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class=\"attachment\">\u003ca href='http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/alzheimer2.jpg' title='alzheimer'>\u003cimg width=\"300\" height=\"200\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/alzheimer2.jpg\" class=\"attachment-medium\" alt=\"alzheimer\" title=\"alzheimer\" 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Barry Starr","firstName":"Dr. Barry","lastName":"Starr","slug":"dr-barry-starr","email":"bstarr@thetech.org","display_author_email":false,"staff_mastheads":[],"title":null,"bio":"Dr. Barry Starr (\u003ca href=\"https://twitter.com/geneticsboy\">@geneticsboy\u003c/a>) is a Geneticist-in-Residence at The Tech Museum of Innovation in San Jose, CA and runs their Stanford at The Tech program. The program is part of an ongoing collaboration between the \u003ca href=\"http://genetics.stanford.edu/\">Stanford Department of Genetics\u003c/a> and \u003ca href=\"http://www.thetech.org/\">The Tech Museum of Innovation\u003c/a>. Together these two partners created the \u003ca href=\"http://www.thetech.org/exhibits/permanent/index.php?sGalKey=gtwt&galKey=lt\">Genetics: Technology with a Twist\u003c/a> exhibition.\r\n\r\nYou can also see \u003ca href=\"https://ww2.kqed.org/science/author/dr-barry-starr/\">additional posts by Barry at KQED Science\u003c/a>, and read his \u003ca href=\"http://science.kqed.org/quest/author/dr-barry-starr/\">previous contributions\u003c/a> to \u003ca href=\"http://science.kqed.org/quest/\">QUEST\u003c/a>, a project dedicated to exploring the Science of Sustainability.","avatar":"https://secure.gravatar.com/avatar/4a5680e4c642ea0f0f3041af16018969?s=600&d=blank&r=g","twitter":"geneticsboy","facebook":null,"instagram":null,"linkedin":null,"sites":[{"site":"science","roles":["author"]},{"site":"quest","roles":["subscriber"]}],"headData":{"title":"Dr. Barry Starr | KQED","description":null,"ogImgSrc":"https://secure.gravatar.com/avatar/4a5680e4c642ea0f0f3041af16018969?s=600&d=blank&r=g","twImgSrc":"https://secure.gravatar.com/avatar/4a5680e4c642ea0f0f3041af16018969?s=600&d=blank&r=g"},"isLoading":false,"link":"/author/dr-barry-starr"}},"breakingNewsReducer":{},"campaignFinanceReducer":{},"firebase":{"requesting":{},"requested":{},"timestamps":{},"data":{},"ordered":{},"auth":{"isLoaded":false,"isEmpty":true},"authError":null,"profile":{"isLoaded":false,"isEmpty":true},"listeners":{"byId":{},"allIds":[]},"isInitializing":false,"errors":[]},"navBarReducer":{"navBarId":"home","fullView":true,"showPlayer":false},"navMenuReducer":{"menus":[{"key":"menu1","items":[{"name":"News","link":"/","type":"title"},{"name":"Politics","link":"/politics"},{"name":"Science","link":"/science"},{"name":"Education","link":"/educationnews"},{"name":"Housing","link":"/housing"},{"name":"Immigration","link":"/immigration"},{"name":"Criminal Justice","link":"/criminaljustice"},{"name":"Silicon Valley","link":"/siliconvalley"},{"name":"Forum","link":"/forum"},{"name":"The California Report","link":"/californiareport"}]},{"key":"menu2","items":[{"name":"Arts & Culture","link":"/arts","type":"title"},{"name":"Critics’ Picks","link":"/thedolist"},{"name":"Cultural Commentary","link":"/artscommentary"},{"name":"Food & Drink","link":"/food"},{"name":"Bay Area Hip-Hop","link":"/bayareahiphop"},{"name":"Rebel Girls","link":"/rebelgirls"},{"name":"Arts Video","link":"/artsvideos"}]},{"key":"menu3","items":[{"name":"Podcasts","link":"/podcasts","type":"title"},{"name":"Bay Curious","link":"/podcasts/baycurious"},{"name":"Rightnowish","link":"/podcasts/rightnowish"},{"name":"The Bay","link":"/podcasts/thebay"},{"name":"On Our Watch","link":"/podcasts/onourwatch"},{"name":"Mindshift","link":"/podcasts/mindshift"},{"name":"Consider This","link":"/podcasts/considerthis"},{"name":"Political Breakdown","link":"/podcasts/politicalbreakdown"}]},{"key":"menu4","items":[{"name":"Live Radio","link":"/radio","type":"title"},{"name":"TV","link":"/tv","type":"title"},{"name":"Events","link":"/events","type":"title"},{"name":"For Educators","link":"/education","type":"title"},{"name":"Support KQED","link":"/support","type":"title"},{"name":"About","link":"/about","type":"title"},{"name":"Help Center","link":"https://kqed-helpcenter.kqed.org/s","type":"title"}]}]},"pagesReducer":{},"postsReducer":{"stream_live":{"type":"live","id":"stream_live","audioUrl":"https://streams.kqed.org/kqedradio","title":"Live Stream","excerpt":"Live Stream information currently unavailable.","link":"/radio","featImg":"","label":{"name":"KQED Live","link":"/"}},"stream_kqedNewscast":{"type":"posts","id":"stream_kqedNewscast","audioUrl":"https://www.kqed.org/.stream/anon/radio/RDnews/newscast.mp3?_=1","title":"KQED Newscast","featImg":"","label":{"name":"88.5 FM","link":"/"}},"quest_19244":{"type":"posts","id":"quest_19244","meta":{"index":"posts_1591205157","site":"quest","id":"19244","score":null,"sort":[1308587263000]},"guestAuthors":[],"slug":"the-cloud-in-the-silver-lining","title":"The Cloud in the Silver Lining","publishDate":1308587263,"format":"standard","headTitle":"QUEST | KQED Science","labelTerm":{"site":"quest"},"content":"\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/06/SilverLining.jpg\" alt=\"\">\u003c/a>\u003cem>My lower risk for Alzheimer's may be the silver lining\u003cbr>to being e2/e2 at APOE.