece in these puzzles.\u003c/p>\n\u003cfigure id=\"attachment_194618\" class=\"wp-caption alignright\" style=\"max-width: 449px\">\u003ca href=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/06/DNAmet.jpg\">\u003cimg class=\"size-full wp-image-194618\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/06/DNAmet.jpg\" alt=\"Adding methyl groups (bright spots) can change how a gene works. (Wikimedia Commons)\" width=\"449\" height=\"375\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/06/DNAmet.jpg 449w, https://ww2.kqed.org/app/uploads/sites/13/2016/06/DNAmet-400x334.jpg 400w\" sizes=\"(max-width: 449px) 100vw, 449px\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Adding methyl groups (bright spots) can change how a gene works. (Wikimedia Commons)\u003c/figcaption>\u003c/figure>\n\u003cp>In this new study, the researchers collected the spit of 121 healthy volunteers and looked at their oxytocin gene. But the team wasn't looking at the A’s, G’s, C’s and T’s that have the genetic instructions for \u003cem>making\u003c/em> oxytocin. Instead, they were looking at something that decorates the gene and affects \u003cem>how much\u003c/em> oxytocin the gene says to make. That something is called methyl groups.\u003c/p>\n\u003cp>In general, the more \u003ca href=\"http://www.nature.com/scitable/topicpage/the-role-of-methylation-in-gene-expression-1070\" target=\"_blank\">methylation \u003c/a>a gene has, the less active it is. And the less active it is, the less product it makes. So an oxytocin gene with a lot of methylation will make less oxytocin. And an oxytocin gene with just a little methylation will make more of it.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Methylation is not, in and of itself, a negative thing. It's a process that helps regulate gene expression so the body gets the right amount of hormones and other critical molecules in the cell. But it can go awry in ways that result in physical or mental disease.\u003c/p>\n\u003cp>What we do and how we live our life can affect the level of methylation on our DNA. We know that enzymes in the cells trigger methylation or demethylation, but we aren't always sure how our experiences causes those enzymes to start working in a specific way\u003cstrong>.\u003c/strong>\u003c/p>\n\u003cp>The researchers in the oxytocin study found that, most of the time, a more methylated oxytocin gene translated to less sociability in these healthy volunteers. They used a variety of tests to look at this.\u003c/p>\n\u003cp>\u003c/p>\u003cp>\u003c/p>\u003cp>The first test was a self-reported survey. The more anxious people said they were about their relationships, the more likely they were to have more methyl groups on the oxytocin gene in their DNA.\u003c/p>\n\u003cp>The second test checked how well people can read emotions on a person’s face. They were shown images of people becoming happy, sad, angry or fearful over a 10-second span of time and were asked to identify the emotion as soon as they were confident in the answer. More methylation meant longer times to tell when someone was getting angry.\u003c/p>\n\u003cp>The last tests looked directly at the brain. In one, researchers studied participants' brains in a couple of different ways while the participants thought about how other people might be feeling or what their point of view might be. Researchers found that, during this test, the parts of the brain involved in sociability were less active in people whose oxytocin genes were more methylated.\u003c/p>\n\u003cp>Taken together, this research points toward the idea that people with a more methylated oxytocin gene are less sociable. Which, if true, is something that can change over our lifetimes. And just might point to a way to treat people who are severely affected by their lack of sociability (think of people toward one end of the autism spectrum).\u003c/p>\n\u003cp>\u003cstrong>Sounds Good But…\u003c/strong>\u003c/p>\n\u003cfigure id=\"attachment_194621\" class=\"wp-caption alignright\" style=\"max-width: 500px\">\u003cimg class=\"size-full wp-image-194621\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/06/GrainOfSalt.jpg\" alt=\"The study is a preliminary one and the results should be taken with a grain of salt. (Flickr)\" width=\"500\" height=\"340\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/06/GrainOfSalt.jpg 500w, https://ww2.kqed.org/app/uploads/sites/13/2016/06/GrainOfSalt-400x272.jpg 400w\" sizes=\"(max-width: 500px) 100vw, 500px\">\u003cfigcaption class=\"wp-caption-text\">The study is a preliminary one and the results should be taken with a grain of salt. (\u003ca href=\"https://c1.staticflickr.com/3/2414/1580792921_f8abfbc901_z.jpg?zz=1\" target=\"_blank\">Flickr\u003c/a>)\u003c/figcaption>\u003c/figure>\n\u003cp>This is all very exciting, but there are a few things to keep in mind.\u003c/p>\n\u003cp>First off, this was a small study: only 121 people. Scientific literature is littered with claims that didn’t hold up when applied to larger groups.\u003c/p>\n\u003cp>Secondly, researchers looked at the DNA in the participants’ spit. Genes often have different levels of methylation in different parts of the body (this is part of the reason a muscle cell is different from a brain cell, even though they have the same DNA). So what is true in spit may not be true in the brain. A \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/25355443\" target=\"_blank\">study\u003c/a> showed that DNA methylation in spit is closer to what's in the brain than is DNA in the blood, but it is still not the same.\u003c/p>\n\u003cp>Third, they didn’t directly look at the levels of oxytocin in the participants. Methylation usually weakens a gene, but not always.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Still, it is an interesting study, giving the first indication that methylation of the oxytocin gene plays a role in sociability. We’ll have to see if it pans out in a larger study. If it does, it might make for an interesting new target to go after for conditions where lack of sociability characterizes the illness.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "Is Red Meat Bad for You? That Might Depend on What Your Ancestors Ate",
"title": "Is Red Meat Bad for You? That Might Depend on What Your Ancestors Ate",
"headTitle": "Future of You | KQED Future of You | KQED Science",
