<h5 class="wp-block-heading" id="h-data-initiative-accelerates-access-to-vital-genetic-and-clinical-insights">Data initiative accelerates access to vital genetic and clinical insights</h5>



<figure class="wp-block-image size-large"><img loading="lazy" decoding="async" width="1200" height="675" src="http://35.88.189.111/wp-content/uploads/2025/09/lung-double-edited-2.png" alt="Illustration of lungs on a background with a larger illustration of lungs" class="wp-image-34192" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2.png 1200w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2-300x169.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2-1024x576.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2-768x432.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2-880x495.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2-1180x664.png 1180w" sizes="auto, (max-width: 1200px) 100vw, 1200px" /></figure>



At the 2025 World Conference on Lung Cancer in Barcelona, the 23andMe Research Institute, in collaboration with Troper Wojcicki Philanthropies and the health data software company Lifebit, introduced an open-source platform that could help fast-track research discoveries through a powerful new cancer data repository.



The announcement comes just a year after the start of the<a href="https://www.23andme.com/lung-cancer" target="_blank" rel="noreferrer noopener"> Lung Cancer Genetics Study</a>, spearheaded by 23andMe and bringing together more than 20 lung cancer advocacy and science organizations to recruit 10,000 people diagnosed with lung cancer. Their goal is to develop new ways to identify those at highest risk for lung cancer early, while also finding possible new treatments for this deadly cancer.



<h2 class="wp-block-heading">The Personal Drive Behind the Mission</h2>



The effort is personal for many of the advocates who are part of the collaboration and also for Anne Wojcicki, founder and CEO of the 23andMe Research Institute. Anne&#8217;s sister Susan Wojcicki died of lung cancer last year, just as the study began.



&#8220;My sister was passionate about understanding the science behind lung cancer so future generations could prevent the disease and treat it. The Lung Cancer Genetics Study is a step towards achieving that.” Anne said.



In the months before her death, <a href="https://blog.23andme.com/articles/a-legacy-of-hope-in-the-fight-against-lung-cancer" target="_blank" rel="noreferrer noopener">Susan had been very involved in helping to create the study with the hope that it could help others</a>. The idea was not just to leverage genetic data for insights into lung cancer but also to create a repository of data that would be available to as many qualified researchers as possible.&nbsp;



The platform — created through the collaboration between the 23andMe Research Institute, Troper Wojcicki Philanthropies, and Lifebit — offers a secure, open-source data platform for researchers to access this novel dataset. Powered by Lifebit&#8217;s Health Data Ecosystem, the platform provides qualified researchers with no-cost access to de-identified data from people diagnosed with lung cancer who have consented to participate in this research.&nbsp;



&#8220;More people die of lung cancer each year than breast, colon, and prostate cancer combined, yet it is one of the least funded for research. It’s important for this powerful new tool to be available at no cost to qualified researchers so that the best minds can work on unlocking the genetic insights that may lead to a cure,&#8221; said Anne.



<h2 class="wp-block-heading">Building a One-of-a-Kind Data Resource</h2>



Since launching the <a href="https://blog.23andme.com/articles/23andme-launches-new-genetic-study-of-lung-cancer" target="_blank" rel="noreferrer noopener">Lung Cancer Genetics Study</a>, more than 1,200 people diagnosed with lung cancer have enrolled to participate in the research. The goal is to enroll 10,000 people by 2027, but the study has already assembled one of the most diverse cohorts ever for lung cancer genetic research.&nbsp;



<figure class="wp-block-image alignright size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="464" src="http://35.88.189.111/wp-content/uploads/2025/09/teal_waldos-1024x464.jpg" alt="" class="wp-image-34183" style="width:242px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/teal_waldos-1024x464.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/teal_waldos-300x136.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/teal_waldos-768x348.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/teal_waldos-880x399.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/teal_waldos-1180x534.jpg 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



Genetics is just one of many factors involved in why some people develop lung cancer. Exposure to tobacco smoke is perhaps the best-known risk factor; however, <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC2409903/" target="_blank" rel="noreferrer noopener">80 to 90%</a> of people with a history of tobacco exposure never get lung cancer, and many people without tobacco exposure get the disease. These facts underscore the importance of investigating other, less well-known risk factors, like air pollution, radon exposure, and workplace-related exposures.



And there&#8217;s much more we don&#8217;t know about lung cancer. Many do not realize, for instance, that lung cancer is the <a href="https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2025/2025-cancer-facts-and-figures-acs.pdf" target="_blank" rel="noreferrer noopener">number one cause of cancer death in women</a> and <a href="https://www.massgeneralbrigham.org/en/about/newsroom/articles/most-common-cancers-in-women#:~:text=It%20may%20not%20surprise%20you,in%20women%20and%20people%20AFAB." target="_blank" rel="noreferrer noopener">the second most common cancer in women</a>. Although lung cancer overall is decreasing because of declines in tobacco use, lung cancer among people who have never smoked <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431055/#:~:text=As%20expected%2C%20the%20primary%20factor%20leading%20to,non%2Dsmokers%20has%20been%20noted%20to%20be%20increasing." target="_blank" rel="noreferrer noopener">is stable or increasing</a>, and <a href="https://www.webmd.com/lung-cancer/features/lung-cancer-women-who-never-smoked" target="_blank" rel="noreferrer noopener">two-thirds of people diagnosed with lung cancer with no smoking history are women</a>.&nbsp;



Understanding the genetics of lung cancer may help unravel some of the factors underlying those statistics. Additionally, learning more about the underlying genetics could provide researchers with more insight into the biological mechanisms of the disease, aiding in the development of improved therapies and new diagnostics.&nbsp;



The de-identified data that participants in the Lung Cancer Genetic Study consented to share isn’t limited to just genetics. Many participants also chose to provide self-reported clinical, lifestyle, and even tumor biomarker data. The study will also follow participants over time, gathering important longitudinal data to help researchers understand the progression of cancer as well as the response to treatments.&nbsp;



<h2 class="wp-block-heading">Empowering Researchers</h2>



By opening up access to qualified researchers, the collaborators aim to address significant gaps in current lung cancer research, break down institutional silos, and remove barriers to dataset access, thereby accelerating research progress.&nbsp;



&#8220;We&#8217;re delivering more than a data system — we&#8217;re enabling an entirely new model for research equity and access,&#8221; said Nadia Litterman, PhD, Director of Scientific Affairs and Partnerships at Troper Wojcicki Philanthropies.



<h2 class="wp-block-heading">Find Out More</h2>



Anyone who has been diagnosed with lung cancer can learn more and enroll in the study at<a href="http://23andme.com/lung-cancer" target="_blank" rel="noreferrer noopener"> 23andme.com/lung-cancer</a>.



Interested researchers can begin the data access request process by contacting TWP study program manager Caitlin Nichols at <a href="mailto:caitlin@twphilanthropies.org">caitlin@twphilanthropies.org</a>.&nbsp;

Illustration of lungs on a background with a larger illustration of lungs

Powerful New Tool Opens Lung Cancer Data for Research Breakthroughs

Health Huddle LIVE from New Orleans brought together top athletes, medical professionals, and community leaders for powerful conversations on health, genetics, and early detection. Hosted at Dillard University during Super Bowl Week, the event was part of 23andMe’s Community Health Huddle, featuring expert panels and free health screenings. 



Watch the Highlights: 



<figure class="wp-block-embed alignwide is-type-video is-provider-youtube wp-block-embed-youtube wp-embed-aspect-16-9 wp-has-aspect-ratio"><div class="wp-block-embed__wrapper">
<iframe loading="lazy" title="The 23andMe Health Huddle: Live from New Orleans" width="500" height="281" src="https://www.youtube.com/embed/5hOR4o5PkAU?feature=oembed" frameborder="0" allow="accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture; web-share" referrerpolicy="strict-origin-when-cross-origin" allowfullscreen></iframe>
</div></figure>



<h2 class="wp-block-heading" id="h-experts-athletes-amp-actionable-insights">Experts, Athletes &amp; Actionable Insights</h2>



Panelists included Dr. Jen Caldwell, Dr. Joel Bervell, and Dr. Mathew Knowles—a breast cancer survivor and 23andMe Global Brand Ambassador—who shared personal stories and insights on health disparities, preventive medicine, and genetic testing. They were joined by NFL Total Health Ambassadors, highlighting how genetic insights shape performance, recovery, and longevity in sports.



<h2 class="wp-block-heading" id="h-key-takeaways">Key Takeaways</h2>



<ul class="wp-block-list">
<li>Genetic Testing Saves Lives – Understanding your genetic risks enables early detection and prevention, reducing the burden of chronic diseases. </li>



<li>Your Family History is Your Health Roadmap – What runs in your family doesn’t have to define your future, but knowing your risks empowers healthier decisions. </li>



<li>Health Inequities Must Be Addressed – Underserved communities continue to lack access to vital genetic and preventive care. This must change. </li>



<li>Athletes Rely on Science to Perform &amp; Recover – The same genetic insights that help pros optimize their health can help everyone make more informed health choices.</li>
</ul>



<h2 class="wp-block-heading" id="h-beyond-the-event-driving-change">Beyond the Event: Driving Change</h2>



Health Huddle LIVE reinforced a core truth: genetic insights aren’t just about ancestry—they’re a tool for taking control of your health and advocating for better healthcare access. By bringing together medicine, sports, and community leadership, 23andMe continues to lead the movement for health equity and empowerment.



 #HealthHuddleLIVE #GeneticHealth #CommunityWellness

Inside Health Huddle LIVE: Athletes, Experts & Doctors on Longevity, Genetics & Wellness

September is Sickle Cell Awareness Month, which offers us another chance to highlight some of the work 23andMe and its collaborators have done over the years.



Earlier this month, researchers from 23andMe,<a target="_blank" href="https://www.nih.gov/" rel="noreferrer noopener"> the the National Institutes of Health</a>, and <a target="_blank" href="https://www.hopkinsmedicine.org/som/" rel="noreferrer noopener">Johns Hopkins University School of Medicine</a> published new data on the association between sickle cell trait and blood clots. The new findings highlight the importance of this ongoing research and our overall efforts to illuminate this condition.



At 23andMe, knowledge is power, and understanding risks offers people opportunities to mitigate them.&nbsp;



<h2 class="wp-block-heading" id="h-awareness-and-research">Awareness and Research</h2>



But more than that, 23andMe also offers a unique research model that allows individuals to learn about their genetic likelihood of developing a condition and participate in innovative genetic research that could potentially find new treatments.



As part of our <a href="http://www.23andme.com/sickle-cell" target="_blank" rel="noreferrer noopener">Sickle Cell Carrier Status Awareness Program</a>, 23andMe has collaborated with academics and advocacy organizations to increase <a href="https://blog.23andme.com/articles/sickle-cell-awareness-2">understanding of sickle cell</a>. In addition, we’re providing resources for those with sickle cell trait and sickle cell disease. With the help of the<a href="https://www.sicklecellga.org/" target="_blank" rel="noreferrer noopener"> Sickle Cell Foundation of Georgia, Inc. (SCFG)</a>,<a href="https://www.btsscycle.org/" target="_blank" rel="noreferrer noopener"> Breaking the SSickle Cell Cycle</a>,<a href="https://www.sc101.org/" target="_blank" rel="noreferrer noopener"> Sickle Cell 101</a>, and the<a href="https://www.msm.edu/" target="_blank" rel="noreferrer noopener"> Morehouse School of Medicine</a>, we’re working with Black communities to promote awareness. 



We are not alone in this effort. Recently, the NBA, the WNBA, and Wilson Sporting Goods began the #IBall4SickleCell social media campaign to raise awareness. The groups participating in the effort are Breaking the SSickle Cell Cycle, the American Red Cross of Tennessee, and New York Presbyterian’s Dalio Center for Health Justice. Learn more about sickle cell, the campaign, and how to help<a href="https://www.sicklecellball.com/" target="_blank" rel="noreferrer noopener"> here</a>. 



From all this work and research, we have learned much about sickle cell and the people it impacts most. However, much work is still needed to improve people’s understanding of sickle cell.



<h2 class="wp-block-heading" id="h-more-on-sickle-cell-anemia-sickle-cell-trait">More on Sickle Cell Anemia, Sickle Cell Trait</h2>



Although many people have heard of sickle cell, often they do not know the difference between sickle cell trait and sickle cell anemia.



To have sickle cell anemia, one must inherit two copies of the HbS variant in the HBB gene—one copy from each biological parent. Typical signs and symptoms include anemia, pain episodes, and frequent infection.



People with just one copy of the HbS variant are called carriers. They’re also said to have <a target="_blank" href="https://www.cdc.gov/ncbddd/sicklecell/traits.html" rel="noreferrer noopener">sickle cell trait</a>. People with sickle cell trait are not expected to have sickle cell anemia. They typically do not experience any health complications. However, in rare cases, people with the sickle cell trait may experience some health impacts. Current research, including our study, is underway to understand better and spread awareness about the complications someone with SCT may experience.



Importantly, carriers can pass their variant on to their future children. If their partner has the HbS variant or another variant in the HBB gene, there’s a 25 percent chance that each child may have sickle cell anemia or a related blood disorder.&nbsp;&nbsp;



<h2 class="wp-block-heading" id="h-23andme-s-sickle-cell-anemia-carrier-status-report">23andMe’s Sickle Cell Anemia Carrier Status Report**</h2>



23andMe’s<a target="_blank" href="https://www.23andme.com/topics/carrier/sickle-cell-anemia/" rel="noreferrer noopener"> Sickle Cell Anemia Carrier Status Report</a>, which meets FDA requirements for clinical and analytical validity, looks at the HbS variant in the HBB gene linked to sickle cell anemia.



Sickle cell anemia is the most severe form of sickle cell disease. Three hundred million people worldwide and one in 13 Black and African Americans in the United States have sickle cell trait, making them carriers for sickle cell anemia.



In addition to informing people if they have one copy of the HbS variant and are carriers for sickle cell anemia, <a href="https://blog.23andme.com/articles/23andme-updates-carrier-status-report-on-sickle-cell-anemia">23andMe’s report </a>can also tell individuals if they have two copies of the tested variant and if they are at risk of developing symptoms. However, the report does not describe one’s overall risk of developing symptoms. 



Because the HbS variant is more common in certain populations, the Sickle Cell Anemia report is most relevant to people of African, Middle Eastern, and South Asian descent, as well as people from the Caribbean, the Mediterranean, and parts of Central and South America.



23andMe Health + Ancestry Service customers and 23andMe+ Premium members can see their <a target="_blank" href="https://you.23andme.com/reports/carrier.sickle_cell_anemia/" rel="noreferrer noopener">Sickle Cell Anemia report here</a>.&nbsp;



Not yet a customer? Learn more about <a target="_blank" href="https://www.23andme.com/compare-dna-tests/?_gl=1*11ns9j4*_ga*OTk4NDAyMjA3LjE3MTgzODA2MTg.*_ga_G330GF3ZFF*MTcyNTQxNDcyOS4xNjQuMS4xNzI1NDE0Nzk4LjAuMC4w" rel="noreferrer noopener">all that 23andMe offers here</a>.