\u003cbr>Image courtesy of \u003ca href=\"http://commons.wikimedia.org/wiki/File:Silver_Lining.JPG\">ImUnicke\u003c/a>\u003c/em>\u003c/span>\u003c/p>\n\u003cp>When last I left you in my \u003ca href=\"http://ww2.kqed.org/quest/2011/05/23/uncovering-risk-one-gene-at-a-time/\">personal genomic journey\u003c/a>, I had just discovered that I was e2/e2 at the APOE gene. I was quietly giddy* about this as it meant I was at a lower risk for getting Alzheimer’s. And even more importantly, it meant I didn’t have e4 which would have significantly increased my chances of getting this form of dementia.\u003c/p>\n\u003cp>Digging a bit deeper I found some more good news. People with e2/e2 usually have lower levels of LDL, the bad cholesterol that increases the risk for a heart attack. This is consistent with my low levels of LDL. Two good effects from one allele!\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>But there are no free lunches in genetics. For example, having two copies of the delta32 version of the CCR5 gene makes you \u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/ask.php?id=336\">pretty resistant to HIV infection\u003c/a>. But it makes you more susceptible to the West Nile Virus. Having one copy of the sickle cell version of the hemoglobin gene makes you \u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/ask.php?id=271\">resistant to malaria\u003c/a>. But your kids might end up with full blown sickle cell anemia. And so on.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The e2 version of the APOE gene is no different. It makes me less likely to get Alzheimer’s and, most of the time, to have a heart attack. But it means that I can end up with higher triglycerides from what I eat. This is consistent with what I have seen at the doctor’s. \u003c/p>\n\u003cp>Triglycerides are actually an independent predictor of heart attack risk. So even though my LDL is low, I need to watch my diet to keep the triglycerides down. If I am not careful, my increased triglycerides might cancel out my decreased LDL and so change my reduced heart attack risk to an increased one. \u003c/p>\n\u003cp>Being e2/e2 also puts me at risk for a relatively rare disease called \u003ca href=\"http://www.kimballgenetics.com/tests-apo_e.html\">hyperlipoproteinemia type III\u003c/a> (HLP type 3). One reason this disease is rare is because being e2/e2 is rare. For example, only around 0.4% of people of European background have this genetic combination.\u003c/p>\n\u003cp>But HLP type 3 is obviously more common for me since I am in that 0.4% group already. Still, only 2% of e2/e2 people end up with HLP type 3 so it is a low risk for me. I decided to look into it anyway.\u003c/p>\n\u003cp>This disease has various symptoms but the most worrisome ones for me are increased risk of heart attack and abnormal glucose tolerance. My fasting glucose levels are stubbornly high whenever I take my yearly blood test. Which makes me wonder if this genetic difference is affecting my glucose tolerance and I am on my way to HLP type 3.\u003c/p>\n\u003cp>Of course, lots of genetic differences are involved in establishing someone’s glucose tolerance. And the environment plays a role too. So my glucose tolerance might have nothing to do with me starting to get HLP type 3.\u003c/p>\n\u003cp>Still, I am definitely going to ask my doctor about it at my next visit. It is rare but there are specific blood tests I can ask for that can tell me if I have this condition. Who’d have thought that a lowered risk of Alzheimer’s would only be a silver lining…\u003c/p>\n\u003cp>*\u003cem>Well, more of a measured giddiness. I know this is just one of the many genes involved in Alzheimer’s but still, it was good news\u003c/em>.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.3393857 -121.8949555\u003c/p>\n\n","blocks":[],"excerpt":"There are no free lunches in genetics. Having a certain version of a gene may protect you from one thing, but make you susceptible to another.","status":"publish","parent":0,"modified":1308587263,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":16,"wordCount":598},"headData":{"title":"The Cloud in the Silver Lining | KQED","description":"There are no free lunches in genetics. Having a certain version of a gene may protect you from one thing, but make you susceptible to another.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"19244 http://www.kqed.org/quest/blog/2011/06/20/the-cloud-in-the-silver-lining/","disqusUrl":"https://ww2.kqed.org/quest/2011/06/20/the-cloud-in-the-silver-lining/","disqusTitle":"The Cloud in the Silver Lining","path":"/quest/19244/the-cloud-in-the-silver-lining","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/06/SilverLining.jpg\" alt=\"\">\u003c/a>\u003cem>My lower risk for Alzheimer's may be the silver lining\u003cbr>to being e2/e2 at APOE.\u003cbr>Image courtesy of \u003ca href=\"http://commons.wikimedia.org/wiki/File:Silver_Lining.JPG\">ImUnicke\u003c/a>\u003c/em>\u003c/span>\u003c/p>\n\u003cp>When last I left you in my \u003ca href=\"http://ww2.kqed.org/quest/2011/05/23/uncovering-risk-one-gene-at-a-time/\">personal genomic journey\u003c/a>, I had just discovered that I was e2/e2 at the APOE gene. I was quietly giddy* about this as it meant I was at a lower risk for getting Alzheimer’s. And even more importantly, it meant I didn’t have e4 which would have significantly increased my chances of getting this form of dementia.