"content": "\u003cp>Some people can get away with eating red meat their whole lives and stay fit as a fiddle. For others, their carnivorous ways may end up contributing to heart disease, cancer or even \u003ca href=\"http://www.foxnews.com/health/2013/08/23/red-meat-consumption-linked-to-alzheimer.html\" target=\"_blank\">Alzheimer's\u003c/a>\u003cstrong>.\u003c/strong>\u003c/p>\n\u003caside class=\"pullquote alignright\">People who have a variation of a certain gene might want to eat more veggies and less red meat to stay healthy, while others may be able to tolerate more meat.\u003c/aside>\n\u003cp>A new \u003ca href=\"http://mbe.oxfordjournals.org/content/early/2016/03/09/molbev.msw049.abstract\">study\u003c/a> in the journal Molecular Biology and Evolution suggests our different responses to diet may stem from where our ancestors lived. That's because the food available to our forebears resulted in differences in DNA that still linger today.\u003c/p>\n\u003cp>In some ways, this isn’t surprising. In the past, if there were mostly vegetables available in a certain geographical area, the people who do best eating vegetables would have thrived. Over the generations, those people would be healthier, have more kids and more frequently pass their genes on. Sooner than you may think, most people in the group would have a set of genes more conducive to eating vegetables and less tolerant of red meat.\u003c/p>\n\u003cp>\u003cstrong>You Are What Your Ancestors Ate\u003c/strong>\u003c/p>\n\u003cp>This is exactly what these researchers found when they looked at the DNA of over 1,000 people. Those whose ancestors ate very little red meat have a key variation in the \u003ca href=\"http://www.genecards.org/cgi-bin/carddisp.pl?gene=FADS2\" target=\"_blank\">FADS2\u003c/a> gene that allows them to flourish on a mostly plant-based diet. The variation boosts their ability to make long-chain polyunsaturated fatty acids (LCPUFA), critical for brain development and the control of inflammation. Thus, when these vegetarian-inclined people eat red meat, they may become more susceptible to inflammation, leading to disease.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The researchers first compared a group of 234 primarily vegetarian people of Indian origin to 311 people from the U.S., who presumably ate a more Western diet with lots of meat and processed food. Sixty-eight percent of the Indian vegetarian group had the genetic difference that optimized their bodies for a plant-based diet while only 18 percent of the group from the U.S. did.\u003c/p>\n\u003cp>The researchers then expanded the study, using the DNA available in the \u003ca href=\"http://www.1000genomes.org/\">1000 Genomes Project\u003c/a>. This public database contains the DNA from people all over the world. The results were similar to what they found with the smaller group. For example, around 70 percent of South Asians had the “vegetarian” DNA difference while only 17 percent of Europeans did.\u003c/p>\n\u003cp>This suggests that what our ancestors ate might affect what our optimal diet is today. People with a “vegetarian” version of this gene might want to eat more veggies and less red meat to stay healthy, while those who lack this variation may be able to tolerate more red meat. There may be no one-size-fits-all diet that works best for everyone.\u003c/p>\n\u003cp>Of course, this calls into question diets like the \u003ca href=\"https://en.wikipedia.org/wiki/Paleolithic_diet\">paleo diet\u003c/a>, which recommends we eat like our ancestors did because that is what our bodies have been configured for. But as this study shows, not everyone's body is the same.\u003c/p>\n\u003cfigure id=\"attachment_139649\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg class=\"size-medium wp-image-139649\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/04/CavePeople-800x463.jpg\" alt=\"Eating what they ate may not be ideal for you depending on your ancestors. Modern people are genetically different from these folks.\" width=\"800\" height=\"463\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople-800x463.jpg 800w, https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople-400x232.jpg 400w, https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople-768x445.jpg 768w, https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople-1180x683.jpg 1180w, https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople.jpg 1920w, https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople-960x556.jpg 960w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">Eating what they ate may not be ideal for you, depending on your ancestors. Modern people are genetically different from these folks. (\u003ca href=\"https://upload.wikimedia.org/wikipedia/commons/a/ae/Diorama,_cavemen_-_National_Museum_of_Mongolian_History.jpg\">Wikimedia Commons\u003c/a>) \u003ccite>(Wikimedia Commons)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Keep in mind, of course, that the genetic difference looked at in this study is one of many bits of DNA that affect how well our bodies process food. There are probably people with the \"vegetarian\" genetic variation who have other DNA that makes them better able to process red meat, and vice versa.\u003c/p>\n\u003cp>We do not yet understand our genetics well enough to predict from our DNA what our ideal diet maybe. This finding is one piece in that puzzle, but we still have a long way to go.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>When we do get there, we will be able to go to our doctor and find out what diet is best for us. But we'll have to see if our future selves are any better at listening to nutritional advice.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Some people can get away with eating red meat their whole lives and stay fit as a fiddle. For others, their carnivorous ways may end up contributing to heart disease, cancer or even \u003ca href=\"http://www.foxnews.com/health/2013/08/23/red-meat-consumption-linked-to-alzheimer.html\" target=\"_blank\">Alzheimer's\u003c/a>\u003cstrong>.\u003c/strong>\u003c/p>\n\u003caside class=\"pullquote alignright\">People who have a variation of a certain gene might want to eat more veggies and less red meat to stay healthy, while others may be able to tolerate more meat.\u003c/aside>\n\u003cp>A new \u003ca href=\"http://mbe.oxfordjournals.org/content/early/2016/03/09/molbev.msw049.abstract\">study\u003c/a> in the journal Molecular Biology and Evolution suggests our different responses to diet may stem from where our ancestors lived. That's because the food available to our forebears resulted in differences in DNA that still linger today.\u003c/p>\n\u003cp>In some ways, this isn’t surprising. In the past, if there were mostly vegetables available in a certain geographical area, the people who do best eating vegetables would have thrived. Over the generations, those people would be healthier, have more kids and more frequently pass their genes on. Sooner than you may think, most people in the group would have a set of genes more conducive to eating vegetables and less tolerant of red meat.\u003c/p>\n\u003cp>\u003cstrong>You Are What Your Ancestors Ate\u003c/strong>\u003c/p>\n\u003cp>This is exactly what these researchers found when they looked at the DNA of over 1,000 people. Those whose ancestors ate very little red meat have a key variation in the \u003ca href=\"http://www.genecards.org/cgi-bin/carddisp.pl?gene=FADS2\" target=\"_blank\">FADS2\u003c/a> gene that allows them to flourish on a mostly plant-based diet. The variation boosts their ability to make long-chain polyunsaturated fatty acids (LCPUFA), critical for brain development and the control of inflammation. Thus, when these vegetarian-inclined people eat red meat, they may become more susceptible to inflammation, leading to disease.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>The researchers first compared a group of 234 primarily vegetarian people of Indian origin to 311 people from the U.S., who presumably ate a more Western diet with lots of meat and processed food. Sixty-eight percent of the Indian vegetarian group had the genetic difference that optimized their bodies for a plant-based diet while only 18 percent of the group from the U.S. did.