<hr class="wp-block-separator has-alpha-channel-opacity"/>



<h2 class="wp-block-heading" id="h-note">Note:</h2>



**The 23andMe PGS test uses qualitative genotyping to detect select clinically relevant variants in the genomic DNA of adults to report carrier status and reporting and interpreting genetic health risks. The relevance of each report may vary based on ethnicity. Our carrier status reports can be used to determine carrier status but cannot determine if you have two copies of any genetic variant. These carrier reports are not intended to tell you anything about your risk for developing a disease in the future, the health of your fetus, or your newborn child’s risk of developing a particular disease later in life. We provide a single report for certain conditions that includes information on carrier status and genetic health risk. For important information and limitations regarding other genetic health risk reports and carrier status reports, click <a target="_blank" href="https://www.23andme.com/test-info/" rel="noreferrer noopener">here</a>.

An illustration for 23andMe's Sickle Cell Carrier Statues Awareness Program.

Learn More About Our Research and Collaborations During Sickle Cell Awareness Month

Editor&#8217;s note 7/8/2024: This post has been updated since 2020. In addition, We do not support uploading DNA data obtained from other testing services to 23andMe. This article explains the risks of uploading your DNA data to third party services.
With all of <a class="waffle-rich-text-link" href="https://www.23andme.com/compare-dna-tests/">23andMe&#8217;s services</a>, you’re in charge of your genetic data. That means we let you decide what information you want to learn and what information you want to share. However, you need to be informed about the risks of sharing your genetic data with other services. This includes understanding the implications if you decide to upload DNA to 23andMe or any third-party service.
After receiving <a class="waffle-rich-text-link" href="https://www.23andme.com/dna-reports-list/">personalized genetic reports</a> from 23andMe, customers can choose to download their raw DNA data. Some customers may do this to upload their data to third-party services, which offer to interpret their raw DNA data to find new genetic relatives or get additional genetic reports. However, 23andMe cannot vouch for the scientific validity or accuracy, or clarity in communication of results of any such third-party services. In fact, only 23andMe offers a consumer genetic test with health reports that have FDA&#8217;s independent assurance of validity and clear results (without requiring a prescription).
Beyond concerns about scientific validity, uploading your raw DNA data to a third-party service can also put <a href="https://www.23andme.com/privacy/">your data privacy</a> at risk. In part, this is why 23andMe provides important warnings to its customers before they choose to download.
<h2>What are some of the risks of uploading your DNA data to a third-party website? </h2>
<div id="attachment_27862" style="width: 310px" class="wp-caption alignright"><a href="https://blog.23andme.com/articles/how-to-be-careful-with-your-raw-dna-data/what-is-dna-upload" rel="attachment wp-att-27862"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-27862" class="size-medium wp-image-27862" src="http://35.88.189.111/wp-content/uploads/2020/01/What-is-DNA-Upload-300x128.jpg" alt="An illustration of the steps for downloading data." width="300" height="128" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/01/What-is-DNA-Upload-300x128.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/01/What-is-DNA-Upload.jpg 512w" sizes="auto, (max-width: 300px) 100vw, 300px" /></a>Most consumer genetics companies, including 23andMe, allow you to download your own raw DNA data. At that point, the customer is free to do what they like with their raw DNA data, such as deciding to upload that raw DNA data to third-party services.</div>
At 23andMe, we’re clear with our users about the risks of using third-party services that provide additional health, wellness or trait insights. This is because only select genotype data used specifically in our Health reports have been individually validated for accuracy. While the rest of your data has undergone a general quality review, it has not been validated to the extent of the data underlying our official 23andMe reports. As a result, raw DNA data should not be used for medical purposes and we do not recommend the use of third-party services that claim to interpret raw DNA data to provide health information.
Consumers also cite concerns about law enforcement uploading crime-scene DNA data to third-party services to crack a cold case. Simply put, uploading crime-scene DNA data into the 23andMe environment is not possible because we do not support the upload of DNA data that has been processed by a third-party laboratory.
Further, 23andMe’s <a href="https://www.23andme.com/transparency-report/">Transparency Report</a> details our policy against releasing customer’s individual DNA data to any third party &#8211; including law enforcement &#8211; without receiving the customer’s explicit consent, unless required by law.
However, this concern about law enforcement upload of crime scene DNA data is a real one that we warn customers about should they choose to upload their DNA data to other third party platforms, including public genealogy services or other third party services that facilitate DNA data upload.
But there’s another form of vulnerability that’s less well-understood: Within databases that allow for raw DNA data uploads with access to relative matching features, people with malicious intent can upload real or fake “<a href="https://en.wikipedia.org/wiki/Trojan_horse_(computing)">Trojan Horse</a>” genetic profiles for access to your personal identifying information. They could even infer your specific DNA variants—such as information about any disease risk variants you might carry. This is one reason why we don&#8217;t support uploading DNA to 23andMe.
<h2>How can that happen?</h2>
<ul>
<li>Many relative-matching services allow you to see the exact section or sections of DNA you share with each relative.*</li>
<li>If uploading DNA data is allowed, it means you no longer know for sure that your relative’s profile is actually controlled by your relative, and a malicious actor could upload real or fake DNA data to deduce information about you based on sections of matching DNA, including any disease risk variants you might have.</li>
<li>Even if shared segments aren’t shown, there are still ways that people with malicious intent can deduce some of your DNA variants.</li>
</ul>
<img loading="lazy" decoding="async" class="size-medium wp-image-27863 alignright" src="https://blog-api.23andme.com/wp-content/uploads/2020/01/How-Uploading-Creates-Risk-300x202.jpg" alt="" width="300" height="202" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/01/How-Uploading-Creates-Risk-300x202.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/01/How-Uploading-Creates-Risk.jpg 512w" sizes="auto, (max-width: 300px) 100vw, 300px" />
This vulnerability was recently described in two reports: one at the University of Washington and another at the University of California, Davis. The authors of these reports explain several ways an “adversary” can deduce people&#8217;s genotypes “either at key positions or at many sites genome-wide” in databases that allow DNA data uploads with relative matching. This highlights the risks associated with uploading DNA to 23andMe or similar services.
Both reports outline specific ways for services to mitigate risk, such as limiting the information displayed in relative-matching features.
While these practices may reduce risk, we believe the simplest and most effective defense is to not allow individuals genotyped through other testing services to upload their DNA data to 23andMe for the purpose of discovering genetic relatives.
In the past, 23andMe has allowed DNA uploads from other consumer genetic testing services in very specific circumstances. Specifically, on DNA Day in April 2018, 23andMe allowed individuals who tested at other companies to upload their results to access a subset of our trait reports, but 23andMe has not enabled the discovery of new relatives for these accounts.
<h2>How does 23andMe ensure that only real, consenting individuals participate in our service? </h2>
In a word, spit.
When you spit into the tube, you’re embarking on the adventure of a lifetime. You’re also trusting 23andMe with some of your most personal information.
Requiring a saliva sample is how 23andMe is able to verify that you’re a real person who chose to participate in the service. While it might be easy to upload fake DNA data, it’s another matter entirely to fake a spit sample, which requires filling a tube with more than two milliliters of spit. It’s how you know that “Linda-your-4th-cousin-who-you-didn’t-know-existed” is a real person who chose to do 23andMe. Linda had to spit in a tube, too.
<h2>What are some key questions you should ask?</h2>
When considering whether or not to upload your raw DNA data to another website, we encourage you to familiarize yourself with their privacy and security policies before you upload your raw DNA data.
Make sure to consider the following questions:
<ol>
<li>Before you upload your DNA data, ask yourself: do I really need to do this? Am I willing to risk the security and privacy of my DNA data by uploading it to a third-party service?</li>
<li>Do your research! Does the third-party service have a track record of strong privacy and data security?</li>
<li>How will the third-party service use your information?  How can your information be further shared with other third parties?</li>
<li>If you are not interested in discovering new relatives but you want additional DNA insights, does the other service explicitly exclude features relating to discovering genetic relatives?</li>
</ol>
An earlier article detailing our stance on protecting customers’ data is available <a href="https://blog.23andme.com/news/our-stance-on-protecting-customers-data/">here</a>. 
<h2>Learn More</h2>
Find out if your <a href="https://www.23andme.com/test-info/genetic-health/">genetics</a> might Increase your risk for any health conditions with 23andMe.
You can also Learn more about common risks associated with uploading raw DNA online and how to protect your DNA information.
*By default, 23andMe does not display your ancestry information or DNA segment information to relatives or connections until you decide to share it with them.

Can You Upload DNA Data to 23andMe? 

<h5 class="wp-block-heading" id="h-fda-now-recommends-genetic-testing-before-prescribing-specific-chemotherapy-medications">FDA Now Recommends Genetic Testing Before Prescribing Specific Chemotherapy Medications</h5>



For years, patient advocates have been calling for stronger safeguards against preventable toxicity from chemotherapy. Last week, the FDA took a major step forward, updating the label for a drug called <a href="https://medlineplus.gov/druginfo/meds/a699003.html" target="_blank" rel="noreferrer noopener">capecitabine</a> to explicitly recommend testing for variants in the DPYD gene before starting treatment. This is more than just a label change—it&#8217;s a long-awaited acknowledgment that genetics matter when it comes to patient safety.



<h2 class="wp-block-heading">What is DPYD?</h2>



The <a href="https://medlineplus.gov/genetics/gene/dpyd/" target="_blank" rel="noreferrer noopener">DPYD gene</a> provides instructions for making an enzyme called DPD (dihydropyrimidine dehydrogenase), which helps the body break down certain chemotherapy drugs like capecitabine and <a href="https://medlineplus.gov/druginfo/meds/a682708.html" target="_blank" rel="noreferrer noopener">5-fluorouracil</a>. These medications are commonly used to treat breast, colorectal, and other cancers. People with certain changes in this gene may not process these drugs properly, causing the drugs to build up in the body and, in some cases, leading to severe or even life-threatening <a href="https://medlineplus.gov/genetics/condition/dihydropyrimidine-dehydrogenase-deficiency/" target="_blank" rel="noreferrer noopener">reactions</a>.



<figure class="wp-block-image alignleft size-full is-resized"><img loading="lazy" decoding="async" width="508" height="531" src="http://35.88.189.111/wp-content/uploads/2025/10/drug-bottle.png" alt="" class="wp-image-34304" style="width:126px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/drug-bottle.png 508w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/drug-bottle-287x300.png 287w" sizes="auto, (max-width: 508px) 100vw, 508px" /></figure>



These reactions can include painful mouth sores, severe diarrhea, low white blood cell counts, and nerve problems. <a href="https://medlineplus.gov/genetics/condition/dihydropyrimidine-dehydrogenase-deficiency/#frequency" target="_blank" rel="noreferrer noopener">Up to 8%</a> of people have a variant in the DPYD gene that affects how well they process these medications. Sadly, some patients with DPYD variants have died after receiving these drugs. Such experiences have fueled years of advocacy calling for genetic testing before treatment, not after. 



<h2 class="wp-block-heading" id="h-a-change-in-the-recommendations">A change in the recommendations</h2>



Until now, the FDA advised doctors they could &#8220;consider testing&#8221; patients before giving capecitabine or similar drugs. The <a href="https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/020896s052lbl.pdf" target="_blank" rel="noreferrer noopener">new label</a> goes much further, adding a warning that says, &#8220;serious adverse reactions or death may occur in patients with complete DPD deficiency&#8221; and telling doctors to test for DPYD variants before prescribing the medication. (Experts predict a similar change to the 5-fluorouracil drug label soon.) It&#8217;s a major win for patient safety and for the <a href="https://test4dpd.org/" target="_blank" rel="noreferrer noopener">advocacy groups</a> who have pushed tirelessly for this change. Organizations that have long advocated for universal DPYD testing hope this update will encourage hospitals and cancer centers across the U.S. to make pretreatment genetic testing standard care.



<figure class="wp-block-image alignright size-large is-resized"><img loading="lazy" decoding="async" width="790" height="1024" src="http://35.88.189.111/wp-content/uploads/2020/09/PGt-Home-790x1024.png" alt="23andMe mobile pharmacogenomics" class="wp-image-28527" style="width:256px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home-790x1024.png 790w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home-231x300.png 231w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home-768x996.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home-679x880.png 679w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home-910x1180.png 910w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home.png 1583w" sizes="auto, (max-width: 790px) 100vw, 790px" /></figure>



We share the belief that genetic insights can empower individuals and help improve outcomes. The 23andMe® <a href="https://www.23andme.com/topics/pharmacogenetics/dpyd/" target="_blank" rel="noreferrer noopener">DPYD Drug Metabolism Pharmacogenetics report</a>*, available to <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members, provides information about two variants associated with reduced DPD enzyme activity. While this report isn&#8217;t a substitute for clinical testing, it can help people learn whether they carry certain DPYD variants and start a conversation with their healthcare provider. 



The FDA&#8217;s new label is an important step toward safer, more personalized cancer treatment and a long-awaited victory for the patients and advocates who made their voices heard.



<hr class="wp-block-separator has-alpha-channel-opacity"/>



 * 23andMe PGS Pharmacogenetics reports: The 23andMe test uses qualitative genotyping to detect 3 variants in the CYP2C19 gene, 2 variants in the DPYD gene and 1 variant in the SLCO1B1 gene in the genomic DNA of adults from saliva for the purpose of reporting and interpreting information about the processing of certain therapeutics to inform discussions with a healthcare professional. It does not describe if a person will or will not respond to a particular therapeutic. Our CYP2C19 Pharmacogenetics report provides certain information about variants associated with metabolism of some therapeutics and provides interpretive drug information regarding the potential effect of citalopram and clopidogrel therapy. Our SLCO1B1 Pharmacogenetics report provides certain information about variants associated with the processing of some therapeutics and provides interpretive drug information regarding the potential effect of simvastatin therapy. Our DPYD Pharmacogenetics report does not describe the association between detected variants and any specific therapeutic. Results for DPYD and certain CYP2C19 results should be confirmed by an independent genetic test prescribed by your own healthcare provider before taking any medical action. Warning: Test information should not be used to start, stop, or change any course of treatment and does not test for all possible variants that may affect metabolism or protein function. The PGS test is not a substitute for visits to a healthcare professional. Making changes to your current regimen can lead to harmful side effects or reduced intended benefits of your medication, therefore consult with your healthcare professional before taking any medical action. For important information and limitations regarding Pharmacogenetic reports, visit <a href="http://23andme.com/test-info/pharmacogenetics/" target="_blank" rel="noreferrer noopener">23andme.com/test-info/pharmacogenetics/</a>

A Big Step Forward for Patient Safety

We often hear about the &#8220;nature versus nurture&#8221; debate, framing it as a battle between our genes and our environment. But in many cases it&#8217;s not a battle at all, it&#8217;s a partnership. The way our genes impact our health and traits may change depending on our environment.