\u003c/p>\n\u003cp>Digging a bit deeper I found some more good news. People with e2/e2 usually have lower levels of LDL, the bad cholesterol that increases the risk for a heart attack. This is consistent with my low levels of LDL. Two good effects from one allele!\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>But there are no free lunches in genetics. For example, having two copies of the delta32 version of the CCR5 gene makes you \u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/ask.php?id=336\">pretty resistant to HIV infection\u003c/a>. But it makes you more susceptible to the West Nile Virus. Having one copy of the sickle cell version of the hemoglobin gene makes you \u003ca href=\"http://www.thetech.org/exhibits/online/ugenetics/ask.php?id=271\">resistant to malaria\u003c/a>. But your kids might end up with full blown sickle cell anemia. And so on.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>The e2 version of the APOE gene is no different. It makes me less likely to get Alzheimer’s and, most of the time, to have a heart attack. But it means that I can end up with higher triglycerides from what I eat. This is consistent with what I have seen at the doctor’s. \u003c/p>\n\u003cp>Triglycerides are actually an independent predictor of heart attack risk. So even though my LDL is low, I need to watch my diet to keep the triglycerides down. If I am not careful, my increased triglycerides might cancel out my decreased LDL and so change my reduced heart attack risk to an increased one. \u003c/p>\n\u003cp>Being e2/e2 also puts me at risk for a relatively rare disease called \u003ca href=\"http://www.kimballgenetics.com/tests-apo_e.html\">hyperlipoproteinemia type III\u003c/a> (HLP type 3). One reason this disease is rare is because being e2/e2 is rare. For example, only around 0.4% of people of European background have this genetic combination.\u003c/p>\n\u003cp>But HLP type 3 is obviously more common for me since I am in that 0.4% group already. Still, only 2% of e2/e2 people end up with HLP type 3 so it is a low risk for me. I decided to look into it anyway.\u003c/p>\n\u003cp>This disease has various symptoms but the most worrisome ones for me are increased risk of heart attack and abnormal glucose tolerance. My fasting glucose levels are stubbornly high whenever I take my yearly blood test. Which makes me wonder if this genetic difference is affecting my glucose tolerance and I am on my way to HLP type 3.\u003c/p>\n\u003cp>Of course, lots of genetic differences are involved in establishing someone’s glucose tolerance. And the environment plays a role too. So my glucose tolerance might have nothing to do with me starting to get HLP type 3.\u003c/p>\n\u003cp>Still, I am definitely going to ask my doctor about it at my next visit. It is rare but there are specific blood tests I can ask for that can tell me if I have this condition. Who’d have thought that a lowered risk of Alzheimer’s would only be a silver lining…\u003c/p>\n\u003cp>*\u003cem>Well, more of a measured giddiness. I know this is just one of the many genes involved in Alzheimer’s but still, it was good news\u003c/em>.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.3393857 -121.8949555\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/19244/the-cloud-in-the-silver-lining","authors":["6177"],"categories":["quest_4"],"tags":["quest_134","quest_135","quest_3458","quest_3546","quest_3553","quest_3555","quest_1192","quest_1197","quest_1332","quest_3610","quest_2162","quest_3804"],"featImg":"quest_15236","label":"quest"},"quest_14037":{"type":"posts","id":"quest_14037","meta":{"index":"posts_1591205157","site":"quest","id":"14037","score":null,"sort":[1303749791000]},"guestAuthors":[],"slug":"better-left-unknown","title":"Better Left Unknown?","publishDate":1303749791,"format":"standard","headTitle":"QUEST | KQED Science","labelTerm":{"site":"quest"},"content":"\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/Redact2.jpg\" alt=\"\">\u003c/a>\u003cem>I might be better off NOT knowing some things about my genes.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Last \u003ca href=\"http://ww2.kqed.org/quest/2011/04/11/dna-diving-for-alzheimer%E2%80%99s/\">blog \u003c/a>I talked about how I was able to wrest information about my APOE gene from my 23andMe data. I wanted to know because of this gene’s link to late onset Alzheimer’s disease.\u003c/p>\n\u003cp>APOE comes in three versions: e2, e3, and e4. People with two e4 versions are around 15 times more likely to end up with Alzheimer’s than are people with two e3 versions. And if these e4 folks do get the disease, it tends to come at an earlier age. \u003c/p>\n\u003cp>I found out that I actually have two e2 versions which protects me somewhat from getting late onset Alzheimer’s. Good news? I guess…\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>In all of this, I didn’t ask whether this information is worth knowing. Being e2/e2 doesn’t mean I won’t get Alzheimer’s…it just means I am at a lower risk. But at least I didn’t find out I was e4/e4. Then I’d know I was more likely to get Alzheimer’s but not be able to do anything medically useful with that information. \u003c/p>\n\u003cp>Being e4/e4 would not have meant that I would for sure end up with Alzheimer’s. So it wouldn’t be like having two copies of the \u003ca href=\"http://www.ornl.gov/sci/techresources/Human_Genome/posters/chromosome/cftr.shtml\">delta-508\u003c/a> marker of the CFTR gene. In that case, I would almost certainly have developed cystic fibrosis. No, two copies of e4 would just mean that I was at a higher risk.