\u003c/p>\n\u003cp>The researchers then expanded the study, using the DNA available in the \u003ca href=\"http://www.1000genomes.org/\">1000 Genomes Project\u003c/a>. This public database contains the DNA from people all over the world. The results were similar to what they found with the smaller group. For example, around 70 percent of South Asians had the “vegetarian” DNA difference while only 17 percent of Europeans did.\u003c/p>\n\u003cp>This suggests that what our ancestors ate might affect what our optimal diet is today. People with a “vegetarian” version of this gene might want to eat more veggies and less red meat to stay healthy, while those who lack this variation may be able to tolerate more red meat. There may be no one-size-fits-all diet that works best for everyone.\u003c/p>\n\u003cp>Of course, this calls into question diets like the \u003ca href=\"https://en.wikipedia.org/wiki/Paleolithic_diet\">paleo diet\u003c/a>, which recommends we eat like our ancestors did because that is what our bodies have been configured for. But as this study shows, not everyone's body is the same.\u003c/p>\n\u003cfigure id=\"attachment_139649\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg class=\"size-medium wp-image-139649\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/04/CavePeople-800x463.jpg\" alt=\"Eating what they ate may not be ideal for you depending on your ancestors. Modern people are genetically different from these folks.\" width=\"800\" height=\"463\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople-800x463.jpg 800w, https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople-400x232.jpg 400w, https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople-768x445.jpg 768w, https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople-1180x683.jpg 1180w, https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople.jpg 1920w, https://ww2.kqed.org/app/uploads/sites/13/2016/04/CavePeople-960x556.jpg 960w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">Eating what they ate may not be ideal for you, depending on your ancestors. Modern people are genetically different from these folks. (\u003ca href=\"https://upload.wikimedia.org/wikipedia/commons/a/ae/Diorama,_cavemen_-_National_Museum_of_Mongolian_History.jpg\">Wikimedia Commons\u003c/a>) \u003ccite>(Wikimedia Commons)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Keep in mind, of course, that the genetic difference looked at in this study is one of many bits of DNA that affect how well our bodies process food. There are probably people with the \"vegetarian\" genetic variation who have other DNA that makes them better able to process red meat, and vice versa.\u003c/p>\n\u003cp>We do not yet understand our genetics well enough to predict from our DNA what our ideal diet maybe. This finding is one piece in that puzzle, but we still have a long way to go.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>When we do get there, we will be able to go to our doctor and find out what diet is best for us. But we'll have to see if our future selves are any better at listening to nutritional advice.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>We think of identical twins as having identical DNA. But a pair of twins \u003ca href=\"http://www.dailymail.co.uk/femail/article-3461832/First-identical-twins-different-skin-colour-born-UK.html\">\u003cu>born in England\u003c/u>\u003c/a> shows that's not exactly true.\u003c/p>\n\u003cp>The two girls started out like all identical twins, developing from the same fertilized egg and the exact same set of DNA. But when they were born last year they didn't look like identical twins. One girl has peach skin and blue eyes and the other has brown sugar skin and brown eyes.\u003c/p>\n\u003cp>At first blush it might seem impossible they could look so different. After all, while huge differences \u003ca href=\"http://genetics.thetech.org/ask/ask304\">\u003cu>can and do happen\u003c/u>\u003c/a> with fraternal twins, identical twins are usually exactly that -- identical in skin, hair and eye color.\u003c/p>\n\u003cp>But, actually, twins who start out with identical DNA always have slightly different DNA by the time they're born. And they also each use their DNA a bit differently too.\u003c/p>\n\u003cp>Even though this is true for all identical twins, we can’t usually tell because the changes happen in parts of the DNA that don’t affect how identical twins look. Which isn’t surprising. DNA is large and very little of it has to do with, for example, skin and eye color.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>By chance, the DNA differences for these girls happened to be in the smallish part of their genome that deals with looks. These two girls let us see what goes on in every identical twin. And in every one of us.\u003c/p>\n\u003cp>\u003cstrong>DNA Differences\u003c/strong>\u003c/p>\n\u003cp>Identical twins do indeed start with identical DNA—they are the result of the same sperm from dad and the same egg from mom.\u003c/p>\n\u003cfigure id=\"attachment_136190\" class=\"wp-caption aligncenter\" style=\"max-width: 655px\">\u003cimg class=\"size-full wp-image-136190\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/03/FerilizationBW.jpg\" alt=\"Even though identical twins come from the same fertilized egg, in the end each twin has slightly different DNA. (Zappys Technology Solutions)\" width=\"655\" height=\"475\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/03/FerilizationBW.jpg 655w, https://ww2.kqed.org/app/uploads/sites/13/2016/03/FerilizationBW-400x290.jpg 400w\" sizes=\"(max-width: 655px) 100vw, 655px\">\u003cfigcaption class=\"wp-caption-text\">Even though identical twins come from the same fertilized egg, in the end each twin has slightly different DNA. (\u003ca href=\"https://www.flickr.com/photos/102642344@N02/10017013846\">Zappys Technology Solutions\u003c/a>)\u003c/figcaption>\u003c/figure>\n\u003cp>The original fertilized egg divides one or more times before the resulting clump of cells splits into two. Each clump of cells goes on to become one of the identical twins.\u003c/p>\n\u003cp>In this process of becoming a brand new baby with trillions of cells, the cells in each clump divide over and over again. DNA differences or mutations can happen any time a cell divides.\u003c/p>\n\u003cp>This is because a cell needs to copy its DNA before it can divide. And while the cellular machinery is astonishingly good at copying DNA, it isn’t perfect. Every now and then it makes a mistake.\u003c/p>\n\u003cp>All of the new cells that come from the one with the mistake will have that same mistake. One consequence is that if it happens early, the baby will have more cells carrying that mistake.\u003c/p>\n\u003cp>Think about it like one of those medieval monks patiently copying manuscripts in a monastery somewhere in medieval Europe. Imagine he makes a mistake during copying and the original manuscript is destroyed. Now every new manuscript contains his mistake.\u003c/p>\n\u003cp>For the English twins, one may have developed a mutation in a gene that affects skin and eye color. Most likely it would be in the lighter child as it is easier to break something than to fix it. And often traits like blue eyes are the result of a gene not working quite right.\u003c/p>\n\u003cp>But this isn’t the only way this could have happened. Another possibility has to do with how cells read their DNA.