<figure class="wp-block-image size-large"><img loading="lazy" decoding="async" width="1024" height="684" src="http://35.88.189.111/wp-content/uploads/2022/09/GettyImages-981323210-1024x684.jpg" alt="" class="wp-image-30209" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/09/GettyImages-981323210-1024x684.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/09/GettyImages-981323210-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/09/GettyImages-981323210-768x513.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/09/GettyImages-981323210-880x587.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/09/GettyImages-981323210-1180x788.jpg 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



Understanding both &#8220;nature&#8221; and &#8220;nurture&#8221; is especially important when we consider complex skills critical to success in life, like reading. Thanks to the contribution of over a million 23andMe® research participants, a <a href="https://pubmed.ncbi.nlm.nih.gov/40991152/" target="_blank" rel="noreferrer noopener">new study</a>, led by scientists from the University of Edinburgh, is helping to untangle how both genes and environment work to shape literacy.



<h2 class="wp-block-heading" id="h-the-reading-puzzle-nbsp">The Reading Puzzle&nbsp;</h2>



Literacy is a powerful predictor of life outcomes, from education level to income. For decades, researchers have tried to understand the roles genetics and environment play in why some people learn to read and spell more easily than others.



<figure class="wp-block-image alignleft size-full is-resized"><img loading="lazy" decoding="async" width="425" height="282" src="http://35.88.189.111/wp-content/uploads/2008/07/twins.jpg" alt="" class="wp-image-392" style="width:309px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2008/07/twins.jpg 425w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2008/07/twins-300x199.jpg 300w" sizes="auto, (max-width: 425px) 100vw, 425px" /></figure>



Several <a href="https://pubmed.ncbi.nlm.nih.gov/23725549/" target="_blank" rel="noreferrer noopener">studies</a> of <a href="https://pubmed.ncbi.nlm.nih.gov/19076484/" target="_blank" rel="noreferrer noopener">twins</a> in the United States suggested an interaction between genes and environment. In these studies, how much influence genetics had on reading skills seemed to be higher in families with a higher socioeconomic status. In other words, genetics appeared to have a bigger impact on a child&#8217;s reading ability when they were in a more advantaged environment. This idea is called a gene-by-environment interaction.



However, the evidence of this gene-by-environment interaction was mixed in studies conducted in the <a href="https://pubmed.ncbi.nlm.nih.gov/19296213/" target="_blank" rel="noreferrer noopener">United Kingdom</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/28832969/" target="_blank" rel="noreferrer noopener">Australia</a>. This puzzle led researchers to ask: can we use modern genetic data to test this theory in large, diverse populations?



<h2 class="wp-block-heading" id="h-a-new-approach">A New Approach</h2>



Researchers utilized summary statistics from a 2022 <a href="https://blog.23andme.com/articles/study-identifies-genetic-links-to-dyslexia" target="_blank" rel="noreferrer noopener">genome-wide association study (GWAS) on dyslexia</a> to construct a polygenic score—a way of estimating someone’s genetic tendency toward a trait by adding up the small effects of thousands of DNA differences.



The team then applied this polygenic score to two large groups of children and adolescents in Australia and the United Kingdom to see if the score&#8217;s effect on reading and spelling skills was moderated by their family&#8217;s socioeconomic status. Socioeconomic status was used as a broad measure of environmental advantage, capturing factors like parental education level and household income.&nbsp;



<h2 class="wp-block-heading" id="h-what-was-discovered-two-parallel-paths">What Was Discovered: Two Parallel Paths</h2>



Both the dyslexia polygenic score (nature) and socioeconomic status (nurture) were significant predictors of reading and spelling performance. Together, demographic, genetic, and socioeconomic factors explained between 8% and 11.6% of the variation in reading skills.



However, the study found no interaction effect. Nature and nurture were both important, but they worked in parallel.



This means the influence of a person&#8217;s genetic predisposition was the same, regardless of their family&#8217;s socioeconomic background. In these groups, a higher genetic predisposition for reading provided a similar boost to children from all socioeconomic backgrounds.&nbsp;



<h2 class="wp-block-heading" id="h-the-bigger-picture">The Bigger Picture</h2>



This finding is an important reminder to scientists to consider different environments when looking for gene-by-environment interactions. While some earlier US-based studies suggested an interaction, the different environments in these large UK and Australian groups showed a different outcome. Suggesting that both our genes and our environment make their own distinct contributions to the development of this fundamental skill.



Of course, every study has its limitations. The 23andMe research participants who contributed to the original GWAS are a self-selecting group and may not be perfectly representative of the general population. Additionally, only about 5% of 23andMe research participants said they had dyslexia, which is on the lower end of the <a href="https://pubmed.ncbi.nlm.nih.gov/18652545/" target="_blank" rel="noreferrer noopener">commonly cited 5–10% range</a>.



Even so, this large-scale study provides a crucial piece of the puzzle, emphasizing how vital it is to test scientific findings in diverse environments to get the full story.

Nature and Nurture: A New Look at the Genetics of Reading Ability

Every year on the third Saturday in October, the world celebrates International Archaeology Day, recognizing the important contributions archaeological research makes to society. This year, to celebrate, we&#8217;re spotlighting one of our favorite archaeological mysteries in the <a href="https://blog.23andme.com/articles/23andmes-historic-matches" target="_blank" rel="noreferrer noopener">Historical Matches</a>SM feature—the skeletons of Roopkund Lake.



<h2 class="wp-block-heading" id="h-about-roopkund-lake">About Roopkund Lake</h2>



Roopkund Lake is a small glacial lake located over 5,000 meters (over 16,000 ft) above sea level in the Nanda Devi National Park, in the Indian Himalayas. In 1942, a forest ranger patrolling the park stumbled upon a chilling scene: hundreds of skeletal remains strewn around the lake. The site has captivated researchers and locals alike ever since.



The mystery of who these individuals were, how they died, and why they were in such a remote and inhospitable location has sparked decades of speculation. Some early researchers proposed that the remains belonged to an army that had lost its way in the mountains, while others suggested they might have been traders following a trans-Himalayan route that had since vanished. A few archaeologists posited that they were pilgrims traveling to nearby shrines, possibly part of the ancient Nanda Devi Raj Jat, a religious procession spanning ~290 kilometers (~180 miles) that is still undertaken in the region every 12 years.



The identification of women and children among the dead, however, made some of the proposed explanations less plausible–especially the claim that they may have been members of an army. Without weapons, trade goods, or written records, no single theory could fully account for the diversity and composition of the group. Local folklore offered its own interpretation: a king, his family, and attendants on a pilgrimage to honor the mountain goddess Nanda Devi had violated sacred protocol and were struck down by a deadly hailstorm in divine retribution.



<h2 class="wp-block-heading" id="h-an-exciting-23andme-connection">An exciting 23andMe connection</h2>



<a href="https://pubmed.ncbi.nlm.nih.gov/31431628/" target="_blank" rel="noreferrer noopener">In 2019</a>, scientists sequenced the genomes of 38 individuals from Roopkund Lake in an effort to better understand the origins of the mysterious remains. But instead of resolving this longstanding mystery, their findings uncovered an even more complex puzzle. 



So what makes this story one of 23andMe’s favorite archaeological mysteries? That 2019 research study was actually led by our very own Dr. Éadaoin Harney—a Scientist on the Population Genetics R&amp;D Team and 23andMe’s “resident ancient DNA expert.” She worked on this study during her PhD at Harvard University where she was a member of Prof. David Reich’s ancient DNA laboratories–one of the largest ancient DNA research laboratories in the world.



“When I first started working with the Roopkund ancient DNA data, I thought that genetics would be a simple and straightforward way to finally help solve the mystery of who they were,” said Dr. Harney. But she was in for a big surprise! “The first hint that this wasn’t going to be as simple as I initially thought was when we discovered how ancestrally diverse the Roopkund individuals were. Then we learned that they didn’t all die at the same time, as had previously been believed. Instead radiocarbon dates generated from the bones spanned over 1,000 years.”



<h2 class="wp-block-heading" id="h-how-dna-adds-to-the-mystery">How DNA adds to the mystery</h2>



The 2019 genetic analysis showed that the individuals fell into three distinct genetic groups, with ancestries from across the globe.



The largest group (which we’ll refer to as Roopkund A) consisted of 23 individuals who died between the 7th and 10th centuries CE, likely during multiple distinct events. Genetically, all appeared South Asian, but with remarkably diverse ancestries–each individual appeared most closely related to different present-day South Asian populations. This finding suggests that they may have traveled to the lake from multiple locations across the subcontinent. Although the exact purpose of their journey to Roopkund Lake remains uncertain, some researchers speculate that they may have been early participants in the Nanda Devi Raj Jat, a traditional pilgrimage that still passes by the lake every 12 years.



The other two groups were even more surprising. One group (Roopkund B) consisted of 14 individuals whose DNA connected them to present-day populations from the eastern Mediterranean—particularly populations in Greece and neighboring regions. The third group (Roopkund C) was represented by a single individual with genetic ancestry most similar to Southeast Asian populations. Radiocarbon dating revealed that these individuals likely died in a single event some time between the 17th and 20th centuries. Why people with ancestry from such distant regions were traveling together in one of the most remote parts of the Himalayas remains a mystery to this day.



Dr. Harney joined 23andMe in 2020 with the goal of creating an approach to identify direct genetic connections between historical and living people. She and her colleagues on the Population Genetics R&amp;D Team succeeded! This technology was first described in their <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC10958645/" target="_blank" rel="noreferrer noopener">2023 study of African Americans from Catoctin Furnace</a>, which was published in (and featured on the cover of) Science. She then helped spearhead the creation of the 23andMe Historical Matches feature, enabling customers to learn how they connect to different historical and ancient individuals.



Over the last five years, one of her secret ambitions was to use this technology to try and finally solve the mystery of the Roopkund individuals&#8217; identities. Could identifying any close genetic relatives of the Roopkund individuals in the 23andMe genetic database help us learn about their identities and answer what brought them to Roopkund?



<h2 class="wp-block-heading" id="h-did-we-solve-the-mystery">Did we solve the mystery?</h2>



We compared the Roopkund individuals to over 11 million research consenting participants in the 23andMe genetic database. While we were hoping this analysis would reveal a number of close genetic relatives, unfortunately, the mystery of Roopkund Lake lives on.



We found that only about 1,240 research participants—less than 0.011% of the individuals included in our analysis—share any sort of genetic connection to the Roopkund individuals. And of those participants, we can count the number of individuals who share over 30 cM of DNA (what we label a “significant genetic connection” in the Historical Matches feature) on just one hand. In fact, we found so few &#8220;significant relatives” that the chances any of those connections trace back to a recent shared common ancestor on a genealogical family tree are extremely slim.



(Although if you happen to be one of those lucky individuals who sees a “significant connection” listed to one of the Roopkund individuals in your 23andMe report, please <a href="https://customercare.23andme.com/hc/en-us/requests/new" target="_blank" rel="noreferrer noopener">reach out to us</a>, as we’d love to learn more!)



<h2 class="wp-block-heading" id="h-what-else-did-we-discover">What else did we discover?</h2>



So, we didn’t solve the mystery of who the Roopkund individuals were, but we did gather fascinating data about their connections to the present day.



First, here is a breakdown of the 17 Roopkund individuals whose DNA was well preserved enough to include in our analyses:



<ul class="wp-block-list">
<li>8 from Roopkund A (South Asian ancestry)</li>



<li>8 from Roopkund B (Eastern Mediterranean ancestry)</li>



<li>1 from Roopkund C (Southeast Asian ancestry)</li>
</ul>



As we mentioned, about 1,240 23andMe research participants shared a genetic connection to the Roopkund individuals. The figure below shows the number of matches each Roopkund group received and highlights the amount of DNA shared. As you can see, the vast majority of the connections we discovered involve less than 20 cM of DNA, meaning that they likely trace back to a shared common ancestor who lived long before any of the Roopkund individuals.



<figure class="wp-block-image size-full is-resized"><img loading="lazy" decoding="async" width="411" height="252" src="http://35.88.189.111/wp-content/uploads/2025/10/image-3.png" alt="" class="wp-image-34359" style="width:625px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/image-3.png 411w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/image-3-300x184.png 300w" sizes="auto, (max-width: 411px) 100vw, 411px" /><figcaption class="wp-element-caption">This figure shows the distribution of total shared DNA that we detected between 23andMe research participants and each of the Roopkund groups (A, B and C). It shows that the vast majority of the connections we identified are to individuals in the Roopkund B group, and the DNA segments they share are shorter than 15 cM. In order to protect participant privacy, all counts less than or equal to 5 are masked and appear equal to 5. </figcaption></figure>



Of those who share a genetic connection, the majority (~1,160) shared a connection to one or more individuals in the Roopkund B group—the one with Eastern Mediterranean-related ancestry. This didn&#8217;t surprise us, since the majority of 23andMe research participants have European ancestry, making them more likely to be related to the Roopkund B individuals.



In addition to occurring more frequently, the Roopkund B individuals also shared some of the strongest genetic connections to 23andMe research participants, as shown in the figure below which depicts the maximum amount of DNA that each Roopkund individual shared with a research participant.



<figure class="wp-block-image size-full"><img loading="lazy" decoding="async" width="643" height="448" src="http://35.88.189.111/wp-content/uploads/2025/10/image-4.png" alt="" class="wp-image-34360" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/image-4.png 643w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/image-4-300x209.png 300w" sizes="auto, (max-width: 643px) 100vw, 643px" /><figcaption class="wp-element-caption">This figure shows the maximum amount of shared DNA that we detected between 23andMe research participants and each of the Roopkund individuals. The individuals are arranged along the x-axis by when they lived, as measured by radiocarbon dating. We masked this result for Roopkund individuals who shared DNA with 5 or fewer 23andMe research participants in order to protect participant privacy, and reported maximum DNA sharing as equal to 0.</figcaption></figure>



We decided to see what Genetic Groups the Roopkund individuals could be connected to, using the same approach that we use to connect customers to these Genetic Groups.&nbsp;&nbsp;&nbsp;



Many of the Roopkund B individuals received matches to Genetic Groups in south eastern Europe, with the strongest connections to groups in Greece and Crete–exactly mirroring the findings of the original study!