\u003c/p>\n\u003cp>And knowing this wouldn’t be able to help me medically at all. There aren’t any good preventative measures I could take to stave off Alzheimer’s. \u003c/p>\n\u003cp>Now this isn’t always true with these kinds of increased risk genetic markers—some are definitely worth knowing. Women who have certain \u003ca href=\"http://www.cancer.gov/cancertopics/factsheet/Risk/BRCA\">BRCA1/BRCA2\u003c/a> markers are at an increased risk for getting breast or ovarian cancer. They can choose to screen early (and often) in the hope of catching the cancer early when it is more treatable. Or, more drastically, they can choose to have their breasts and/or ovaries removed. Neither is really an option for Alzheimer’s.\u003c/p>\n\u003cp>So knowing my APOE status isn’t really that useful medically (at least not yet). I can’t do anything useful with the information other than wait and see if I end up with Alzheimer’s. Which is pretty much what I would have done without the test.\u003c/p>\n\u003cp>I’m bringing all of this up because 23andMe is now offering people their APOE information (with an upgrade to their new chip, of course). People can now find out their particular combination of e2, e3, and e4 markers*. \u003c/p>\n\u003cp>In the past, the question was whether or not direct to consumer (DTC) genetic testing companies should offer such a test. That ship has either sailed or is getting ready to leave the harbor. The test will be made available to people who really want the information.\u003c/p>\n\u003cp>So now the key question is whether knowing your APOE status is worth it. The answer to this question will be different for different people. Given this, the most important thing is for people to have the information they need to make the right choice about whether they want to know their APOE status or not.\u003c/p>\n\u003cp>One way to figure this out is with a genetic counselor but most DTC tests don’t mandate that you need to talk to one before you are tested. This means it is absolutely critical that the online information provided by DTC companies are presented in an easy to understand way that does not oversell the genetic test. The DTC companies need to be upfront in the fact that this test is not predictive and that there are no proven preventative measures that can keep Alzheimer’s at bay.\u003c/p>\n\u003cp>I’ll let you all judge how well 23andMe has done at letting people know about what you can learn from the APOE test and what you can do with that knowledge. Click \u003ca href=\"https://www.23andme.com/health/alzheimers/\">here \u003c/a>to read what they have to say.\u003c/p>\n\u003cp>* \u003cem>You have always been able to get your APOE status with a more expensive genetic test from \u003ca href=\"http://www.decodeme.com/\">deCODEme\u003c/a>.\u003c/em>\u003c/p>\n\u003cp>\u003ca href=\"http://www.thetech.org/genetics/ask.php?id=405\">Learn more about how genes and the environment work together to cause Alzheimer's.\u003c/a> \u003c/p>\n\u003cp>\u003cem>I put this video in the last blog but it probably should have gone in this one. It shows the unintended consequences of finding out you are e4/e4.\u003c/em>\u003c/p>\n\u003cp style=\"text-align: center\">\n\u003ciframe width=\"425\" height=\"349\" src=\"http://www.youtube.com/embed/oGuvzlD7Yx8\" frameborder=\"0\">\u003c/iframe>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n","blocks":[],"excerpt":"Just because we can find out about some of our genetic information, should we? Even though the results are often not very useful or even very informative, they can sometimes be a real burden.","status":"publish","parent":0,"modified":1303749791,"stats":{"hasAudio":false,"hasVideo":true,"hasChartOrMap":true,"iframeSrcs":["http://www.youtube.com/embed/oGuvzlD7Yx8"],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":21,"wordCount":777},"headData":{"title":"Better Left Unknown? | KQED","description":"Just because we can find out about some of our genetic information, should we? Even though the results are often not very useful or even very informative, they can sometimes be a real burden.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"14037 http://www.kqed.org/quest/blog/2011/04/25/better-left-unknown/","disqusUrl":"https://ww2.kqed.org/quest/2011/04/25/better-left-unknown/","disqusTitle":"Better Left Unknown?","path":"/quest/14037/better-left-unknown","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"left\">\u003ca href=\"http://www.kqed.org/quest\">\u003cimg src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/Redact2.jpg\" alt=\"\">\u003c/a>\u003cem>I might be better off NOT knowing some things about my genes.\u003c/em>\u003c/span>\u003c/p>\n\u003cp>Last \u003ca href=\"http://ww2.kqed.org/quest/2011/04/11/dna-diving-for-alzheimer%E2%80%99s/\">blog \u003c/a>I talked about how I was able to wrest information about my APOE gene from my 23andMe data. I wanted to know because of this gene’s link to late onset Alzheimer’s disease.