\u003c/p>\n\u003cp>\u003cstrong>Using DNA Differently\u003c/strong>\u003c/p>\n\u003cp>Imagine Louis C.K., Meryl Streep and Kevin Hart are all going up for the same role. Even though they all have the exact same lines to read, odds are there will be real differences in how they say them.\u003c/p>\n\u003cfigure id=\"attachment_136192\" class=\"wp-caption aligncenter\" style=\"max-width: 650px\">\u003cimg class=\"size-full wp-image-136192\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/03/LouisCKMerylStreepKevinHart.jpg\" alt=\"Just like different actors will read the same script differently, so too will different people's cells read the same genes differently.\" width=\"650\" height=\"277\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/03/LouisCKMerylStreepKevinHart.jpg 650w, https://ww2.kqed.org/app/uploads/sites/13/2016/03/LouisCKMerylStreepKevinHart-400x170.jpg 400w\" sizes=\"(max-width: 650px) 100vw, 650px\">\u003cfigcaption class=\"wp-caption-text\">Just like different actors will read the same script differently, so too will different people's cells read the same genes differently. \u003ccite>(Wikimedia Commons)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>This is sort of what happens in different people’s cells. One person's cells will read a gene one way and another person’s cells will read the exact same gene a different way. If that gene controls skin and/or eye color, then it will affect a person’s skin or eye color.\u003c/p>\n\u003cp>Here's how it might work: Near the genes there little chemical markers that can, for example, tell the cell how often to read a gene.\u003c/p>\n\u003cp>In the case of the twins, it could be that a set of these “epigenetic” marks is telling the cells of one twin to read her skin and eye color genes just a little bit. That means she would make less pigment and so have fair skin and blue eyes.\u003c/p>\n\u003cp>Or her sister might have marks on her DNA telling her cells to read her skin and eye color genes much more often. This would explain her brown eyes and cafe au lait skin.\u003c/p>\n\u003cp>What is fascinating about these epigenetic marks is that they're reversible. This means that, for example, the twin with blue eyes and fair skin may eventually end up with her sister’s eye and skin color. Which wouldn’t be surprising as it isn’t uncommon for babies to be born with lighter skin and eyes that darken over time.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>If the girls' differences are the result of a mutation in the DNA itself, they'll probably go through life as different-looking identical twins. But if the reason is in how their cells read their DNA, these girls might someday look more identical than they do now.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>We think of identical twins as having identical DNA. But a pair of twins \u003ca href=\"http://www.dailymail.co.uk/femail/article-3461832/First-identical-twins-different-skin-colour-born-UK.html\">\u003cu>born in England\u003c/u>\u003c/a> shows that's not exactly true.\u003c/p>\n\u003cp>The two girls started out like all identical twins, developing from the same fertilized egg and the exact same set of DNA. But when they were born last year they didn't look like identical twins. One girl has peach skin and blue eyes and the other has brown sugar skin and brown eyes.\u003c/p>\n\u003cp>At first blush it might seem impossible they could look so different. After all, while huge differences \u003ca href=\"http://genetics.thetech.org/ask/ask304\">\u003cu>can and do happen\u003c/u>\u003c/a> with fraternal twins, identical twins are usually exactly that -- identical in skin, hair and eye color.\u003c/p>\n\u003cp>But, actually, twins who start out with identical DNA always have slightly different DNA by the time they're born. And they also each use their DNA a bit differently too.\u003c/p>\n\u003cp>Even though this is true for all identical twins, we can’t usually tell because the changes happen in parts of the DNA that don’t affect how identical twins look. Which isn’t surprising. DNA is large and very little of it has to do with, for example, skin and eye color.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>By chance, the DNA differences for these girls happened to be in the smallish part of their genome that deals with looks. These two girls let us see what goes on in every identical twin. And in every one of us.\u003c/p>\n\u003cp>\u003cstrong>DNA Differences\u003c/strong>\u003c/p>\n\u003cp>Identical twins do indeed start with identical DNA—they are the result of the same sperm from dad and the same egg from mom.\u003c/p>\n\u003cfigure id=\"attachment_136190\" class=\"wp-caption aligncenter\" style=\"max-width: 655px\">\u003cimg class=\"size-full wp-image-136190\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/03/FerilizationBW.jpg\" alt=\"Even though identical twins come from the same fertilized egg, in the end each twin has slightly different DNA. (Zappys Technology Solutions)\" width=\"655\" height=\"475\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/03/FerilizationBW.jpg 655w, https://ww2.kqed.org/app/uploads/sites/13/2016/03/FerilizationBW-400x290.jpg 400w\" sizes=\"(max-width: 655px) 100vw, 655px\">\u003cfigcaption class=\"wp-caption-text\">Even though identical twins come from the same fertilized egg, in the end each twin has slightly different DNA. (\u003ca href=\"https://www.flickr.com/photos/102642344@N02/10017013846\">Zappys Technology Solutions\u003c/a>)\u003c/figcaption>\u003c/figure>\n\u003cp>The original fertilized egg divides one or more times before the resulting clump of cells splits into two. Each clump of cells goes on to become one of the identical twins.\u003c/p>\n\u003cp>In this process of becoming a brand new baby with trillions of cells, the cells in each clump divide over and over again. DNA differences or mutations can happen any time a cell divides.\u003c/p>\n\u003cp>This is because a cell needs to copy its DNA before it can divide. And while the cellular machinery is astonishingly good at copying DNA, it isn’t perfect. Every now and then it makes a mistake.\u003c/p>\n\u003cp>All of the new cells that come from the one with the mistake will have that same mistake. One consequence is that if it happens early, the baby will have more cells carrying that mistake.\u003c/p>\n\u003cp>Think about it like one of those medieval monks patiently copying manuscripts in a monastery somewhere in medieval Europe. Imagine he makes a mistake during copying and the original manuscript is destroyed. Now every new manuscript contains his mistake.\u003c/p>\n\u003cp>For the English twins, one may have developed a mutation in a gene that affects skin and eye color. Most likely it would be in the lighter child as it is easier to break something than to fix it. And often traits like blue eyes are the result of a gene not working quite right.\u003c/p>\n\u003cp>But this isn’t the only way this could have happened. Another possibility has to do with how cells read their DNA.\u003c/p>\n\u003cp>\u003cstrong>Using DNA Differently\u003c/strong>\u003c/p>\n\u003cp>Imagine Louis C.K., Meryl Streep and Kevin Hart are all going up for the same role. Even though they all have the exact same lines to read, odds are there will be real differences in how they say them.\u003c/p>\n\u003cfigure id=\"attachment_136192\" class=\"wp-caption aligncenter\" style=\"max-width: 650px\">\u003cimg class=\"size-full wp-image-136192\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/03/LouisCKMerylStreepKevinHart.jpg\" alt=\"Just like different actors will read the same script differently, so too will different people's cells read the same genes differently.