<figure class="wp-block-image size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="849" src="http://35.88.189.111/wp-content/uploads/2025/10/roopkund_b_2-1024x849.png" alt="" class="wp-image-34352" style="width:575px" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_b_2-1024x849.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_b_2-300x249.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_b_2-768x636.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_b_2-880x729.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_b_2-1180x978.png 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /><figcaption class="wp-element-caption">This map shows the location of the different Genetic Groups that we compared the Roopkund B individuals to. Groups shown in darker colors shared the strongest genetic matches to one or more of the Roopkund B individuals.</figcaption></figure>



Since the Roopkund A and Roopkund C individuals shared far fewer genetic connections to 23andMe research participants, it was hard to localize their ancestry in the same way. But we were able to connect the Roopkund C individual to a single Genetic Group, located in China. This finding is generally consistent with the original study, where this individual exhibited connections to populations in East and Southeast Asia.&nbsp;



<figure class="wp-block-image size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="874" src="http://35.88.189.111/wp-content/uploads/2025/10/roopkund_c_2-1024x874.png" alt="" class="wp-image-34353" style="width:592px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_c_2-1024x874.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_c_2-300x256.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_c_2-768x655.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_c_2-880x751.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_c_2-1180x1007.png 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /><figcaption class="wp-element-caption">This map shows the location of the different Genetic Groups that we compared the Roopkund C individual to. Groups shown in darker colors shared the strongest genetic matches to the Roopkund C individual.</figcaption></figure>



We couldn’t connect the Roopkund A individuals to any of the Genetic Groups that we have identified. That doesn’t mean they aren’t genetically related to any of these groups. Instead it is likely just because the original research team was only able to sequence a small amount of DNA from these individuals, making it harder to connect them to research participants in the 23andMe database.&nbsp;



<h2 class="wp-block-heading" id="h-what-s-next">What’s Next?</h2>



So for now, all we can say is that the mystery of Roopkund Lake continues. But we promise this archaeological site is one that is close to our hearts. If we have any updates in the future, we’ll be sure to let you know.



<h2 class="wp-block-heading" id="h-learn-more">Learn more</h2>



Want to see if you share a genetic connection with any of the individuals who died at Roopkund Lake—or hundreds of other historical people? The Historical Matches feature is available to <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members.



And if you are interested in finding ways to celebrate International Archaeology Day, check out organizations like the Archaeological Institute of America, which has an exciting <a href="https://www.archaeological.org/events/category/international-archaeology-day/list/" target="_blank" rel="noreferrer noopener">calendar of Archaeology-related events</a>.

New Historical Matches Could Connect You to the Mysterious Skeletons of Roopkund Lake

This week the American Society of Human Genetics (ASHG) is having its <a href="https://meetings.ashg.org/event/ASHG25/home/" target="_blank" rel="noreferrer noopener">annual meeting</a> in Boston. Attending the ASHG annual meeting is about more than just presenting our work, it&#8217;s one way we are working to ensure that the 23andMe® Research Institute contributes to a healthier future for everyone.



<ul class="wp-block-list">
<li>Amplifying impact: Sharing our discoveries with a global audience helps our work reach those who can build upon it, accelerating the path from discovery to clinic.</li>



<li>Fostering collaboration: It&#8217;s where we connect with the brightest minds in the field. These conversations spark new ideas and forge partnerships that are essential for tackling complex diseases.</li>



<li>Staying on the cutting edge: Exposure to the latest technologies and unpublished data keeps our research relevant and innovative.</li>
</ul>



<h2 class="wp-block-heading" id="h-23andme-research-institute-at-ashg">23andMe Research Institute at ASHG</h2>



For those attending, stop by our posters in the following sessions:



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WEDNESDAY, OCTOBER 15TH 2:30 &#8211; 4:30 PM (Posters; Board #2004W) Sustaining Research Ethics in Times of Change: A Framework from the 23andMe Research Program



presented by Emily DelloRusso, Principal Regulatory Science Manager
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THURSDAY, OCTOBER 16TH 2:30 &#8211; 4:30 PM (Posters; Board #2035T) Explore23: a privacy-forward, secure, extensible, and easy-to-use web application for exploration of a large genomic research cohort



presented by Julie Granka, Director, Statistical Genetics
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FRIDAY, OCTOBER 17TH 2:30 &#8211; 4:30 PM (Posters; Board #3014F) Learning about a genetic predisposition to depression is psychologically well tolerated among those with high polygenic risk scores



presented by Rebecca Berns, Sr. Product Scientist I, Genomic Health and Sciences
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Interested in reading more? 23andMe has contributed to <a href="https://research.23andme.com/publications/" target="_blank" rel="noreferrer noopener">more than 300 research publications</a>.

23andMe Research Institute Attending ASHG 2025

Cannabis is already one of the most widely used drugs globally, and its use will likely grow even more as it becomes more socially accepted and legally available. For many the recreational use of cannabis poses few problems, but for as many as a third of users, it becomes problematic developing into an addiction or what scientists call cannabis use disorder. Research suggests that genetics may explain why.



<h2 class="wp-block-heading" id="h-searching-the-genome-for-clues">Searching the Genome for Clues</h2>



In collaboration with 23andMe Research Institute, researchers at the University of California, San Diego <a href="https://www.nature.com/articles/s41380-025-03219-2" target="_blank" rel="noreferrer noopener">published a study</a> today that found genetic links to cannabis use as well as links to psychiatric, cognitive, and physical health. The researchers used data from more than 130,000 people who consented to participate in 23andMe research. Participants answered survey questions on whether they had ever used cannabis (“lifetime use”) and, for those who had, how often they used it during their heaviest 30-day period (“frequency of use”). The team then conducted genome-wide association studies searching for genetic variants linked to ever trying cannabis and how often people used the drug.



<h2 class="wp-block-heading" id="h-what-the-data-revealed">What the Data Revealed</h2>



Researchers found that having ever used cannabis was associated with two genetic regions: CADM2—a gene <a href="https://blog.23andme.com/articles/scientists-identify-genes-associated-with-cannabis-use" target="_blank" rel="noreferrer noopener">previously linked</a> to cannabis and other substance use, impulsivity, and risk-taking—and GRM3. While GRM3 has been tied to alcohol use, schizophrenia, and certain personality traits, this is the first time it’s been linked to cannabis use. How often someone used cannabis was associated with a different variant also near CADM2, strengthening this gene’s role in cannabis behaviors. Both having ever used cannabis and how frequently someone used cannabis were genetically linked to other substance use, pain, and psychiatric conditions like depression. Researchers also created polygenic scores—which tally the effects of many different genetic variants—to estimate both the likelihood of ever having used cannabis and the frequency of cannabis use. These polygenic scores were able to replicate associations between cannabis use and substance use and mood disorders in two other independent research datasets (All of Us and BioVU). The researchers also uncovered novel associations with anxiety, celiac disease, HIV, and viral hepatitis.



<h2 class="wp-block-heading" id="h-why-this-research-matters">Why This Research Matters</h2>



Most genetic research on cannabis has focused on two points in the spectrum: first use and cannabis use disorder. But the stages in between—like how often someone uses cannabis—are just as important. Studying these “pre-addiction” traits may help determine who is more likely to progress from a casual user to someone with cannabis use disorder. This study was one of the first genome wide association studies to look at traits that may lead to cannabis use disorder.&nbsp;



Traits like frequency of cannabis use can reveal genetic factors that shape vulnerability before addiction develops. Understanding these factors could eventually help predict risk for cannabis use disorder and related health conditions.



<h2 class="wp-block-heading" id="h-more-than-just-dna">More Than Just DNA</h2>



Like all research there are some important considerations to keep in mind for this study:



<ul class="wp-block-list">
<li>While this research focused on genetics, many non-genetic factors may also play a significant role in a person&#8217;s likelihood of using cannabis or developing cannabis use disorder.</li>



<li>The study was conducted in people of European descent (based on an analysis of their local genetic ancestry), so the findings may not fully apply to people of other ancestries.</li>



<li>The measure of frequency (use days in a 30-day window) of using cannabis doesn’t capture full patterns such as the duration of regular use or quantity consumed.</li>



<li>While GRM3 is a promising lead, more work is needed to understand how the genetic variant in this region affects cannabis use biology.</li>
</ul>



<h2 class="wp-block-heading" id="h-the-road-ahead">The Road Ahead</h2>



Future research will need to expand to larger and more diverse cohorts and include other cannabis-related traits such as craving, withdrawal, and response to cannabis. Combining genetic insights from multiple stages of cannabis use could:



<ul class="wp-block-list">
<li>Improve the discovery of new genetic variants</li>



<li>Help build predictive models for problematic use</li>



<li>Clarify how cannabis genetics intersect with physical and mental health</li>
</ul>



Takeaway: Studying genetic influences on early cannabis use behaviors could eventually help predict risk for cannabis use disorder and related health conditions, and may help shed light on who is most at risk for cannabis use disorder.&nbsp; These findings mark an important step toward understanding the genetics of cannabis use and its health consequences.

New Genetic Insights Into Cannabis Use

Late in the first quarter in only his third game this season, one professional football team’s star edge-rusher limped off the field, gesturing to his trainers with his thumb down. Apparently, he already knew what he&#8217;d find out a short time later with an MRI: he&#8217;d again torn his ACL, the anterior cruciate ligament.



While a hard tackle or awkward fall can tear an ACL, some people may be more prone to an ACL tear than others, and their genetics may explain why.



A new 23andMe polygenic risk score (PRS) report sheds light on that genetic connection. The report examines how a person&#8217;s genetics may impact their likelihood of experiencing an ACL tear, an injury particularly common among those involved in high-impact sports.



<h2 class="wp-block-heading" id="h-how-genetics-may-influence-acl-tear-risk">How Genetics May Influence ACL Tear Risk</h2>



First, it&#8217;s important to note that your genetics is only one part of the story – many other factors can influence the risk of an ACL tear. 



<figure class="wp-block-image alignright size-full"><img loading="lazy" decoding="async" width="306" height="126" src="http://35.88.189.111/wp-content/uploads/2025/10/ACL-tear-PRS-Hero.png" alt="" class="wp-image-34316" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/ACL-tear-PRS-Hero.png 306w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/ACL-tear-PRS-Hero-300x124.png 300w" sizes="auto, (max-width: 306px) 100vw, 306px" /></figure>



Tears typically occur when the knee twists or extends beyond its normal range, often seen in sports that involve jumping and sudden stops, pivots, or changes in direction. That might be in sports such as football, soccer, basketball, or downhill skiing. The ACL is the most commonly injured ligament in the knee.&nbsp;&nbsp;



We also know that ACL tears are more common in female athletes. However, because more males participate in high-risk sports, the total number of ACL tears may actually be higher in males. They are also more likely in people with a family history of an ACL injury or a personal history of an ACL tear. Indeed, genetics plays an important role, with one 2020 sports medicine journal study estimating the <a href="https://bjsm.bmj.com/content/55/7/385" target="_blank" rel="noreferrer noopener">genetic contribution to an ACL tear at approximately 69 percent</a>. 



While the exact biological mechanism involved is not yet known, the genetic associations do offer some hints. Among the many genetic variants associated with ACL tears are variants in or near genes involved in the formation of collagen, a building block for ligaments. Scientists have discovered other variants linked to tears, but most of those associations are inconclusive, and more research is needed.&nbsp;



<h2 class="wp-block-heading" id="h-23andme-s-new-acl-tear-prs-report">23andMe&#8217;s New ACL Tear PRS Report</h2>



Knowing how genetics influences the risk for an ACL tear can empower athletes, who are at the highest risk, train smarter and work toward preventing them.&nbsp;



To create the new ACL Tear PRS Report* 23andMe scientists analyzed data from people who consented to participate in research to identify thousands of variants associated with ACL tears. The 23andMe scientists then created a genetic model that incorporated those variants to calculate the genetic likelihood of an ACL tear.



This PRS report, like other 23andMe PRS reports, is research-based and not validated for medical diagnostic use; it may have limitations for people with mixed or less-studied ancestries and does not account for every possible factor influencing ACL health. In addition, polygenic risk scores integrate many common variants, but they do not account for rare genetic variants or lifestyle factors that can heavily impact risk.&nbsp;



For individuals with an elevated genetic or family risk, creating a personalized prevention plan and scheduling regular check-ins with sports medicine professionals are great ways to keep knees healthy.&nbsp;



<h2 class="wp-block-heading" id="h-mitigating-the-risk-of-acl-tears">Mitigating the Risk of ACL Tears</h2>



Whether you’re a pro athlete or not, and especially if you’ve already had an ACL tear before, proper training and technique&nbsp; are simple ways to help lower the likelihood of injury.



Here are a few things you can do to help lower the risk of an ACL tear:



<ul class="wp-block-list">
<li>Build muscle strength in the hamstrings, and core to stabilize the knee.</li>



<li>Maintain proper technique for movements such as jumping, pivoting, and squatting — like landing on the balls of your feet with knees bent and keeping knees aligned over your toes.</li>



<li>Warm up and cool down before and after physical activity to increase flexibility.</li>



<li>Wear supportive, activity-appropriate footwear for correct alignment.</li>



<li>Consulting with physical therapists or trainers for form and strength assessments can further reduce the risk, regardless of one&#8217;s genetic background.</li>
</ul>



We continue to learn about the role genetics plays in sports-related injuries, including ACL tears, but genetics is just one factor.&nbsp;



<h2 class="wp-block-heading" id="h-learn-more">Learn More</h2>



<a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members can view this report with their other Wellness reports.



<a href="https://you.23andme.com/" target="_blank" rel="noreferrer noopener">Sign in</a> to learn more about what 23andMe&#8217;s ACL Tear PRS can tell you. 



* The 23andMe ACL Tear PRS report is based on a genetic model that includes data and insights from 23andMe consented research participants and incorporates more than 6,000 genetic variants to provide information on the likelihood of experiencing an ACL tear. The report does not describe a person’s overall likelihood, does not account for lifestyle or family history and has not been reviewed by the US Food and Drug Administration. The ACL Tear PRS report is not intended to tell you anything about your current state of health, or to be used to make medical decisions or determine any treatment.

Genetics May Explain Why Some Athletes Are More Prone to ACL Tears

<h6 class="wp-block-heading" id="h-a-new-study-may-help-identify-and-more-quickly-help-the-60-of-people-with-major-depression-who-do-not-get-relief-from-their-initial-treatments">A new study may help identify and more quickly help the 60% of people with major depression who do not get relief from their initial treatments. </h6>



It is estimated that 60% of patients with major depressive disorder don&#8217;t find relief from their first medication, and as many as one-third develop <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC10503923/" target="_blank" rel="noreferrer noopener">treatment-resistant depression</a>, which is often defined as still experiencing symptoms after trying at least two antidepressants.



Researchers at Johnson &amp; Johnson and the 23andMe Research Institute used advanced machine learning techniques to accurately identify those at most risk for treatment-resistant depression, a massive breakthrough for those suffering with this condition.



The groundbreaking research, published this week in the journal <a href="https://pubmed.ncbi.nlm.nih.gov/41028019/" target="_blank" rel="noreferrer noopener">Scientific Reports</a>, used only self-reported information from about 23,000 people who consented to participate in 23andMe research. The model included a total of 101 predictive factors, including such things as age, symptoms that persist between episodes of depression, the duration of episodes of depression, stress levels, and suicidal thoughts. 



Using this predictive model, researchers were able to accurately predict those at the highest risk for treatment-resistant depression 78% of the time, according to the study.&nbsp;



The predictive model did not use either genetics or lab results, just questions that can be easily assessed by a clinician.