\u003c/p>\n\u003cp>APOE comes in three versions: e2, e3, and e4. People with two e4 versions are around 15 times more likely to end up with Alzheimer’s than are people with two e3 versions. And if these e4 folks do get the disease, it tends to come at an earlier age. \u003c/p>\n\u003cp>I found out that I actually have two e2 versions which protects me somewhat from getting late onset Alzheimer’s. Good news? I guess…\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>In all of this, I didn’t ask whether this information is worth knowing. Being e2/e2 doesn’t mean I won’t get Alzheimer’s…it just means I am at a lower risk. But at least I didn’t find out I was e4/e4. Then I’d know I was more likely to get Alzheimer’s but not be able to do anything medically useful with that information. \u003c/p>\n\u003cp>Being e4/e4 would not have meant that I would for sure end up with Alzheimer’s. So it wouldn’t be like having two copies of the \u003ca href=\"http://www.ornl.gov/sci/techresources/Human_Genome/posters/chromosome/cftr.shtml\">delta-508\u003c/a> marker of the CFTR gene. In that case, I would almost certainly have developed cystic fibrosis. No, two copies of e4 would just mean that I was at a higher risk.\u003c/p>\n\u003cp>And knowing this wouldn’t be able to help me medically at all. There aren’t any good preventative measures I could take to stave off Alzheimer’s. \u003c/p>\n\u003cp>Now this isn’t always true with these kinds of increased risk genetic markers—some are definitely worth knowing. Women who have certain \u003ca href=\"http://www.cancer.gov/cancertopics/factsheet/Risk/BRCA\">BRCA1/BRCA2\u003c/a> markers are at an increased risk for getting breast or ovarian cancer. They can choose to screen early (and often) in the hope of catching the cancer early when it is more treatable. Or, more drastically, they can choose to have their breasts and/or ovaries removed. Neither is really an option for Alzheimer’s.\u003c/p>\n\u003cp>So knowing my APOE status isn’t really that useful medically (at least not yet). I can’t do anything useful with the information other than wait and see if I end up with Alzheimer’s. Which is pretty much what I would have done without the test.\u003c/p>\n\u003cp>I’m bringing all of this up because 23andMe is now offering people their APOE information (with an upgrade to their new chip, of course). People can now find out their particular combination of e2, e3, and e4 markers*. \u003c/p>\n\u003cp>In the past, the question was whether or not direct to consumer (DTC) genetic testing companies should offer such a test. That ship has either sailed or is getting ready to leave the harbor. The test will be made available to people who really want the information.\u003c/p>\n\u003cp>So now the key question is whether knowing your APOE status is worth it. The answer to this question will be different for different people. Given this, the most important thing is for people to have the information they need to make the right choice about whether they want to know their APOE status or not.\u003c/p>\n\u003cp>One way to figure this out is with a genetic counselor but most DTC tests don’t mandate that you need to talk to one before you are tested. This means it is absolutely critical that the online information provided by DTC companies are presented in an easy to understand way that does not oversell the genetic test. The DTC companies need to be upfront in the fact that this test is not predictive and that there are no proven preventative measures that can keep Alzheimer’s at bay.\u003c/p>\n\u003cp>I’ll let you all judge how well 23andMe has done at letting people know about what you can learn from the APOE test and what you can do with that knowledge. Click \u003ca href=\"https://www.23andme.com/health/alzheimers/\">here \u003c/a>to read what they have to say.\u003c/p>\n\u003cp>* \u003cem>You have always been able to get your APOE status with a more expensive genetic test from \u003ca href=\"http://www.decodeme.com/\">deCODEme\u003c/a>.\u003c/em>\u003c/p>\n\u003cp>\u003ca href=\"http://www.thetech.org/genetics/ask.php?id=405\">Learn more about how genes and the environment work together to cause Alzheimer's.\u003c/a> \u003c/p>\n\u003cp>\u003cem>I put this video in the last blog but it probably should have gone in this one. It shows the unintended consequences of finding out you are e4/e4.\u003c/em>\u003c/p>\n\u003cp style=\"text-align: center\">\n\u003ciframe width=\"425\" height=\"349\" src=\"http://www.youtube.com/embed/oGuvzlD7Yx8\" frameborder=\"0\">\u003c/iframe>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/14037/better-left-unknown","authors":["6177"],"categories":["quest_4"],"tags":["quest_43","quest_134","quest_135","quest_3458","quest_377","quest_3530","quest_3553","quest_3554","quest_3555","quest_3587","quest_1195","quest_1197","quest_3652","quest_2161"],"featImg":"quest_13535","label":"quest"},"quest_13504":{"type":"posts","id":"quest_13504","meta":{"index":"posts_1591205157","site":"quest","id":"13504","score":null,"sort":[1302537708000]},"guestAuthors":[],"slug":"dna-diving-for-alzheimer%e2%80%99s","title":"DNA Diving for Alzheimer’s","publishDate":1302537708,"format":"standard","headTitle":"DNA Diving for Alzheimer’s | KQED","labelTerm":{"site":"quest"},"content":"\u003ctable align=\"left\">\n\u003ctbody>\n\u003ctr>\n\u003ctd>\u003cimg decoding=\"async\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/AlzPetScan22.gif\" alt=\"\">\u003cbr>\n\u003cspan style=\"color: #999999\">My 23andMe test tells me I am less likely to end up\u003cbr>\nwith the brain on the left.\u003cbr>\nImage courtesy of \u003ca href=\"http://commons.wikimedia.org/wiki/File:PiB_PET_Images_AD.jpg\">Klunkwe\u003c/a>.