\" width=\"650\" height=\"277\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/03/LouisCKMerylStreepKevinHart.jpg 650w, https://ww2.kqed.org/app/uploads/sites/13/2016/03/LouisCKMerylStreepKevinHart-400x170.jpg 400w\" sizes=\"(max-width: 650px) 100vw, 650px\">\u003cfigcaption class=\"wp-caption-text\">Just like different actors will read the same script differently, so too will different people's cells read the same genes differently. \u003ccite>(Wikimedia Commons)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>This is sort of what happens in different people’s cells. One person's cells will read a gene one way and another person’s cells will read the exact same gene a different way. If that gene controls skin and/or eye color, then it will affect a person’s skin or eye color.\u003c/p>\n\u003cp>Here's how it might work: Near the genes there little chemical markers that can, for example, tell the cell how often to read a gene.\u003c/p>\n\u003cp>In the case of the twins, it could be that a set of these “epigenetic” marks is telling the cells of one twin to read her skin and eye color genes just a little bit. That means she would make less pigment and so have fair skin and blue eyes.\u003c/p>\n\u003cp>Or her sister might have marks on her DNA telling her cells to read her skin and eye color genes much more often. This would explain her brown eyes and cafe au lait skin.\u003c/p>\n\u003cp>What is fascinating about these epigenetic marks is that they're reversible. This means that, for example, the twin with blue eyes and fair skin may eventually end up with her sister’s eye and skin color. Which wouldn’t be surprising as it isn’t uncommon for babies to be born with lighter skin and eyes that darken over time.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>If the girls' differences are the result of a mutation in the DNA itself, they'll probably go through life as different-looking identical twins. But if the reason is in how their cells read their DNA, these girls might someday look more identical than they do now.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"disqusTitle": "Discovery May Lead to Earlier Diagnosis for Breast Cancer",
"title": "Discovery May Lead to Earlier Diagnosis for Breast Cancer",
"headTitle": "Women’s Health | KQED Future of You | KQED Science",
"content": "\u003cp>Doctors and patients know the earlier someone gets a cancer diagnosis, the better the chance that treatment will work. So anything that helps catch cancer at an earlier stage could help save lives.\u003c/p>\n\u003cp>Most cancers happen because of mistakes or mutations in the DNA of key genes. When any key gene is damaged, the chances the cell will grow uncontrollably go up. And cells growing uncontrollably is the very definition of cancer.\u003c/p>\n\u003caside class=\"pullquote alignright\">Most women are not born with a mutation in this gene. Instead, over a lifetime, they develop the mutations in their breast cells that can induce tumors.\u003c/aside>\n\u003cp>In a new \u003ca href=\"http://ajp.amjpathol.org/article/S0002-9440(16)00087-0/abstract\" target=\"_blank\">study\u003c/a> out this week researchers at the \u003ca href=\"http://www.augusta.edu/mcg/\" target=\"_blank\">Medical College of Georgia at Augusta University\u003c/a> have \u003ca href=\"http://jagwire.augusta.edu/archives/31680\" target=\"_blank\">found a gene\u003c/a> that may make it easier for doctors to find certain breast and possibly ovarian cancers at an earlier stage. Results from this study in the \u003ca href=\"http://ajp.amjpathol.org/\" target=\"_blank\">American Journal of Pathology\u003c/a> may even point to new treatments.\u003c/p>\n\u003cp>The researchers looked at 249 breast cancer samples and found that in more than 70 percent of them, a gene that is normally turned off in adults has mutated and turned on. And because the mutated gene is harder to detect in some of the later stage cancers the researchers looked at, it could be even more common than this.\u003c/p>\n\u003cp>The identified gene, GT198, has been associated with breast and ovarian cancer in the past but it is in this study where the researchers determined at least one way the mutated gene can cause a tumor to grow.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>When GT198 is mutated, it can turn on other genes that encourage tumor growth.\u003c/p>\n\u003cp>\u003cstrong>How Might This Change Diagnosis or Treatment?\u003cbr>\n\u003c/strong>\u003cbr>\nThis finding suggests that doctors who find something suspicious in a breast exam could look for signs of a mutated GT198. The doctor would remove some tissue from the breast to see if the GT198 gene is on in a set of cells called stromal cells. If it is, a red flag would go up and the doctor could do some additional testing in order to discern whether there's a young tumor, leading to early treatment that could perhaps nip the breast cancer in the bud.\u003c/p>\n\u003caside class=\"pullquote alignright\">If the results hold up, a diagnostic test to find out whether the gene has mutated should be pretty straightforward to design.\u003c/aside>\n\u003cp>In the more distant future, scientists may design new treatments based on this mutated gene. For example, they might look for how to goose a patient’s immune system to attack only the cells where the gene is turned on. If we had \u003ca href=\"http://www.cancer.org/treatment/treatmentsandsideeffects/treatmenttypes/immunotherapy/immunotherapy-toc\" target=\"_blank\">immunotherapy\u003c/a> that killed only cancer cells, there might be fewer side effects than with current treatments like radiation and chemotherapy.\u003c/p>\n\u003cp>Another avenue for treatment based on this work would be to go after the protein that the GT198 gene \u003ca href=\"https://en.wikipedia.org/wiki/Genetic_code\" target=\"_blank\">helps build\u003c/a>. As is usually the case, it is the protein and not the gene itself that is doing the dirty work and causing the cancer. So perhaps researchers could find some small molecule that stops the protein from turning on tumor-encouraging genes. Ideally, this would at least slow down tumor growth.\u003c/p>\n\u003cp>The results will need to be confirmed at least in part by analyzing additional breast cancer samples. If the results hold up, then the diagnostic test to find out whether GT198 is turned on should be pretty straightforward to design. Treatments based on these findings would not be. They may not be available for quite a while.\u003c/p>\n\u003cp>\u003cstrong>Inherited or Spontaneous\u003c/strong>\u003c/p>\n\u003cp>Cancer happens when key genes are damaged. The DNA can be damaged from things in the environment like cigarette smoke or the ultraviolet light from the sun, or a cell can simply make a mistake when copying its DNA.