<h2 class="wp-block-heading">Why This Matters</h2>



<figure class="wp-block-image alignright size-full is-resized"><img loading="lazy" decoding="async" width="508" height="531" src="http://35.88.189.111/wp-content/uploads/2025/10/drug-bottle.png" alt="" class="wp-image-34304" style="width:161px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/drug-bottle.png 508w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/drug-bottle-287x300.png 287w" sizes="auto, (max-width: 508px) 100vw, 508px" /></figure>



Typically, antidepressants used to treat major depression take a little time to work, up to a month or a month and a half. When a treatment does not work, clinicians often prescribe an alternative medication. When someone with depression fails to respond to at least two different medications, they are deemed to have treatment-resistant depression. In many cases, it can take around a year for someone to finally be diagnosed with treatment-resistant depression.



That long delay in finding effective treatment has a cost, not just in the time it takes to identify treatment but in the prolonged suffering for those in the throes of depression, unable to get relief.&nbsp;



The promise of the kind of predictive modeling described in this new study is that it would give both people with depression and clinicians who treat them a tool to flag those who might not respond to standard therapies.



Instead of waiting to see if initial treatments are effective, it may accelerate the process of finding alternatives. Additionally, this predictive model only utilizes patient-reported information; no expensive testing is required.&nbsp;



<h2 class="wp-block-heading">More About the Predictive Model</h2>



The model identified eight primary factors that predict treatment resistance, as reported by research participants. Each offers different dimensions of their depression.



<figure class="wp-block-image alignleft size-full is-resized"><img loading="lazy" decoding="async" width="275" height="252" src="http://35.88.189.111/wp-content/uploads/2025/10/depression.png" alt="" class="wp-image-34307" style="width:184px;height:auto"/></figure>



Participants reported on the different symptoms that persisted between the episodes of depression. They reported on how long each episode of depression lasted, and how many years they&#8217;d experienced these periodic episodes. Also included in the self-reported data were levels of stress, or whether they had recurring post-traumatic stress, and two critical factors that looked at more external stressors and life events. Also factored into the modeling was a participant&#8217;s age and whether they had suicidal thoughts. Finally, the model included the self-reported timing between episodes of depression, which was significant when the time between episodes was shorter.



Using these factors and advanced machine learning the researchers were able to accurately distinguish between those who were treatment-resistant and those who responded to treatment. An accurate way to identify if someone will or will not respond to treatment could translate into meaningful clinical benefits. It could mean the difference between waiting months for effective treatment instead of years.&nbsp;



<h2 class="wp-block-heading">More Personalized Depression Care</h2>



This research represents a crucial step toward more personalized mental health treatment and a move away from a &#8220;one-size-fits-all&#8221; approach to treatment of depression.&nbsp;



For the millions of people living with depression, this work represents a path toward precision care, shortening the time to effective treatment and improving quality of life.



The future of depression treatment lies not just in developing new medications, but in better understanding who needs what treatment when. This predictive model brings us measurably closer to that goal, promising a world where effective depression treatment is not a matter of luck, but of precision.



If you or someone you know is struggling with depression, please reach out to a mental health professional. The <a href="https://988lifeline.org/" target="_blank" rel="noreferrer noopener">National Suicide Prevention Lifeline</a> (988) provides 24/7 support for those in crisis.

Predicting Treatment-Resistant Depression Using the 23andMe Survey Data

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This October, for Breast Cancer Awareness Month, we will be sharing some of the latest research on this important topic.
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What if the same genetic factors that put you at higher risk for developing cancer could potentially increase the chances you&#8217;d survive longer if you do get cancer? This counterintuitive possibility is exactly what researchers discovered in a groundbreaking collaboration between the 23andMe Research Institute and the Dana-Farber Cancer Institute.



<h2 class="wp-block-heading" id="h-understanding-cancer-risk-and-polygenic-scores">Understanding cancer risk and polygenic scores</h2>



Like most common diseases, cancer is multifactorial – it&#8217;s caused by a combination of genetic factors and non-genetic factors like environmental exposures and lifestyle. Polygenic risk scores are tools that can estimate an individual&#8217;s inherited genetic risk of developing many common conditions, such as cancers.&nbsp;



A <a href="https://pubmed.ncbi.nlm.nih.gov/40877800/" target="_blank" rel="noreferrer noopener">recent study</a> conducted at the Dana-Farber Cancer Institute investigated whether  polygenic risk scores may be associated not just with risk of disease, but with clinical outcomes. The study analyzed nearly 24,000 cancer patients to ask whether having a high <a href="https://blog.23andme.com/articles/three-new-prs-cancer-reports" target="_blank" rel="noreferrer noopener">polygenic risk score, predicting a high likelihood of cancer</a>, also could tell you anything about the prognosis for a person who does go on to develop cancer.



In collaboration with 23andMe, researchers looked at polygenic risk scores for more than 200 diseases to see if any could also predict the prognosis of six common cancer types: non-small cell lung cancer, colorectal cancer, breast carcinoma, glioma, ovarian cancer, and prostate cancer.&nbsp;



<h2 class="wp-block-heading" id="h-an-unexpected-finding">An unexpected finding</h2>



Surprisingly, they found that among breast cancer patients, those with high polygenic risk scores for breast cancer actually showed longer average survival times than those with low scores. This finding held up even when accounting for other factors like a patient&#8217;s age, treatment, or different kinds of tumors.



Why might this be the case?&nbsp;



Cancer-causing genetic changes come in two types: those you&#8217;re born with (germline mutations) that appear in every cell, and those that develop over time in specific tissues (somatic mutations) due to factors like smoking or aging. Polygenic risk scores measure only germline mutations.



The researcher&#8217;s results raise the possibility that tumors driven more by germline mutations — and corresponding high polygenic risk scores — may tend to be less aggressive compared to tumors that are more driven by somatic mutations.&nbsp;



<h2 class="wp-block-heading" id="h-what-comes-next">What comes next</h2>



While these results are statistically robust, they&#8217;ll need to be confirmed in other studies before changing how doctors might treat cancer patients. With additional investigation, these findings could eventually help doctors provide more personalized prognoses and potentially identify patients who might benefit from different treatment approaches based on their genetic risk profiles.

Study Reveals an Unexpected Link Between Genetic Cancer Risk Scores and Survival

This update is currently available to all eligible customers on the latest, V5, genotyping chip. 



The 23andMe Ancestry Team has been working hard on <a href="https://blog.23andme.com/articles/a-major-update-to-ancestry-composition-is-coming-soon" target="_blank" rel="noreferrer noopener">a major update to the Ancestry Composition report</a>, and results are now available! Our goal is to provide the most accurate and meaningful genetic ancestry results in the industry. We ground our models in rigorous science, guided by established population genetics research, to ensure your results are consistent, reliable, and can help guide your personal journey of discovery.



<h2 class="wp-block-heading" id="h-what-changes-you-ll-see">What changes you&#8217;ll see</h2>



<ul class="wp-block-list">
<li>New granularity in your ancestry percentages: 33 new populations in Europe and 6 in the Americas to explore. Plus we&#8217;ve updated our algorithm to eliminate “Broadly” and “Unassigned” categories in the default results view.&nbsp;</li>



<li>More accurate results: A new state-of-the-art DNA phasing pipeline reduces errors and gives a more accurate estimate of your percentages, even if your ancestry isn&#8217;t from Europe or the Americas.&nbsp;</li>



<li>New features: A new “Version History” section lets you compare your new results to your previous result, and <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members can also access all previous versions of their results at different confidence thresholds.</li>
</ul>



This update powers your Ancestry Composition, Ancestry Timeline, Parental Inheritance, DNA Painting, and more.



<h2 class="wp-block-heading" id="h-our-focus-for-this-update">Our focus for this update</h2>



For this update we focused on improving the entire Ancestry Composition pipeline integrating the latest research. Throughout the rounds of development we look at two major metrics: precision and recall. Precision lets us know how often we correctly predict that a piece of DNA is from a specific population. Recall tells us how much DNA from a specific population we can correctly identify. Working to maximize both precision and recall is critical to making Ancestry Composition and other ancestry features as accurate as possible.



<figure class="wp-block-image alignleft size-full is-resized"><img loading="lazy" decoding="async" width="366" height="368" src="http://35.88.189.111/wp-content/uploads/2025/09/AC78_wheel.png" alt="" class="wp-image-34276" style="width:170px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/AC78_wheel.png 366w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/AC78_wheel-298x300.png 298w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/AC78_wheel-150x150.png 150w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/AC78_wheel-271x271.png 271w" sizes="auto, (max-width: 366px) 100vw, 366px" /></figure>



The final models in this update had good precision and recall across the new populations, ensuring the accuracy of the ancestry breakdown predictions while also expanding the specificity and granularity of the populations. One example of the improvements gained by this update is the reduced amount of North Asian ancestry predicted for some Indigenous North American customers. You can learn more about the development process and see precision and recall metrics for each population in the <a href="https://www.23andme.com/ancestry-composition-guide/" target="_blank" rel="noreferrer noopener">Ancestry Composition Guide</a>.



While this update focused on increasing granularity in Europe and the Americas, customers from other parts of the world will still benefit thanks to the improvements to the science and the removal of broadly and unassigned ancestry.



<a href="https://you.23andme.com/" target="_blank" rel="noreferrer noopener">Sign in</a> and check out your new results.&nbsp;



Not yet a 23andMe member? Learn more about what <a href="https://www.23andme.com/compare-dna-tests/" target="_blank" rel="noreferrer noopener">23andMe has to offer</a>.



<h2 class="wp-block-heading" id="h-some-questions-you-might-be-wondering-about">Some questions you might be wondering about</h2>



Why are certain populations combined?



To define the 78 Ancestry Composition populations, we analyzed the reference datasets, chose candidate populations that appeared to cluster together, and then evaluated whether we can distinguish those groups in practice. Some populations tend to cluster on their own, but most country-level populations overlap to some degree. In these cases, we experiment with different groupings of country-level populations to find combinations that we can distinguish with high confidence. Check out the <a href="https://www.23andme.com/ancestry-composition-guide/" target="_blank" rel="noreferrer noopener">Ancestry Composition Guide</a> to learn more.



Does this mean that the people in those groups are the same? No. Each group has its own history, culture, and often different languages. These groupings are a reflection of our current genetic understanding and scientific methods, not a statement about cultural identity.



Does this mean DNA that is assigned to these populations is from all groups? Not necessarily. For example, DNA assigned to the Belarusian, Polish &amp; Ukrainian group might mean your ancestors were from one, two, or all three of those country-level populations. Sometimes other information from your DNA, such as your Genetic Groups, might help you identify more specific locations your ancestors may have come from.&nbsp;



Why are some reference panels smaller than before?



A reference panel, or a reference population or reference dataset, is a collection of DNA samples from people with some common connection. We compare your DNA to these reference panels to determine which ancestry most closely corresponds to your DNA. We often use 23andMe research participants who tell us they have four grandparents all born in the same country for reference panels.



However, sometimes when we look at the ancestry prediction for individuals in a reference panel for a specific population a few individuals don&#8217;t end up being predicted to have a reasonably large percentage of their DNA from that population. These individuals are considered outliers. As part of this update we systematically reviewed our reference panels around the world to remove these outliers. But don&#8217;t worry; even though some reference panels might be smaller, we still check that the models perform as well as (or better than) before for people with ancestry from these regions.&nbsp;



Why is there no Indigenous Caribbean population?



To define a new ancestry population we need reference panels made up of individuals who have deep genetic roots from one place. However, many individuals from the Caribbean are highly admixed (“admixture” refers to places where there was mixing of previously separate populations). This makes it incredibly difficult to identify a sufficient number of individuals with primarily indigenous DNA from the Caribbean. The reference panels for the new Indigenous American populations are almost entirely unadmixed, which is why we are able to provide ancestry percentages for these populations.&nbsp;



<figure class="wp-block-image alignright size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="502" src="http://35.88.189.111/wp-content/uploads/2019/08/avg_ancestry_caribbean-1024x502.png" alt="" class="wp-image-27359" style="width:371px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/08/avg_ancestry_caribbean-1024x502.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/08/avg_ancestry_caribbean-300x147.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/08/avg_ancestry_caribbean-768x376.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/08/avg_ancestry_caribbean-880x431.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/08/avg_ancestry_caribbean-1180x578.png 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



So where does Indigenous Caribbean ancestry show up? We tend to see that Indigenous American ancestry in individuals from the Caribbean is spread among several of the new Indigenous American populations (especially North American, Southern Mesoamerican, Central Andean &amp; Amazonian, and Northern Andean).



Does this mean Indigenous Caribbean ancestors came from those places? Not necessarily. It simply means that of the options available today, those populations are the closest genetic match.&nbsp;



Why weren&#8217;t other parts of the world updated?



While we would love to be able to make major updates around the world more frequently, each new population requires new reference data and major updates in the prediction models. Throughout the years we have increased the number of populations across the rest of the world; however, we have not updated the populations in Europe since 2012. This update was an important opportunity to provide more detail in Europe and the Americas.



We will continue to work towards providing more specificity and granularity around the world in your ancestry percentages as well as Genetic Groups (keep an eye out over the next few months for new Genetic Groups in Africa), <a href="https://blog.23andme.com/articles/23andmes-historic-matches" target="_blank" rel="noreferrer noopener">Historical Matches</a>SM, and other features.



Why did the colors change?



Adding 39 new colors to the color palette was quite the task for the 23andMe Design Team. The team took this opportunity to think about the colors holistically, coming up with a new system that provides a gradient across the world, allowing for nearby populations that are closer together geographically to be represented by more similar colors, while at the same time providing a system that can work for more populations in the future.



Who will get this update?



All customers genotyped on the current (V5) chip and with access to the ancestry service will see this update. A genotyping chip (or array) tests for a fixed set of genetic variants (SNPs) across the genome. Different chip versions (V1, V2, V3, V4, V5, etc.) test for different sets of SNPs. More recent chips often include better coverage for certain populations, recently discovered variants, or better genetic markers that help improve ancestry?composition algorithms or detect health?associated variants.



Ancestry Composition is trained on specific genotyping chip versions, and these latest models were only trained on the latest chip version. The models are incompatible with data from older genotyping chips, as older chips don’t include most of the genetic markers used by these new ancestry models. More recent chip versions are also designed with better coverage for diverse populations. If you&#8217;re on an older chip version (or not sure which chip version you have) learn about chip upgrades <a href="https://customercare.23andme.com/hc/en-us/articles/360025014494-How-Do-I-Upgrade-My-Genotyping-Chip" target="_blank" rel="noreferrer noopener">here</a>.



What happens if my family deleted data and I want to connect with them?



When you connect with a biological parent through Your Connections, we use the additional information we learn from your parents&#8217; DNA to improve the resolution of your Ancestry Composition results. You will also be able to see the proportions of each ancestry that you inherited from each parent in the Parental Inheritance section in your Ancestry Composition report. If a family member has deleted their account they will need to purchase a new kit and create a new account before you can connect with them.

It’s Finally Here: A New Version of Ancestry Composition

Obsessive-compulsive disorder (OCD) is a complex and often debilitating condition that affects up to three percent of people, but the biological basis of the disorder has remained largely elusive. While we’ve known that genetics play a role, previous genetic studies have been limited by their relatively small sample size and have only identified a few of the specific genetic variants involved.



But that is now changing.