\u003c/span>\u003c/td>\n\u003c/tr>\n\u003c/tbody>\n\u003c/table>\n\u003cp>I was having lunch with a colleague the other day and we got to talking about genetic testing (yes, we are that geeky). I told him about how my 23andMe test had missed my being prediabetic. This says a lot about what 23andMe’s test can tell me about my risk for diabetes. Not much.\u003c/p>\n\u003cp>Now as I have \u003ca href=\"http://ww2.kqed.org/quest/2009/10/12/do-these-genes-make-me-look-diabetic/\">said before\u003c/a>, the fact that 23andMe can’t tell me that I’m likely to become diabetic from their DNA test isn’t their fault (other than, perhaps, some overselling on their part). Diabetes research just isn’t far enough along to be able to accurately predict whether someone will get diabetes or not. Or to make any really meaningful prediction about diabetes at all.\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>We then got to talking about Alzheimer’s. Turns out his family tree is littered with Alzheimer’s on both his mother’s and father’s side. He ran into a similar problem–23andMe doesn’t report anything for Alzheimer’s.\u003c/p>\n\u003cp>But here the situation is a bit different than for diabetes. There are a couple of DNA markers that can tell us a lot about our future risk for late onset Alzheimer’s. It just so happens that 23andMe doesn’t report on them.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>These markers deal with the APOE gene. This gene comes in three common versions: e2, e3, and e4. People with two copies of the e4 version are 15 times more likely to develop Alzheimer’s and if they do end up with the disease, it tends to come earlier. (One copy of e4 increases your risk about 3 times.)\u003c/p>\n\u003cp>With a little help from my colleague, I decided to dig a bit deeper into Alzheimer’s and see what I could figure out from what 23andMe did provide. Turns out I can figure out a whole lot about my APOE status. And that I can help other people figure out more from their results too.\u003c/p>\n\u003cp>The two markers (also called \u003ca href=\"http://www.ncbi.nlm.nih.gov/About/primer/snps.html\">SNP\u003c/a>s) that deal with APOE and Alzheimer’s are rs429358 and rs7412. Here, according to \u003ca href=\"http://www.snpedia.com/index.php/ApoE\">SNPedia\u003c/a>, are the combinations of these markers that tell you your APOE status:\u003c/p>\n\u003cp style=\"text-align: center\">\u003cimg decoding=\"async\" class=\"alignnone\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/APOEtable2.jpg\" alt=\"\">\u003c/p>\n\u003cp>To my surprise, 23andMe gives information on one of them, rs7412. Even though this isn’t usually enough to tell whether you have the dreaded e4 version or not, in my case it was. I almost certainly do not have any versions of e4 (yay!).\u003c/p>\n\u003cp>See, my results at rs7412 are TT*. If I am interpreting these results correctly, this means I almost certainly have two copies of the e2 version of the APOE gene. In terms of my Alzheimer’s risk this is great news as being e2/e2 actually lowers your risk for getting the disease. (There is a chance I could be e1 but this doesn’t seem to be a very common version at all.)\u003c/p>\n\u003cp>Of course this doesn’t mean I won’t get Alzheimer’s…I still might. After all, the \u003ca href=\"http://www.alz.org/alzheimers_disease_causes_risk_factors.asp#familyhistory\">risk \u003c/a>for someone over 85 getting Alzheimer’s is almost 50%. Even though this number lumps e4 and e2 folks together, e2 people do not have a 0% risk for Alzheimer’s nor do e4 people have a 100% chance. People with e4 are just more likely to have Alzheimer’s than e2 people.\u003c/p>\n\u003cp>It might help to think about getting Alzheimer’s like drawing an inside straight in poker. Everyone might do it but people who are playing with wildcards are more likely to get it. These are the e4 folks. But it isn’t a for sure thing…you still may not draw the straight even with deuces wild.\u003c/p>\n\u003cp>Same thing with not having e4. Now I am less likely to draw that inside straight because there are no wild cards but it can still happen.\u003c/p>\n\u003cp>Because I was TT at rs7412, my case was pretty easy to figure out. Next blog I’ll try to help people out who are TC or CC at rs7412.\u003c/p>\n\u003cp>*\u003cem>Remember, we have two copies of each of our genes. So I have a T at rs7412 in one copy and a T at rs7412 in my other copy.\u003c/em>\u003c/p>\n\u003cp>\u003cem>A video showing why knowing your APOE status isn’t necessarily a good thing.\u003c/em>\u003c/p>\n\u003cp style=\"text-align: center\">\n\u003ciframe loading=\"lazy\" width=\"425\" height=\"349\" src=\"http://www.youtube.com/embed/oGuvzlD7Yx8\" frameborder=\"0\">\u003c/iframe>\u003c/p>\n\u003cp>Learn more about current Bay Area genetic research from \u003ca href=\"http://www.kqed.org/a/forum/R201104050900\">KQED’s Forum. \u003c/a>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n","blocks":[],"excerpt":"I was able to figure out my APOE status and so one of my key risk factors for developing late onset Alzheimer's from my 23andMe test even though 23andMe doesn't officially report any results for Alzheimer's.","status":"publish","parent":0,"modified":1684974330,"stats":{"hasAudio":false,"hasVideo":true,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":20,"wordCount":777},"headData":{"title":"DNA Diving for Alzheimer’s | KQED","description":"I was able to figure out my APOE status and so one of my key risk factors for developing late onset Alzheimer's from my 23andMe test even though 23andMe doesn't officially report any results for Alzheimer's.