\u003c/p>\n\u003cfigure id=\"attachment_132980\" class=\"wp-caption aligncenter\" style=\"max-width: 620px\">\u003cimg class=\"size-full wp-image-132980\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/03/DNAmutUV.jpg\" alt=\"Most cancers happen when key DNA is damaged or is copied incorrectly. (Wikimedia Commons)\" width=\"620\" height=\"364\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/03/DNAmutUV.jpg 620w, https://ww2.kqed.org/app/uploads/sites/13/2016/03/DNAmutUV-400x235.jpg 400w\" sizes=\"(max-width: 620px) 100vw, 620px\">\u003cfigcaption class=\"wp-caption-text\">Most cancers happen when key DNA is damaged or is copied incorrectly. (\u003ca href=\"https://upload.wikimedia.org/wikipedia/commons/thumb/f/fd/DNA_UV_mutation.svg/2000px-DNA_UV_mutation.svg.png\">Wikimedia Commons\u003c/a>)\u003c/figcaption>\u003c/figure>\n\u003cp>Some people inherit mutated genes that make it more likely they'll develop cancer. \u003ca href=\"http://ww5.komen.org/BreastCancer/BRCA1andBRCA2.html\" target=\"_blank\">BRCA1\u003c/a>, the gene made famous by Angelina Jolie, is one of these. She inherited a mutated BRCA1 gene that raised her risk of developing breast (and ovarian) cancer later in life.\u003c/p>\n\u003cp>The authors of this study estimated from previous work that 4% of breast cancers that run in the family may have the mutated GT198 gene. But in the study, more than 70 percent of the breast cancers had a mutated GT198 gene, so it's clear many women had not inherited the mutation.\u003c/p>\n\u003cp>It turns out most women are not born with a mutated GT198 gene, but develop mutations in this gene in their breast cells over their lifetime.\u003c/p>\n\u003cp>This is how the vast majority of cancers develop. Mutations happen in our DNA as we live our lives.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Still, researchers are working on a genetic test that looks for people born with a mutated GT198 gene. Like the test for mutant BRCA1/2 genes, it would help people find out if they're at a higher risk for developing breast cancer.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Doctors and patients know the earlier someone gets a cancer diagnosis, the better the chance that treatment will work. So anything that helps catch cancer at an earlier stage could help save lives.\u003c/p>\n\u003cp>Most cancers happen because of mistakes or mutations in the DNA of key genes. When any key gene is damaged, the chances the cell will grow uncontrollably go up. And cells growing uncontrollably is the very definition of cancer.\u003c/p>\n\u003caside class=\"pullquote alignright\">Most women are not born with a mutation in this gene. Instead, over a lifetime, they develop the mutations in their breast cells that can induce tumors.\u003c/aside>\n\u003cp>In a new \u003ca href=\"http://ajp.amjpathol.org/article/S0002-9440(16)00087-0/abstract\" target=\"_blank\">study\u003c/a> out this week researchers at the \u003ca href=\"http://www.augusta.edu/mcg/\" target=\"_blank\">Medical College of Georgia at Augusta University\u003c/a> have \u003ca href=\"http://jagwire.augusta.edu/archives/31680\" target=\"_blank\">found a gene\u003c/a> that may make it easier for doctors to find certain breast and possibly ovarian cancers at an earlier stage. Results from this study in the \u003ca href=\"http://ajp.amjpathol.org/\" target=\"_blank\">American Journal of Pathology\u003c/a> may even point to new treatments.\u003c/p>\n\u003cp>The researchers looked at 249 breast cancer samples and found that in more than 70 percent of them, a gene that is normally turned off in adults has mutated and turned on. And because the mutated gene is harder to detect in some of the later stage cancers the researchers looked at, it could be even more common than this.\u003c/p>\n\u003cp>The identified gene, GT198, has been associated with breast and ovarian cancer in the past but it is in this study where the researchers determined at least one way the mutated gene can cause a tumor to grow.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>When GT198 is mutated, it can turn on other genes that encourage tumor growth.\u003c/p>\n\u003cp>\u003cstrong>How Might This Change Diagnosis or Treatment?\u003cbr>\n\u003c/strong>\u003cbr>\nThis finding suggests that doctors who find something suspicious in a breast exam could look for signs of a mutated GT198. The doctor would remove some tissue from the breast to see if the GT198 gene is on in a set of cells called stromal cells. If it is, a red flag would go up and the doctor could do some additional testing in order to discern whether there's a young tumor, leading to early treatment that could perhaps nip the breast cancer in the bud.\u003c/p>\n\u003caside class=\"pullquote alignright\">If the results hold up, a diagnostic test to find out whether the gene has mutated should be pretty straightforward to design.\u003c/aside>\n\u003cp>In the more distant future, scientists may design new treatments based on this mutated gene. For example, they might look for how to goose a patient’s immune system to attack only the cells where the gene is turned on. If we had \u003ca href=\"http://www.cancer.org/treatment/treatmentsandsideeffects/treatmenttypes/immunotherapy/immunotherapy-toc\" target=\"_blank\">immunotherapy\u003c/a> that killed only cancer cells, there might be fewer side effects than with current treatments like radiation and chemotherapy.\u003c/p>\n\u003cp>Another avenue for treatment based on this work would be to go after the protein that the GT198 gene \u003ca href=\"https://en.wikipedia.org/wiki/Genetic_code\" target=\"_blank\">helps build\u003c/a>. As is usually the case, it is the protein and not the gene itself that is doing the dirty work and causing the cancer. So perhaps researchers could find some small molecule that stops the protein from turning on tumor-encouraging genes. Ideally, this would at least slow down tumor growth.\u003c/p>\n\u003cp>The results will need to be confirmed at least in part by analyzing additional breast cancer samples. If the results hold up, then the diagnostic test to find out whether GT198 is turned on should be pretty straightforward to design. Treatments based on these findings would not be. They may not be available for quite a while.\u003c/p>\n\u003cp>\u003cstrong>Inherited or Spontaneous\u003c/strong>\u003c/p>\n\u003cp>Cancer happens when key genes are damaged. The DNA can be damaged from things in the environment like cigarette smoke or the ultraviolet light from the sun, or a cell can simply make a mistake when copying its DNA.\u003c/p>\n\u003cfigure id=\"attachment_132980\" class=\"wp-caption aligncenter\" style=\"max-width: 620px\">\u003cimg class=\"size-full wp-image-132980\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/03/DNAmutUV.jpg\" alt=\"Most cancers happen when key DNA is damaged or is copied incorrectly. (Wikimedia Commons)\" width=\"620\" height=\"364\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/03/DNAmutUV.jpg 620w, https://ww2.kqed.org/app/uploads/sites/13/2016/03/DNAmutUV-400x235.jpg 400w\" sizes=\"(max-width: 620px) 100vw, 620px\">\u003cfigcaption class=\"wp-caption-text\">Most cancers happen when key DNA is damaged or is copied incorrectly. (\u003ca href=\"https://upload.wikimedia.org/wikipedia/commons/thumb/f/fd/DNA_UV_mutation.svg/2000px-DNA_UV_mutation.svg.png\">Wikimedia Commons\u003c/a>)\u003c/figcaption>\u003c/figure>\n\u003cp>Some people inherit mutated genes that make it more likely they'll develop cancer. \u003ca href=\"http://ww5.komen.org/BreastCancer/BRCA1andBRCA2.html\" target=\"_blank\">BRCA1\u003c/a>, the gene made famous by Angelina Jolie, is one of these. She inherited a mutated BRCA1 gene that raised her risk of developing breast (and ovarian) cancer later in life.