<a href="https://pubmed.ncbi.nlm.nih.gov/40360802/" target="_blank" rel="noreferrer noopener">In a recent study</a>, the largest of its kind ever conducted for OCD, researchers identified dozens of genetic variants associated with the disorder, offering unprecedented insight into its underlying biology.



<h2 class="wp-block-heading" id="h-the-power-of-numbers">The Power of Numbers</h2>



For complex conditions like OCD, genetic discovery is a numbers game. To find the subtle genetic variations that contribute to risk, scientists need to compare the DNA of vast numbers of people with and without the condition. This is where the research model of the 23andMe Research Institute makes a world of difference.



<figure class="wp-block-image alignright size-full is-resized"><img loading="lazy" decoding="async" width="600" height="600" src="http://35.88.189.111/wp-content/uploads/2017/05/your_dna_family.png" alt="" class="wp-image-25345" style="width:141px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family.png 600w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family-150x150.png 150w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family-300x300.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family-271x271.png 271w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family-372x372.png 372w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family-574x574.png 574w" sizes="auto, (max-width: 600px) 100vw, 600px" /></figure>



This study combined data from 28 different cohorts. The result was a dataset of incredible scale, including 53,660 individuals with OCD and more than 2 million controls. Consented 23andMe research participants made up about half of the entire cohort in this study. This immense contribution, made possible by those who choose to participate in research, was critical to achieving the statistical power needed to make these new discoveries.



<h2 class="wp-block-heading" id="h-what-the-study-found">What the Study Found</h2>



By scanning the genomes of millions of individuals, the researchers identified 30 independent genetic variants that were significantly associated with OCD. Of these 30 genetic variants, half are entirely new discoveries, while the others confirm and strengthen findings from previous, smaller studies. Researchers mapped these genetic variants to 25 genes that are likely impacted by those variants.



<h3 class="wp-block-heading" id="h-zeroing-in-on-the-brain">Zeroing In on the Brain</h3>



Identifying the genes is just the first step. The next question is: where in the body do these genes do their work?



<figure class="wp-block-image alignleft size-full is-resized"><img loading="lazy" decoding="async" width="438" height="458" src="http://35.88.189.111/wp-content/uploads/2015/06/Brain-Logo.jpg" alt="Brain Logo" class="wp-image-22635" style="width:157px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/Brain-Logo.jpg 438w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/Brain-Logo-287x300.jpg 287w" sizes="auto, (max-width: 438px) 100vw, 438px" /></figure>



To find out, the researchers performed tissue and single-cell enrichment analyses. The results were striking. The genetic signals for OCD were highly enriched in six different types of human brain tissue. In contrast, there was no enrichment found in tissues outside the brain.



The study drilled down even further, pinpointing specific cell types and found that these genes are at work in the same cells identified by neuroimaging and deep brain stimulation studies of OCD. By independently identifying these precise brain regions and cell types through genetics, this study provides additional supporting evidence that these genes and neurons play a direct role in the biology of OCD.



<h3 class="wp-block-heading" id="h-shared-genetics">Shared Genetics</h3>



The study also investigated the genetic relationship between OCD and other psychiatric and behavioral conditions. The researchers found statistically significant positive genetic correlations between OCD and a range of other disorders, including anxiety, depression, anorexia nervosa, and Tourette syndrome



This finding reinforces a growing body of evidence that many psychiatric conditions, while appearing different on the surface, are likely to share some underlying genetic susceptibility factors. Understanding this genetic overlap may be key to understanding mental health as a whole.



<h2 class="wp-block-heading" id="h-a-foundation-for-the-future">A Foundation for the Future</h2>



This study represents a pivotal moment for OCD research. By dramatically expanding the list of known genetic variants associated with OCD and grounding them in the specific biology of the brain, this work opens doors for researchers to explore the precise mechanisms by which these genes influence brain circuits and contribute to OCD symptoms.



Ultimately, these findings may be a critical step toward developing novel and more effective treatments for a disorder that has long been misunderstood.



And once again, we want to extend our deepest gratitude to 23andMe research participants. Your contribution to this landmark study has advanced our understanding of OCD and paved the way for a healthier future.

A Major Leap Forward in Understanding the Genetics of OCD

In the article <a href="https://www.nytimes.com/2017/01/11/magazine/neanderthals-were-people-too.html?_r=0">Neanderthals Were People Too</a>, Jon Mooallem describes an electric moment where he felt a visceral connection to our long lost human cousins.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-25260" src="https://blog-api.23andme.com/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-212x300.jpg" alt="" width="212" height="300" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-212x300.jpg 212w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-768x1084.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-725x1024.jpg 725w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-623x880.jpg 623w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-836x1180.jpg 836w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/01/EGrhX_Flint-Nana-Kennis-Kennis-reconstructions-of-the-Gibraltar-12-skulls-Photo-S.Finlayson-scaled.jpg 1813w" sizes="auto, (max-width: 212px) 100vw, 212px" />
Watching a group of archeologist painstakingly excavate a small hearth in a cave in Gibraltar, Mooallen is suddenly struck by what he’s seeing. The bits of charcoal, the fire stained ground where embers are scattered and the smoke stained walls where the cinders from the fire had pushed up against the rock wall.


“Suddenly, it struck me — though it should have earlier — that what we were looking at were the remnants of a single event: a specific fire, on a specific night, made by specific Neanderthals. Maybe this won’t sound that profound, but it snapped that prehistoric abstraction into focus. This wasn’t just a “hearth,” I realized; it was a campfire.”


<h6>The Connection</h6>

He was looking at the remains of a fire that warmed these human cousins of ours on a night 50,000 years ago, and he felt connected.
Whether we feel it or not, most humans living today are connected to Neanderthals.
All non-Africans have between one and three percent Neanderthal DNA, a remnant of interbreeding as modern humans migrated out of Africa and met Neanderthals for the first time. And we likely carry remnants of other hominids in our DNA, such as the Denisovans.
Perhaps it’s that genetic connection that fuels our fascination with Neanderthal, or maybe it’s that what we learn is informing us all more about what it means to be human.
We know that we owe much to the Neanderthals. It’s likely that interbreeding with Neanderthals helped give humans an evolutionary advantage to adapt — beneficial immune response and blood clotting for instance — but it also left us with a subtle risk for certain diseases, according to <a href="http://www.sciencemag.org/news/2016/02/our-hidden-neandertal-dna-may-increase-risk-allergies-depression">research published early last year</a>.

<h6>The Neanderthal Advantage</h6>

Vanderbilt University&#8217;s John Anthony Capra, was the lead author of that study, which we previously wrote about in the <a href="https://blog.23andme.com/news/the-lasting-legacy-of-neanderthals/">blog</a>. Capra recently spoke with <a href="https://www.nytimes.com/2017/01/20/science/john-anthony-capra-neanderthals-dna-humans.html">The New York Times</a> about that research.
Over time humans <a href="https://blog.23andme.com/23andme-research/new-neanderthal-research/">purged</a> all but the last vestiges of Neanderthal DNA — but some of what remains, even some of what previously could have been beneficial, is deleterious, according to Capra.


“What we’ve been finding is that Neanderthal DNA has a subtle influence on risk for disease,” Capra said.


For the research, Capra and his team looked at electronic health records from 50,000 individuals and found associations with Neanderthal DNA and immune response, blood clotting, and depression.
These findings and others indicate that Neanderthals were much more like us than we previously thought.


“We tend to think of them as dumb and brutish,” Capra said. “There’s no reason to believe that. Maybe those of us of European heritage should be thinking, “Let’s improve their standing in the popular imagination. They’re our ancestors, too.’”

The Neanderthal Within

Scientists have unearthed a trove of bones in a South African cave belonging to a previously unidentified early human relative.
<div id="attachment_22837" style="width: 277px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-22837" class="size-medium wp-image-22837" src="https://blog-api.23andme.com/wp-content/uploads/2015/09/F1.large-1-267x300.jpg" alt="Composite skeleton of Homo nadeli along with other bones found at the Rising Star Cave in South Africa. Photo: Lee Berger, Wits, photographed at Evolutionary Studies Institute" width="267" height="300" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/09/F1.large-1-267x300.jpg 267w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/09/F1.large-1-768x863.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/09/F1.large-1-911x1024.jpg 911w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/09/F1.large-1-783x880.jpg 783w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/09/F1.large-1-1050x1180.jpg 1050w" sizes="auto, (max-width: 267px) 100vw, 267px" />Composite skeleton of Homo nadeli along with other bones found at the Rising Star Cave in South Africa. Photo: Lee Berger, Wits, photographed at Evolutionary Studies Institute</div>
<h2>Rising Star</h2>
Found in the “Rising Star Cave,” the new species has been dubbed homo naledi – naledi is the Sosetho word for star – and fills in more detail about the story of human evolution.
“We’ve found a new species that we are placing in the genus Homo, which is really quite remarkable,” <a href="https://twitter.com/LeeRberger">Lee Berger</a>, a paleoanthropologist, who led the research told the <a href="http://www.theguardian.com/science/2015/sep/10/new-species-of-ancient-human-discovered-claim-scientists">Guardian</a>.
There’s much to ponder with the new finding and some intriguing implications discussed at length in two <a href="http://elifesciences.org/content/4/e09560">new papers</a> about the bones as well as a new <a href="https://www.pbs.org/wgbh/nova/evolution/dawn-of-humanity.html">Nova</a> special. For one, the find adds more information in the big gap in the fossil record tracing back to the dawn of humanity. 
<h2>Homo Naledi</h2>
One of the papers also details where and how the bones were found and covers various theories about how they got there. The implication from that paper is that the bones – more than a 1,000 bones and bone fragments from at least 15 individuals – were possibly brought there for burial. If true this would suggest that homo naledi were advanced enough to actually have a ritual for burying their dead.
“If true it points to advance behavior,” <a href="http://bluelionphotos.blogspot.co.za/2015/09/the-rising-star-interviews.html">said John Hawkes</a>, and paleoanthropologist from the University of Wisconsin who is a co-author of the paper.
That would also point to such things as social bonds, and other kinds of communal structures.
The excavation and its implications are covered at length in the upcoming issue of <a href="http://news.nationalgeographic.com/2015/09/150910-human-evolution-change/">National Geographic</a>.
<h2>Ancient Human Relative</h2>
The team believes the bones &#8211; as yet undated &#8211; represent a new ancient human relative that adds another chapter in the human story.
The bones have some characteristics that are similar to both modern humans and other ancient human species that pre-date it. They were long-legged and slender with hands and feet similar to humans, but their brains were only about a third of the size of modern humans.
In the wonderful <a href="https://www.pbs.org/wgbh/nova/evolution/dawn-of-humanity.html">Nova</a> program, scientists say the find should more clearly change how we look at the human family tree, where there were likely many different species that branched out in different ways, some crossing back to contribute to what ultimately became modern humans, while others went extinct.

Hello Cousin

Consider the cow, and this humble herbivore’s contribution to the human story.<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/dairy-cow-300x200.jpg" alt="dairy cow" class="alignright size-medium wp-image-22620" width="300" height="200" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/dairy-cow-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/dairy-cow-768x511.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/dairy-cow.jpg 849w" sizes="auto, (max-width: 300px) 100vw, 300px" />


We’re not just talking burgers and ice cream, archeological evidence suggests that cows were likely first domesticated from aurochs (extinct wild oxen) as long as 11,000 years ago when farmers used their milk to <a href="https://www.npr.org/sections/thesalt/2012/12/27/168144785/an-evolutionary-whodunit-how-did-humans-develop-lactose-tolerance" target="_blank" rel="noopener noreferrer">make cheese</a> and yogurt.
Nutrient-rich with plenty of vitamin D for the sun-starved in Northern Europe, milk was a kind of superfood of the Bronze Age.
But <a href="https://www.nature.com/news/dna-data-explosion-lights-up-the-bronze-age-1.17723" target="_blank" rel="noopener noreferrer">new research</a> suggests that it took a long time before Europeans could actually benefit from this potent potable.
Looking at DNA samples from the remains for more than 100 individuals who lived in Eurasia from 3,000 to 5,000 years ago, researchers in Norway found that it took a surprisingly long time before Europeans could tolerate milk.
The study looked at much more than whether those early Europeans could tolerate dairy, and focused more broadly on a wide variety of physical and physiological traits including hair thickness, height and skin color.
But the DNA samples indicate that those early Europeans were mostly lactose intolerant, suggesting that even though they had domesticated cows at the time they were unable to digest raw milk as adults. The exception appears to be among the Yamnaya, a group of people who migrated into Northern Europe from an area near the Altai Mountains in what is now central Russia. Researchers speculate that natural selection favored this trait, giving those with it a rich source of nutrition that could sustained them during times of famine when harvests failed. 
 
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/milk-287x300.jpg" alt="Glass of milk isolated on white. Vector illustration" class="alignright size-medium wp-image-22621" width="287" height="300" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/milk-287x300.jpg 287w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/milk-768x802.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/milk-980x1024.jpg 980w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/milk-843x880.jpg 843w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/milk-1130x1180.jpg 1130w" sizes="auto, (max-width: 287px) 100vw, 287px" />

<h5>
Intolerant, even today 
</h5>

Most people are actually lactose intolerant as adults. Only about <a href="https://www.sciencedirect.com/science/article/pii/S0958694611002536" target="_blank" rel="noopener noreferrer">35 percent of people worldwide</a> can digest lactose beyond the age of about seven or eight.
The numbers tell a deeper story when demographically divided. While the majority of people of European ancestry <a href="https://www.nature.com/news/archaeology-the-milk-revolution-1.13471" target="_blank" rel="noopener noreferrer">can tolerate milk</a> into adulthood, only a small minority of people of Asian ancestry can. Among 23andMe customers who consented to research only about 16 percent of those of European ancestry reported that they were <a href="https://www.23andme.com/topics/wellness/lactose-intolerance/">lactose intolerant</a> compared to about 85 percent of people of Asian ancestry.

<h5>
So what gives? 
</h5>

There are a number of <a href="https://www.npr.org/sections/thesalt/2012/12/27/168144785/an-evolutionary-whodunit-how-did-humans-develop-lactose-tolerance" target="_blank" rel="noopener noreferrer">theories</a> about why there are differences among people of different ancestry, and a recent study of ancient Northern European DNA suggests the ability to digest dairy is a relatively new phenomena.
Drinking milk is a problem for most adults. It contains high amounts of a sugar named lactose. As children, we all produce lactase, an enzyme that allows us to break up lactose in our mother&#8217;s milk. As we grow older lactase levels go down, making it harder for adults to breakdown the lactose sugars and causing gastrointestinal &#8220;discomfort.&#8221;
In populations with domesticated cattle, however, there may have been an evolutionary incentive to being able to drink milk as adults and several populations – including populations in Northern Europe – developed genetic variants that enabled adults to continue to breakdown lactose into adulthood. This genetic variant offered a likely evolutionary advantage because milk is nutrient rich, plentiful, and cleaner than many sources of water. In times of famine it offered an alternative source of food for those who could tolerate it.