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"templateType":"standard","featuredImageType":"standard","excludeFromSiteSearch":"Include","articleAge":"0","path":"/quest/13504/dna-diving-for-alzheimer%e2%80%99s","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003ctable align=\"left\">\n\u003ctbody>\n\u003ctr>\n\u003ctd>\u003cimg decoding=\"async\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/AlzPetScan22.gif\" alt=\"\">\u003cbr>\n\u003cspan style=\"color: #999999\">My 23andMe test tells me I am less likely to end up\u003cbr>\nwith the brain on the left.\u003cbr>\nImage courtesy of \u003ca href=\"http://commons.wikimedia.org/wiki/File:PiB_PET_Images_AD.jpg\">Klunkwe\u003c/a>.\u003c/span>\u003c/td>\n\u003c/tr>\n\u003c/tbody>\n\u003c/table>\n\u003cp>I was having lunch with a colleague the other day and we got to talking about genetic testing (yes, we are that geeky). I told him about how my 23andMe test had missed my being prediabetic. This says a lot about what 23andMe’s test can tell me about my risk for diabetes. Not much.\u003c/p>\n\u003cp>Now as I have \u003ca href=\"http://ww2.kqed.org/quest/2009/10/12/do-these-genes-make-me-look-diabetic/\">said before\u003c/a>, the fact that 23andMe can’t tell me that I’m likely to become diabetic from their DNA test isn’t their fault (other than, perhaps, some overselling on their part). Diabetes research just isn’t far enough along to be able to accurately predict whether someone will get diabetes or not. Or to make any really meaningful prediction about diabetes at all.\u003c/p>\n\u003cp>\u003c!--more-->\u003c/p>\n\u003cp>We then got to talking about Alzheimer’s. Turns out his family tree is littered with Alzheimer’s on both his mother’s and father’s side. He ran into a similar problem–23andMe doesn’t report anything for Alzheimer’s.\u003c/p>\n\u003cp>But here the situation is a bit different than for diabetes. There are a couple of DNA markers that can tell us a lot about our future risk for late onset Alzheimer’s. It just so happens that 23andMe doesn’t report on them.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>These markers deal with the APOE gene. This gene comes in three common versions: e2, e3, and e4. People with two copies of the e4 version are 15 times more likely to develop Alzheimer’s and if they do end up with the disease, it tends to come earlier. (One copy of e4 increases your risk about 3 times.)\u003c/p>\n\u003cp>With a little help from my colleague, I decided to dig a bit deeper into Alzheimer’s and see what I could figure out from what 23andMe did provide. Turns out I can figure out a whole lot about my APOE status. And that I can help other people figure out more from their results too.\u003c/p>\n\u003cp>The two markers (also called \u003ca href=\"http://www.ncbi.nlm.nih.gov/About/primer/snps.html\">SNP\u003c/a>s) that deal with APOE and Alzheimer’s are rs429358 and rs7412. Here, according to \u003ca href=\"http://www.snpedia.com/index.php/ApoE\">SNPedia\u003c/a>, are the combinations of these markers that tell you your APOE status:\u003c/p>\n\u003cp style=\"text-align: center\">\u003cimg decoding=\"async\" class=\"alignnone\" src=\"http://ww2.kqed.org/quest/wp-content/uploads/sites/39/2011/04/APOEtable2.jpg\" alt=\"\">\u003c/p>\n\u003cp>To my surprise, 23andMe gives information on one of them, rs7412. Even though this isn’t usually enough to tell whether you have the dreaded e4 version or not, in my case it was. I almost certainly do not have any versions of e4 (yay!).\u003c/p>\n\u003cp>See, my results at rs7412 are TT*. If I am interpreting these results correctly, this means I almost certainly have two copies of the e2 version of the APOE gene. In terms of my Alzheimer’s risk this is great news as being e2/e2 actually lowers your risk for getting the disease. (There is a chance I could be e1 but this doesn’t seem to be a very common version at all.)\u003c/p>\n\u003cp>Of course this doesn’t mean I won’t get Alzheimer’s…I still might. After all, the \u003ca href=\"http://www.alz.org/alzheimers_disease_causes_risk_factors.asp#familyhistory\">risk \u003c/a>for someone over 85 getting Alzheimer’s is almost 50%. Even though this number lumps e4 and e2 folks together, e2 people do not have a 0% risk for Alzheimer’s nor do e4 people have a 100% chance. People with e4 are just more likely to have Alzheimer’s than e2 people.\u003c/p>\n\u003cp>It might help to think about getting Alzheimer’s like drawing an inside straight in poker. Everyone might do it but people who are playing with wildcards are more likely to get it. These are the e4 folks. But it isn’t a for sure thing…you still may not draw the straight even with deuces wild.\u003c/p>\n\u003cp>Same thing with not having e4. Now I am less likely to draw that inside straight because there are no wild cards but it can still happen.\u003c/p>\n\u003cp>Because I was TT at rs7412, my case was pretty easy to figure out. Next blog I’ll try to help people out who are TC or CC at rs7412.\u003c/p>\n\u003cp>*\u003cem>Remember, we have two copies of each of our genes. So I have a T at rs7412 in one copy and a T at rs7412 in my other copy.\u003c/em>\u003c/p>\n\u003cp>\u003cem>A video showing why knowing your APOE status isn’t necessarily a good thing.