\u003c/p>\n\u003cp>The authors of this study estimated from previous work that 4% of breast cancers that run in the family may have the mutated GT198 gene. But in the study, more than 70 percent of the breast cancers had a mutated GT198 gene, so it's clear many women had not inherited the mutation.\u003c/p>\n\u003cp>It turns out most women are not born with a mutated GT198 gene, but develop mutations in this gene in their breast cells over their lifetime.\u003c/p>\n\u003cp>This is how the vast majority of cancers develop. Mutations happen in our DNA as we live our lives.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Still, researchers are working on a genetic test that looks for people born with a mutated GT198 gene. Like the test for mutant BRCA1/2 genes, it would help people find out if they're at a higher risk for developing breast cancer.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>Last Thursday, Veritas Genetics \u003ca href=\"http://www.prnewswire.com/news-releases/veritas-genetics-launches-999-whole-genome-and-sets-new-standard-for-genetic-testing-300230258.html\" target=\"_blank\">announced\u003c/a> it will make available your entire genetic sequence for just $999. That's all of your body's instructions for making and running the machine known as you for roughly the price of a big-screen TV.\u003c/p>\n\u003caside class=\"pullquote alignright\">If you buy your whole genome, make sure it's been read a minimum of 30 times to ensure accuracy.\u003c/aside>\n\u003cp>The sequencing, which will be available for order on March 30, needs to be requested through a physician. Veritas said you will also receive interpretation and on-demand genetic counseling -- just as important as the sequence itself. After all, without this analysis, you'd be staring at your specific combination of 6 billion or so\u003ca href=\"http://www.nature.com/scitable/content/the-four-bases-atcg-6491969\" target=\"_blank\"> As, Gs, Cs and Ts\u003c/a> with no way to decode it.\u003c/p>\n\u003cp>While Veritas isn't the first company to provide you with access to your DNA, it's the first to offer your whole genome for that low a price. A company called Sure Genomics, for example, launched a \u003ca href=\"http://www.businesswire.com/news/home/20160209005530/en/Genomics-Introduces-Full-DNA-Sequence-Consumers-Delivered\" target=\"_blank\">whole genome service\u003c/a> last month, costing $2,500 plus $150 annually for biannual updated analyses that will take into account newly found genetic markers.\u003c/p>\n\u003cp>Given the complexity of the possible results, it will be interesting to see what you get for such a low price.\u003c/p>\n\u003cp>\u003cstrong>With Genetic Sequencing, Is Less More?\u003c/strong>\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Whole genome sequencing is different than what the company 23andMe offers, for as little as $199. Rather than looking at your entire genome, 23andMe searches for already known genetic variations, like those for cystic fibrosis, sickle cell anemia, and other diseases and traits.\u003c/p>\n\u003cp>Because 23andMe only looks for the parts of your DNA known to be associated with certain traits or diseases, it can’t report on variations that are present but have yet to be determined as significant. Or on rare variants that they know what effect they have but do not test for.\u003c/p>\n\u003cfigure id=\"attachment_125387\" class=\"wp-caption aligncenter\" style=\"max-width: 700px\">\u003cimg class=\"size-full wp-image-125387\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/03/MotherBaby.jpg\" alt=\"You are special and so is your DNA. (Pixabay)\" width=\"700\" height=\"466\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/03/MotherBaby.jpg 700w, https://ww2.kqed.org/app/uploads/sites/13/2016/03/MotherBaby-400x266.jpg 400w\" sizes=\"(max-width: 700px) 100vw, 700px\">\u003cfigcaption class=\"wp-caption-text\">You are special and so is your DNA. (\u003ca href=\"https://pixabay.com/en/baby-care-caucasian-cheek-child-17327/\">Pixabay\u003c/a>) \u003ccite>(Pixabay)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Remember how your mom told you you're \"special.\" Well, that's technically true, because everyone’s DNA is unique.\u003c/p>\n\u003cp>But it also means scientists trying to interpret vast stretches of your genetic code is like Egyptologists staring at hieroglyphics without the benefit of the Rosetta Stone. So even though your entire genome has the potential to one day tell you a whole lot about yourself, currently it's not saying much. And anyone looking at it won't know how or whether the majority of combinations in your genetic code determine your health and other traits.\u003c/p>\n\u003cp>For example, if a unique sequence falls within a gene implicated in a disease, then you may or may not be at a higher risk for that disease. Sometimes scientists can make a reasonable prediction, but often they can’t. Now imagine these types of unknowns strewn throughout your genome.\u003c/p>\n\u003cp>But this will not always be the case. As scientists learn more and more about what different parts of the human genome can tell us, your own sequence will become more and more communicative, so to speak. Meaning one day, that information could be found to impact your health.\u003c/p>\n\u003cp>\u003cstrong>You Need Coverage\u003c/strong>\u003c/p>\n\u003cp>If you do choose to spend more money to explore the unknown reaches of your genome, you want to make sure that data is high quality. Good quality genomes don’t contain a lot of mistakes, and they aren’t missing big sections.\u003c/p>\n\u003cp>The key thing to look for is something called \"coverage.\"\u003c/p>\n\u003cp>Basically, coverage is how many times on average your genome has been read. One rule of thumb: If a whole genome sequence (WGS) is going to be used to predict individual characteristics, it should be read a \u003ca href=\"http://www.ccmb.med.umich.edu/node/1186\">bare minimum of 30 times\u003c/a>.\u003c/p>\n\u003cp>Dr. Michael Snyder, chair of the Department of Genetics at Stanford University, says even more is better. \"I would do at least 60X and even that will not give adequate coverage in a lot of regions.\"\u003c/p>\n\u003cp>Why do scientists need to read the same DNA over and over again? Mainly because while new technologies have made sequencing much cheaper, they have also made it vulnerable to a greater number of mistakes. Scientists now need a lot of reads to ensure the sequence is correct.\u003c/p>\n\u003cp>Another reason so many reads are required is that some parts of the genome just don’t sequence very well. You need to do a lot of sequencing to get these regions to appear in the data.\u003c/p>\n\u003cp>\u003cstrong>More than DNA\u003c/strong>\u003c/p>\n\u003cp>Of course with Veritas and other services that provide you with your entire genome, you are paying for more than your genetic code. You are also paying for the interpretation and the counseling that comes with your results.\u003c/p>\n\u003cp>How valuable that is to you will depend on which results the company interprets, how much counseling it will offer, and, finally, how you will respond to the data. Handled right, information about your genetic predispositions can be extremely helpful. But handled poorly, it can be confusing, worrying, and perhaps lead to \u003ca href=\"http://ww2.kqed.org/futureofyou/2016/02/08/student-was-asked-to-leave-school-because-of-his-dna/\" target=\"_blank\">unintended consequences\u003c/a>.