In the book 10,000 Year Explosion: How Civilization Accelerated Human Evolution, anthropologists Gregory Cochran and Henry Harpending called humans with this variant “<a href="https://westhunt.wordpress.com/2012/10/23/mampires/" target="_blank" rel="noopener noreferrer">mampires</a>,” because it allowed people to feed on the milk of other animals. It’s a clever term, but maybe with a little darker connotations than necessary. As the anthropologist <a href="http://johnhawks.net/weblog/reviews/accel/question-on-selection-and-lactase-2014.html" target="_blank" rel="noopener noreferrer">John Hawkes noted</a> in his blog, milk from domesticated animals is a much more efficient use of farm animals than raising them for meat. In places in Europe, Arabia and in parts of Africa where cold or arid climates made consistent yields from farming grain difficult, milk was a good alternative source of nutrition.

23andMoo

A skull found in a previously undisturbed cave in Israel may hold important new evidence about human migration and intermixing with Neanderthals.
The paper <a href="https://www.nature.com/nature/journal/vaop/ncurrent/full/nature14134.html" target="_blank" rel="noopener noreferrer"> published last month</a> by scientists from Tel Aviv University, offers new evidence about the timing of human migration out of Africa, and when those modern humans mixed with Neanderthals. not 
<div id="attachment_22187" style="width: 310px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-22187" src="https://blog-api.23andme.com/wp-content/uploads/2015/02/skull580-300x171.jpg" alt="Photo: Clara Amit, Israel Antiquities Authority" class="size-medium wp-image-22187" width="300" height="171" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/02/skull580-300x171.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/02/skull580-574x330.jpg 574w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/02/skull580.jpg 580w" sizes="auto, (max-width: 300px) 100vw, 300px" />Photo: Clara Amit, Israel Antiquities Authority</div>
&nbsp;

<h6>A New Timeline?</h6>
The first anatomically modern humans emerged in Africa about 200,000 years ago. This latest finding appears to support several theories about the timing of the human migration <a href="https://www.nature.com/news/2011/110809/full/476136a/box/1.html" target="_blank" rel="noopener noreferrer">out of Africa</a> as well as the timing of intermixing between humans and Neanderthals.
All non-African people today carry traces of Neanderthal DNA. Based on DNA tests scientists have suggested that the interbreeding likely happened between 50,000 and 60,000 years ago.
A study last year, that used new techniques to more accurately date Neanderthal remains, suggested that Neanderthals and humans may have lived side-by-side for <a href="http://www.bbc.com/news/science-environment-28693371" target="_blank" rel="noopener noreferrer">up to 5,000 years</a>. But when and where the Neanderthals and modern humans mixed has been harder to pinpoint.
That’s what makes this study so interesting.
<h6>How Old?</h6>
Uranium-thorium dating of the skull shows that the remains are about 60,000-to-70,000 years old. Known as the Manot cave, the site is near the town of Haifa and within miles of several other archeological sites where Neanderthal remains dating from that same period have also been found. This suggests that at the very least the two species, homo sapiens and homo neanderthalensis, lived side-by-side in the Middle East during that time.
But the researchers involved in this study believe that the bones show more than that.
<h6>New Insights</h6>
According to the author of the study, <a href="http://english.tau.ac.il/news/discovery_ancient_skull" target="_blank" rel="noopener noreferrer">Tel Aviv University Professor Israel Hershkovitz</a>, the shape of the skull bears characteristics found in early modern humans. They are similar to remains found both in Africa and Europe. The skull also shares some characteristics found in Neanderthals. But whether the skull was of a human who had interbred with Neanderthals cannot be determined without recovering DNA from the skull.
Unfortunately, extracting DNA from this skull could prove very difficult. Unlike the remains of other ancient humans that were found in much colder climates where DNA can be preserved longer, these remains have been exposed to much higher temperatures. DNA begins to break down as it&#8217;s exposed to microbes, water and oxygen. Ancient DNA tends to be found in very small quantities and is often fragmentary or damaged.
So far the <a href="http://www.sciencemag.org/content/343/6178/1417.summary" target="_blank" rel="noopener noreferrer">oldest human DNA</a> was extracted from a bone found along a Siberian riverbank of a man who lived 45,000 years ago.
<img loading="lazy" decoding="async" class="alignright wp-image-14049" title="neanderthal icon" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2012/06/neanderthal-icon-96x150.jpg" width="50" height="77" />
Got Neanderthal DNA?
23andMe customers can <a href="https://www.23andme.com/you/labs/neanderthal/">find their inner Neanderthal</a> or at least how much Neanderthal DNA they have. Not yet a customer? <a href="https://www.23andme.com/store">Visit our store</a>!

Meeting At the Crossroads

Svante Paabo and his team in Leipzig are up to it again, <img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2014/10/Svante-Paabo-and-Nikolay-Peristov-200x200.jpg" alt="Svante PÃ¤Ã¤bo and Nikolay Peristov discuss the Ust'-Ishim discovery" class="alignright size-thumbnail wp-image-21817" width="200" height="200" />and revealing more detail about interbreeding between modern humans and our early human cousins, the Neanderthals.
No stranger to extracting ancient DNA, Paabo, the director of evolutionary genetics at the <a href="http://www.mpg.de/eva-en?section=eb-evb-g" target="_blank" rel="noopener noreferrer">Max Planck Institute for Evolutionary Anthropology</a> in Leipzig, Germany, was the first to decode the Neanderthal genome.

<h6>Neanderthals and Modern Humans</h6>
That was when researchers first learned that Neanderthal and humans mated, and that all human with Asian or European ancestry, who are living today carry remnants of that Neanderthal DNA.
Beyond the marvel of actually extracting DNA from the femur of the ancient human known as the “Ust’-Ishim man,” and sequencing that DNA to the same accuracy as that achieved from sequences for living people, is what this sequence is telling scientists about human evolution and migration.
“The population to which the individual belonged may have split from the ancestors of present-day West Eurasian and East Eurasian populations before, or at about the same time, when these two first split from each other,” Paabo in an <a href="http://www.mpg.de/8710423/genome-earliest-modern-human?filter_order=L&#038;research_topic=" target="_blank" rel="noopener noreferrer">announcement</a> regarding the paper. 
<h6>Interbreeding</h6>
Although some of the <a href="https://www.npr.org/blogs/health/2014/10/22/358047524/a-45-000-year-old-leg-bone-reveals-the-oldest-human-genome-yet" target="_blank" rel="noopener noreferrer">coverage</a> this week, has focused on the fact that humans and Neanderthals were interbreeding, that really is old news. What’s more significant is what that DNA is telling us about <a href="https://www.nytimes.com/2014/10/23/science/research-humans-interbred-with-neanderthals.html?ref=science&#038;_r=0" target="_blank" rel="noopener noreferrer">when the interbreeding occurred</a> and hinted at when and where humans first migrated out of Africa and then into Asia and Europe.
The sequence indicated that this early human also had about the same percentage of Neanderthal DNA as we do today, but that the segments of that DNA were much longer. Because of how DNA recombines with each generation, this is what researchers thought they would see. It also helped them more precisely pinpoint when interbreeding between humans and Neanderthals occurred to sometime between 50,000 and 60,000 years ago.
<h6>Migration Timeline</h6>
Previous estimates ranged much wider saying that it occurred between 30,000 and 80,000 years ago. Pinpointing the time is significant because that period also corresponds with when humans were first migrating out of Africa and through the Middle East, according to Janet Kelso, who did the computer based analyses of the sequence. Humans likely migrated out of Africa about 100,000 years ago, and perhaps came into contact with Neanderthals in the Middle East, mixing with them there before migrating into Europe and Asia.
There is much more value in this ancient genome for researchers as they compare it to the genomes of modern humans. For instance, it allowed researchers to estimate that between one and two mutations per year accumulated in human populations in Europe and Asia since the Ust’-Ishim walked the earth.
Not much is known about this one man, however. There were no artifacts found with him. But looking at his DNA, researcher learned that he has more in common with modern Asians than with modern day Europeans. In their paper the researchers suggested that this lends weight to a theory that there were waves of migration into Europe, but that modern humans descend from a population who “did not participate in the initial dispersal of modern humans into Europe and Asia.”
<img loading="lazy" decoding="async" class="alignright wp-image-14049" title="neanderthal icon" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2012/06/neanderthal-icon-96x150.jpg" width="50" height="77" />
Got Neanderthal DNA?
23andMe customers can <a href="https://www.23andme.com/you/labs/neanderthal/">find their inner Neanderthal</a> or at least how much Neanderthal DNA they have. Not yet a customer? <a href="https://www.23andme.com/store">Visit our store</a>!

Dem Bones

<img loading="lazy" decoding="async" class="aligncenter wp-image-10750 size-full" title="top10ten" src="http://35.88.189.111/wp-content/uploads/2011/12/top10ten.jpg" alt="" width="306" height="345" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2011/12/top10ten.jpg 306w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2011/12/top10ten-266x300.jpg 266w" sizes="auto, (max-width: 306px) 100vw, 306px" />
Take a moment to look back at the ten most interesting and significant genetic findings of 2012 or at least the ones that drew our attention.
In the last 12 months we’ve seen huge strides in genetic research giving us new insight into serious conditions such as Alzheimer’s as well as new treatments for cystic fibrosis. And in the last year scientists have made huge leaps in our understanding of the human genome itself with the culmination of a massive study of the so-called uncharted non-coding portions of our DNA – the ENCODE project.
Researchers at 23andMe continue to contribute to some of these important findings with groundbreaking work on the relative importance of family health history versus genetics when determining disease risk and a new method to screen for the genetic risk for certain types of blood disorders.
It’s been another great year of discovery and here’s our top ten.
<img loading="lazy" decoding="async" class="alignright wp-image-5677 size-full" title="alzheimers" src="http://35.88.189.111/wp-content/uploads/2009/12/alzheimers.jpg" alt="" width="435" height="310" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2009/12/alzheimers.jpg 435w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2009/12/alzheimers-300x214.jpg 300w" sizes="auto, (max-width: 435px) 100vw, 435px" />
1) &nbsp;A Genetic Variant Protective Against Alzheimer’s Disease – The T version of rs63750847 &nbsp;– also known as the A673T variant in the APP gene – was associated with about five times lower odds of <a href="https://www.ncbi.nlm.nih.gov/pubmed?cmd=Search&amp;db=pubmed&amp;term=22801501">Alzheimer&#8217;s</a>. While this is a very rare variant – only about one in 10,000 people of European descent have it – the research, done by the Icelandic company deCODE Genetics in association with Genentech, adds more insight into the development of the disease. Many mutations in the APP gene actually cause Alzheimer’s through an overproduction of beta amyloid protein in the brain (a hallmark of Alzheimer’s), but the protective variant appears to do the opposite, according to the study. New drugs built on this finding could help protect against Alzheimer’s, or even the mental ravages of normal aging. 23andMe does offer customers reports on their own Alzheimer’s risk based on the more common APOE variant, as well as a report on this protective APP variant.
<img loading="lazy" decoding="async" class="aligncenter wp-image-15558 size-full" title="encode" src="http://35.88.189.111/wp-content/uploads/2012/09/encode.jpg" alt="" width="574" height="334" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/09/encode.jpg 574w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/09/encode-300x175.jpg 300w" sizes="auto, (max-width: 574px) 100vw, 574px" />
2) &nbsp;ENCODE Project Creates a Map of the Uncharted Areas of the Genome – Much of the work in genetics has been focused on the areas in our DNA that code for proteins, but this is a very small part – just 1 percent – of our genome. The<a href="https://www.wired.com/wiredscience/2012/09/encode-human-genome/"> ENCODE project</a>, which has enlisted more than 400 scientists over several years, is attempting to map the rest of it, the so called<a href="https://blog.23andme.com/news/a-map-of-the-uncharted-genome/"> “dark matter” of the genome</a>. What they’ve created is the foundation of a sort of encyclopedia of the functions of many of these uncharted areas of the genome. It’s a resource that will be used by many scientists in the years to come.
3) &nbsp;Noninvasive Prenatal Sequencing – Two separate research groups reported within weeks of each other that they had<a href="https://blog.23andme.com/health-traits/noninvasive-sequencing-of-a-human-fetus/"> successfully sequenced a human fetus</a> and done so noninvasively. The breakthrough offers an opportunity for earlier prenatal screening than currently offered with amniocentesis or chorionic villous sampling (CVS) without the same risks for a developing fetus.
4) &nbsp;New insights into a group of rare blood disorders known as MPNs – In less than a year, 23andMe recruited a 1,000-person cohort with a group of rare blood disorders known as myeloproliferative neoplasms, or MPNs. Within months of reaching that goal we began reporting our<a href="https://blog.23andme.com/23andme-research/novel-genetic-findings-for-myeloproliferative-neoplasms/"> new findings</a>. Among them were replications of known genetic associations with the disease as well as new ones including an association between these conditions and variants in the TERT and ATM genes.
<img loading="lazy" decoding="async" class="aligncenter wp-image-6487 size-full" title="neanderthal_bones" src="http://35.88.189.111/wp-content/uploads/2010/05/neanderthal_bones.jpg" alt="" width="350" height="421" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/neanderthal_bones.jpg 350w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/neanderthal_bones-249x300.jpg 249w" sizes="auto, (max-width: 350px) 100vw, 350px" />
5) &nbsp;New Insights into Human Origins and Evolution – Several different studies highlight ongoing research on our early ancestors and the evolution of modern humans. Beyond the compelling tale of our early ancestors, the journey out of African and the intermixing with Neanderthals and Denisovans, the new research also gives us insight into the<a href="https://www.wired.com/wiredscience/2012/11/recent-human-evolution-2/"> significance of rare genetic variants</a>.
6) &nbsp;Family Medical and Genetics Used Together to Predict Disease – 23andMe <a href="https://blog.23andme.com/23andme-research/using-genetics-and-family-history-for-health/">developed a model</a> to show that both family history and genetic tests have strengths in predicting disease risks, but when used together they provide the best predictor for disease.
&nbsp;7) &nbsp;Older Dads’ Biological Clocks – For a long time prospective fathers could wile away the years without much worry about when to have kids, while prospective moms were constantly checking their ticking biological clocks.<a href="https://www.nature.com/nature/journal/v488/n7412/full/nature11396.html"> A study</a> may turn the tables a bit, pushing men to think a little more about how long they wait to start a family. The study says that as men grow older the number of de novo mutations they<a href="https://blog.23andme.com/health-traits/for-older-dads/"> pass onto their children increases</a>, and preliminary studies suggest that the more de novo mutations passed onto a child the higher the risk that child could develop certain types of conditions, such as autism and schizophrenia. That said becoming a dad can actually be good for you. There’s evidence linking <a href="https://blog.23andme.com/health-traits/ah-fatherhood-dirty-diapers-skinned-knees-and-healthier-hearts/">fatherhood to healthier hearts.</a>
8) &nbsp;Breast Size Matters, But Not How You Think – Researchers at 23andMe found that genetic factors influence breast size and that in turn these factors are connected to the genetics of breast cancer.
&nbsp;9) &nbsp;New Treatment for Cystic Fibrosis – &nbsp;Early in 2012 the FDA approved ivacaftor (Kalydeco ®) as a new treatment for cystic fibrosis, one of the most common recessively inherited diseases. The drug<a href="https://online.wsj.com/article/SB10000872396390444024204578046911440223842.html?mod=WSJ_TechInnovationAwards1012_MiddleSecondSummaries%20."> developed by Vertex Pharmaceuticals Inc</a>. is the first treatment that targets one of the underlying causes of cystic fibrosis – a specific genetic mutation – rather than its symptoms.
10) &nbsp;Autism Study Reveals No Genetic Associations – It may be strange to <a href="https://blog.23andme.com/health-traits/autism-study-reveals-no-genetic-associations/" target="_blank" rel="noopener noreferrer">point to a study that finds no genetic associations</a>, but sometimes an absence of evidence can hint toward new routes of study. Cases of Autism spectrum disorders – which run the gamut from mild to severe impairment and include autism, Asperger syndrome and other disorders – have become increasingly common in the U.S. Why that is, is not so easy to discern. The lack of an association doesn’t mean that genetics isn’t important. In fact twin studies suggest that autism is at least moderately heritable, but it may be that genetic variations play a smaller role than rare mutations or copy number variation in the risk of a person developing autism.