\u003c/em>\u003c/p>\n\u003cp style=\"text-align: center\">\n\u003ciframe loading=\"lazy\" width=\"425\" height=\"349\" src=\"http://www.youtube.com/embed/oGuvzlD7Yx8\" frameborder=\"0\">\u003c/iframe>\u003c/p>\n\u003cp>Learn more about current Bay Area genetic research from \u003ca href=\"http://www.kqed.org/a/forum/R201104050900\">KQED’s Forum. \u003c/a>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp> 37.7749295 -122.4194155\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/quest/13504/dna-diving-for-alzheimer%e2%80%99s","authors":["6177"],"categories":["quest_4"],"tags":["quest_43","quest_134","quest_135","quest_3457","quest_3458","quest_377","quest_3530","quest_3553","quest_3554","quest_3555","quest_1195","quest_1197","quest_3652","quest_2161"],"featImg":"quest_13535","label":"quest"}},"programsReducer":{"possible":{"id":"possible","title":"Possible","info":"Possible is hosted by entrepreneur Reid Hoffman and writer Aria Finger. Together in Possible, Hoffman and Finger lead enlightening discussions about building a brighter collective future. The show features interviews with visionary guests like Trevor Noah, Sam Altman and Janette Sadik-Khan. Possible paints an optimistic portrait of the world we can create through science, policy, business, art and our shared humanity. It asks: What if everything goes right for once? How can we get there? Each episode also includes a short fiction story generated by advanced AI GPT-4, serving as a thought-provoking springboard to speculate how humanity could leverage technology for good.","airtime":"SUN 2pm","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/Possible-Podcast-Tile-360x360-1.jpg","officialWebsiteLink":"https://www.possible.fm/","meta":{"site":"news","source":"Possible"},"link":"/radio/program/possible","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/possible/id1677184070","spotify":"https://open.spotify.com/show/730YpdUSNlMyPQwNnyjp4k"}},"1a":{"id":"1a","title":"1A","info":"1A is home to the national conversation. 1A brings on great guests and frames the best debate in ways that make you think, share and engage.","airtime":"MON-THU 11pm-12am","imageSrc":"https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/1a.jpg","officialWebsiteLink":"https://the1a.org/","meta":{"site":"news","source":"npr"},"link":"/radio/program/1a","subscribe":{"npr":"https://rpb3r.app.goo.gl/RBrW","apple":"https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?s=143441&mt=2&id=1188724250&at=11l79Y&ct=nprdirectory","tuneIn":"https://tunein.com/radio/1A-p947376/","rss":"https://feeds.npr.org/510316/podcast.xml"}},"all-things-considered":{"id":"all-things-considered","title":"All Things Considered","info":"Every weekday, \u003cem>All Things Considered\u003c/em> hosts Robert Siegel, Audie Cornish, Ari Shapiro, and Kelly McEvers present the program's trademark mix of news, interviews, commentaries, reviews, and offbeat features. 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You can also visit the MindShift website for episodes and supplemental blog posts or tweet us \u003ca href=\"https://twitter.com/MindShiftKQED\">@MindShiftKQED\u003c/a> or visit us at \u003ca href=\"/mindshift\">MindShift.KQED.org\u003c/a>","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/Mindshift-Podcast-Tile-703x703-1.jpg","imageAlt":"KQED MindShift: How We Will Learn","officialWebsiteLink":"/mindshift/","meta":{"site":"news","source":"kqed","order":"2"},"link":"/podcasts/mindshift","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/mindshift-podcast/id1078765985","google":"https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM1NzY0NjAwNDI5","npr":"https://www.npr.org/podcasts/464615685/mind-shift-podcast","stitcher":"https://www.stitcher.com/podcast/kqed/stories-teachers-share","spotify":"https://open.spotify.com/show/0MxSpNYZKNprFLCl7eEtyx"}},"morning-edition":{"id":"morning-edition","title":"Morning Edition","info":"\u003cem>Morning Edition\u003c/em> takes listeners around the country and the world with multi-faceted stories and commentaries every weekday. 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On Our Watch brings listeners into the rooms where officers are questioned and witnesses are interrogated to find out who this system is really protecting. Is it the officers, or the public they've sworn to serve?","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/On-Our-Watch-Podcast-Tile-703x703-1.jpg","imageAlt":"On Our Watch from NPR and KQED","officialWebsiteLink":"/podcasts/onourwatch","meta":{"site":"news","source":"kqed","order":"1"},"link":"/podcasts/onourwatch","subscribe":{"apple":"https://podcasts.apple.com/podcast/id1567098962","google":"https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5ucHIub3JnLzUxMDM2MC9wb2RjYXN0LnhtbD9zYz1nb29nbGVwb2RjYXN0cw","npr":"https://rpb3r.app.goo.gl/onourwatch","spotify":"https://open.spotify.com/show/0OLWoyizopu6tY1XiuX70x","tuneIn":"https://tunein.com/radio/On-Our-Watch-p1436229/","stitcher":"https://www.stitcher.com/show/on-our-watch","rss":"https://feeds.npr.org/510360/podcast.xml"}},"on-the-media":{"id":"on-the-media","title":"On The Media","info":"Our weekly podcast explores how the media 'sausage' is made, casts an incisive eye on fluctuations in the marketplace of ideas, and examines threats to the freedom of information and expression in America and abroad. 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