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>They say a little information can be dangerous. But too much can be overwhelming.\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Last Thursday, Veritas Genetics \u003ca href=\"http://www.prnewswire.com/news-releases/veritas-genetics-launches-999-whole-genome-and-sets-new-standard-for-genetic-testing-300230258.html\" target=\"_blank\">announced\u003c/a> it will make available your entire genetic sequence for just $999. That's all of your body's instructions for making and running the machine known as you for roughly the price of a big-screen TV.\u003c/p>\n\u003caside class=\"pullquote alignright\">If you buy your whole genome, make sure it's been read a minimum of 30 times to ensure accuracy.\u003c/aside>\n\u003cp>The sequencing, which will be available for order on March 30, needs to be requested through a physician. Veritas said you will also receive interpretation and on-demand genetic counseling -- just as important as the sequence itself. After all, without this analysis, you'd be staring at your specific combination of 6 billion or so\u003ca href=\"http://www.nature.com/scitable/content/the-four-bases-atcg-6491969\" target=\"_blank\"> As, Gs, Cs and Ts\u003c/a> with no way to decode it.\u003c/p>\n\u003cp>While Veritas isn't the first company to provide you with access to your DNA, it's the first to offer your whole genome for that low a price. A company called Sure Genomics, for example, launched a \u003ca href=\"http://www.businesswire.com/news/home/20160209005530/en/Genomics-Introduces-Full-DNA-Sequence-Consumers-Delivered\" target=\"_blank\">whole genome service\u003c/a> last month, costing $2,500 plus $150 annually for biannual updated analyses that will take into account newly found genetic markers.\u003c/p>\n\u003cp>Given the complexity of the possible results, it will be interesting to see what you get for such a low price.\u003c/p>\n\u003cp>\u003cstrong>With Genetic Sequencing, Is Less More?\u003c/strong>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Whole genome sequencing is different than what the company 23andMe offers, for as little as $199. Rather than looking at your entire genome, 23andMe searches for already known genetic variations, like those for cystic fibrosis, sickle cell anemia, and other diseases and traits.\u003c/p>\n\u003cp>Because 23andMe only looks for the parts of your DNA known to be associated with certain traits or diseases, it can’t report on variations that are present but have yet to be determined as significant. Or on rare variants that they know what effect they have but do not test for.\u003c/p>\n\u003cfigure id=\"attachment_125387\" class=\"wp-caption aligncenter\" style=\"max-width: 700px\">\u003cimg class=\"size-full wp-image-125387\" src=\"http://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/03/MotherBaby.jpg\" alt=\"You are special and so is your DNA. (Pixabay)\" width=\"700\" height=\"466\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/03/MotherBaby.jpg 700w, https://ww2.kqed.org/app/uploads/sites/13/2016/03/MotherBaby-400x266.jpg 400w\" sizes=\"(max-width: 700px) 100vw, 700px\">\u003cfigcaption class=\"wp-caption-text\">You are special and so is your DNA. (\u003ca href=\"https://pixabay.com/en/baby-care-caucasian-cheek-child-17327/\">Pixabay\u003c/a>) \u003ccite>(Pixabay)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Remember how your mom told you you're \"special.\" Well, that's technically true, because everyone’s DNA is unique.\u003c/p>\n\u003cp>But it also means scientists trying to interpret vast stretches of your genetic code is like Egyptologists staring at hieroglyphics without the benefit of the Rosetta Stone. So even though your entire genome has the potential to one day tell you a whole lot about yourself, currently it's not saying much. And anyone looking at it won't know how or whether the majority of combinations in your genetic code determine your health and other traits.\u003c/p>\n\u003cp>For example, if a unique sequence falls within a gene implicated in a disease, then you may or may not be at a higher risk for that disease. Sometimes scientists can make a reasonable prediction, but often they can’t. Now imagine these types of unknowns strewn throughout your genome.\u003c/p>\n\u003cp>But this will not always be the case. As scientists learn more and more about what different parts of the human genome can tell us, your own sequence will become more and more communicative, so to speak. Meaning one day, that information could be found to impact your health.\u003c/p>\n\u003cp>\u003cstrong>You Need Coverage\u003c/strong>\u003c/p>\n\u003cp>If you do choose to spend more money to explore the unknown reaches of your genome, you want to make sure that data is high quality. Good quality genomes don’t contain a lot of mistakes, and they aren’t missing big sections.\u003c/p>\n\u003cp>The key thing to look for is something called \"coverage.\"\u003c/p>\n\u003cp>Basically, coverage is how many times on average your genome has been read. One rule of thumb: If a whole genome sequence (WGS) is going to be used to predict individual characteristics, it should be read a \u003ca href=\"http://www.ccmb.med.umich.edu/node/1186\">bare minimum of 30 times\u003c/a>.\u003c/p>\n\u003cp>Dr. Michael Snyder, chair of the Department of Genetics at Stanford University, says even more is better. \"I would do at least 60X and even that will not give adequate coverage in a lot of regions.\"\u003c/p>\n\u003cp>Why do scientists need to read the same DNA over and over again? Mainly because while new technologies have made sequencing much cheaper, they have also made it vulnerable to a greater number of mistakes. Scientists now need a lot of reads to ensure the sequence is correct.\u003c/p>\n\u003cp>Another reason so many reads are required is that some parts of the genome just don’t sequence very well. You need to do a lot of sequencing to get these regions to appear in the data.\u003c/p>\n\u003cp>\u003cstrong>More than DNA\u003c/strong>\u003c/p>\n\u003cp>Of course with Veritas and other services that provide you with your entire genome, you are paying for more than your genetic code. You are also paying for the interpretation and the counseling that comes with your results.\u003c/p>\n\u003cp>How valuable that is to you will depend on which results the company interprets, how much counseling it will offer, and, finally, how you will respond to the data. Handled right, information about your genetic predispositions can be extremely helpful. But handled poorly, it can be confusing, worrying, and perhaps lead to \u003ca href=\"http://ww2.kqed.org/futureofyou/2016/02/08/student-was-asked-to-leave-school-because-of-his-dna/\" target=\"_blank\">unintended consequences\u003c/a>.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>They say a little information can be dangerous. But too much can be overwhelming.\u003c/p>\n\n\u003c/div>\u003c/p>",
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"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.",
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"soldout": {
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"title": "SOLD OUT: Rethinking Housing in America",
"tagline": "A new future for housing",
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