Top Genetic Findings of 2012

Soon children will be filling their backpacks with new notebooks and pencils and piling into yellow school buses.   Even if your school days are long past, you need not be left behind.
Learning is life-long, and you can continue your education using 23andMe&#8217;s short animated guides to human prehistory.
Distributed on-line both on our website (just the first three videos) and at the <a href="https://www.khanacademy.org/" target="_blank" rel="noopener noreferrer">Khan Academy</a> (all five videos), watching these free educational videos couldn&#8217;t be easier.
To learn a little more about genetics you don&#8217;t even need to get on a bus, just your computer.  It is time to go back-to-school!
To take the 23andMe course in Human Prehistory 101, watch the following five videos below. This is the first of three educational courses we&#8217;ll be posting in honor of the &#8220;Back-to-School&#8221; season.
You can check how well you really were paying attention by trying our &#8220;quiz&#8221; after the videos (and you stand a chance of winning a $25 Amazon Gift Card).   We&#8217;ll be announcing the correct answers and the winner of the contest on Wednesday, September 5th. Upon completion, you can take pride in your new knowledge by printing out a certificate that signifies your new human prehistory expert status!

<table id="movies" border="1" width="603" cellspacing="10" cellpadding="20">
<tbody>
<tr>
<td style="padding: 15px;"><img loading="lazy" decoding="async" class="alignright wp-image-15085 size-medium" src="http://35.88.189.111/wp-content/uploads/2012/08/Prologue-300x235.jpg" alt="" width="300" height="235" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/Prologue-300x235.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/Prologue.jpg 542w" sizes="auto, (max-width: 300px) 100vw, 300px" /></td>
<td style="padding: 15px;">
<h3>Prologue</h3>
Description: 
This <a href="https://youtu.be/Mm-IxK1GrYE" target="_blank" rel="noopener noreferrer">first video</a> sets the stage. You&#8217;ll learn about our ancestors and evolutionary cousins &#8212; who they were and how they lived.
 Time: 
4 min 41 sec</td>
</tr>
<tr>
<td style="padding: 15px;"><img loading="lazy" decoding="async" class="aligncenter wp-image-15124 size-medium" src="http://35.88.189.111/wp-content/uploads/2012/08/Part11-300x228.jpg" alt="" width="300" height="228" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/Part11-300x228.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/Part11.jpg 603w" sizes="auto, (max-width: 300px) 100vw, 300px" /></td>
<td style="padding: 15px;">
<h3>Part 1: Out of (Eastern) Africa</h3>
Description: 
In this<a href="https://youtu.be/8183HPmA2_I" target="_blank" rel="noopener noreferrer"> second video</a> learn about the birthplace of humanity &#8212; Africa &#8212; and why non-Africans may be descended from as few as 100 travelers.
 Time: 
5 min 35 sec</td>
</tr>
<tr>
<td style="padding: 15px;"><img loading="lazy" decoding="async" class="size-medium wp-image-15092 alignleft" src="https://blog-api.23andme.com/wp-content/uploads/2012/08/Part2-300x232.jpg" alt="" width="300" height="232" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/Part2-300x232.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/Part2.jpg 586w" sizes="auto, (max-width: 300px) 100vw, 300px" /></td>
<td style="padding: 15px;">
<h3 style="text-align: left;">Part 2: Weathering the Storm</h3>
Description: 
Hot weather got your down?   This <a href="https://youtu.be/T9Nw66RCMhg" target="_blank" rel="noopener noreferrer">third video</a> is sure to cool you off.
 Time: 
3 min 25 sec</td>
</tr>
<tr>
<td style="padding: 15px;"><img loading="lazy" decoding="async" class="wp-image-15093 aligncenter" src="https://blog-api.23andme.com/wp-content/uploads/2012/08/Part3-300x211.jpg" alt="" width="300" height="211" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/Part3-300x211.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/Part3.jpg 736w" sizes="auto, (max-width: 300px) 100vw, 300px" /></td>
<td style="padding: 15px;">
<h3>Part 3: Agriculture Rocks Our World</h3>
Description: 
In this <a href="https://youtu.be/IVHD9wGlbho" target="_blank" rel="noopener noreferrer">fourth video</a> you learn about how agriculture not only changed our diets but also many social aspects of human society.
 Time: 
7 min 00 sec</td>
</tr>
<tr>
<td style="padding: 15px;"><img loading="lazy" decoding="async" class="size-medium wp-image-15094 aligncenter" src="https://blog-api.23andme.com/wp-content/uploads/2012/08/Epilogue-300x202.jpg" alt="" width="300" height="202" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/Epilogue-300x202.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/Epilogue.jpg 732w" sizes="auto, (max-width: 300px) 100vw, 300px" /></td>
<td style="padding: 15px;">
<h3>Epilogue</h3>
Description: 
This <a href="https://youtu.be/F-zRXHAo4-U" target="_blank" rel="noopener noreferrer">last video</a> tells the story of how humankind is being reunited.
 Time: 
2 min 45 sec</td>
</tr>
</tbody>
</table>
Update: This quiz is officially over! <a href="https://blog.23andme.com/articles/human-prehistory-101-results">Check out the answers here.</a> 
<div style="border: 1px solid #000; padding: 5px; font-style: italic; margin: 15px; width: 550px; float: center;">
<img loading="lazy" decoding="async" class="alignleft size-full wp-image-12163" style="float: left; margin-right: 15px;" src="https://blog-api.23andme.com/wp-content/uploads/2012/04/JRBgdIBXKIeVIdETJrxYIw_ttam_logo.jpg" alt="" width="24" height="40" />You have now completed the entire 23andMe Human Prehistory course, the first in a three-part Back-to-School educational course series! Click on the certificate below get a larger image which you can print out and display it with pride.
<img loading="lazy" decoding="async" class="aligncenter wp-image-15149 size-medium" src="http://35.88.189.111/wp-content/uploads/2012/08/PreHistoryPostCertificate-300x199.jpg" alt="" width="300" height="199" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/PreHistoryPostCertificate-300x199.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/PreHistoryPostCertificate-768x509.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/08/PreHistoryPostCertificate.jpg 852w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Want to continue your education? You can learn about <a href="https://www.23andme.com/you/" target="_blank" rel="noopener noreferrer">your self from both a health and ancestry perspective </a> on 23andMe. Not yet a customer? Visit our <a href="https://www.23andme.com/store/cart/" target="_blank" rel="noopener noreferrer">store</a>.
</div>

Back-to-School: Human Prehistory 101

by Mike Macpherson, Shirley Wu, and Joanna Mountain
<img loading="lazy" decoding="async" class="alignright wp-image-8628 size-medium" title="Hadza-hunter" src="http://35.88.189.111/wp-content/uploads/2011/03/Hadza-hunter-300x200.jpg" alt="A photo of a smiling young Hadza hunter girl." width="300" height="200" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2011/03/Hadza-hunter-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2011/03/Hadza-hunter.jpg 424w" sizes="auto, (max-width: 300px) 100vw, 300px" />A young Hadza hunter
From just flecks of bone and specks of DNA, scientists have been able to piece together a story of the origin of our species.
<h2>Out of East Africa?</h2>
That story, by most accounts, begins in eastern Africa 100-200,000 years ago. After all, multiple lines of evidence point to eastern Africa &#8212; it’s where the oldest recognizable human bones have been found, where the linguistic diversity is richest, and it fits the available genetic data.
However, in this week’s issue of PNAS, researchers, including those from Stanford, UCSF, and 23andMe, present much more extensive genetic evidence suggesting that humans may have originated not in eastern but in southern Africa.
<h2>Using DNA</h2>
How can genetics tell you where a species originated? A general principle is that you tend to find the highest levels of genetic variation in the portion of the population that’s been around the longest. That’s because sub-populations that split off from an original population start out with just a sample of the original population’s gene pool, and it takes a very long time for new genetic variation to build up in the new sub-population.
Using this principle, one strategy for identifying a species&#8217; origin is to measure genetic variation in several places where the species lives and look for the place where the genetic variation is highest.
For this study, the authors gathered new genome-wide data from three click-speaking peoples from southern Africa living for millennia in relative isolation and seven northern African peoples. They also assembled existing genome-wide data from 14 further African populations, covering eastern, western, and central Africa, resulting in a continent-wide representation of genetic variation.
<h2>Different Theories</h2>
With this much coverage, the researchers would have been in a position to find evidence for human origins in any part of Africa; eastern Africa would be the front-runner, but researchers have argued that northern, central, and southern Africa are also plausible candidates.
However, they found that among all the populations they looked at, the highest levels of genetic variation were found in southern Africa. This suggests, the authors conclude that each of us may trace our ancestry (ignoring any contributions from Neandertals for now!) back to southern Africa, sometimes less than 100,000 years ago.
Although this new genetic evidence is intriguing, it’s not the end of the story. There’s some archaeological evidence to support a southern African origin, but for now, it’s fairly limited. These new data are also consistent with a scenario where humankind arose in eastern Africa but later migrated to southern Africa. Studies sampling genetic diversity in further African populations may help clarify the early history of our species.
<img loading="lazy" decoding="async" class="alignright wp-image-6513 size-medium" title="joanna_africa4" src="http://35.88.189.111/wp-content/uploads/2010/05/joanna_africa4-300x207.jpg" alt="" width="300" height="207" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/joanna_africa4-300x207.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/joanna_africa4.jpg 357w" sizes="auto, (max-width: 300px) 100vw, 300px" />Dr. Mountain in Africa during her time in the Peace Corps
<h2>Using GWAS</h2>
The insights of this study were enabled by genome-wide genetic data of the sort that 23andMe generates. In fact, they used exactly the kind of data that 23andMe generates; the southern African Sandawe, Hadza, and Khomani individuals were all genotyped on our 580,000-SNP v2 platform, just like many of our customers.
23andMe was proud to participate in this study, which was actually launched almost 15 years ago by 23andMe’s Senior Director of Research, Joanna Mountain. Dr. Mountain collected samples for the Hadza in Tanzania and initiated the recent sample collection in South Africa.
We are also proud to note that the study’s lead and second authors, Brenna Henn, and Christopher Gignoux, are former members of Team 23andMe. Brenna and Chris made many contributions to 23andMe’s product, most visibly to the Maternal and Paternal Line features.

Location, Location, Location: Did Humans Start Out in Southern Africa?

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-4589" title="chimp" src="https://blog-api.23andme.com/wp-content/uploads/2009/09/chimp-300x200.jpg" alt="chimp" width="300" height="200" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2009/09/chimp-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2009/09/chimp.jpg 600w" sizes="auto, (max-width: 300px) 100vw, 300px" />
We may be another step closer to discovering what makes us human.
A new study published online this week in <a href="https://genome.cshlp.org/content/early/2009/08/31/gr.095026.109.abstract" target="_blank" rel="noopener noreferrer">Genome Research</a> has pinpointed three genes in humans that may genetically differentiate us from chimps and other primates.
<h6>Shared DNA</h6>
Genetically we are very similar to chimps, so most of the differences researchers have observed to date regard physical appearance and <a href="http://www.archive.org/details/comparative_tests_on_human_chimp_infants" target="_blank" rel="noopener noreferrer">behaviors</a>.
The new study found several genes that were once silent and nonfunctional in our primate ancestors. They seem to have awakened around the time that humans formed a new evolutionary branch.
Researchers at the University of Dublin compared sections of the human genome with those of chimps and other primates. They found active genes that are absent from the chimp genome.
<h6>Human Genes</h6>
They found three human genes, CLLU1, C22orf45 and DNAHI0OS, that were present but inactive in non-human primates.

At the location of each of the three human genes, a disabling sequence of DNA was found in the genomes of the chimp, macaque, gorilla, gibbon and partially in the orangutan.
The study suggests that the awakened human genes shed their disabling components. But these awakened genes gained &#8220;enabling&#8221; sequences that helped them do the work of forming proteins in the body.
<h6>Awakened Genes</h6>
Previous research found that genes arising from inactive DNA were present in flies and yeast. The study suggests there may be a total of 18 awakened genes in humans. Yet researchers were limited to analyzing only a part of the 24,000-gene human genome.
The functions of these novel genes are not yet known. However, it is tempting to infer that these genes, specific to humans, are responsible for the attributes that differentiate us from other primates.

What Makes Us Human? Study Finds Hints By Comparing Chimp and Human DNA

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3359" title="neanderthaler_278" src="https://blog-api.23andme.com/wp-content/uploads/2009/04/neanderthaler_278.jpg" alt="" width="278" height="206">
Over the past decade, there has been no shortage of studies focused on the relationship between Neanderthals and our own species, Homo sapiens. Researchers have dug deep into the fossil record and our genomes to uncover how closely related we are to the Neanderthals, whether we interacted with them, and even whether our two species shared offspring.
But what about the Neanderthals themselves? We know that beginning around 400,000 years ago, they occupied over 3 million square miles of Europe and Western Asia, from Spain to Iraq. &nbsp; We know that they developed a unique tool technology and that they buried their dead. &nbsp; But what we really don&#8217;t know is how they compared to each other: &nbsp; were there in fact distinct Neanderthal sub-groups, shaped by the vastly different environments in which they lived? &nbsp; Or can they all be considered a single, genetically similar population? These questions are addressed in the most recent issue of <a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0005151" target="_blank" rel="noopener">PLoS One</a> by anthropologists from the UniversitÃ© de la MÃ©diterranÃ©e in France, using a method that is both unique and comprehensive. 
 
This study is of interest not only because it attempts to understand Neanderthal diversity, but also because it utilized data from a various sources. &nbsp; First, the researchers collected data from the mitochondrial DNA sequences of 12 separate Neanderthal skeletons. These skeletons ranged in age from 29,000 to 100,000 years and were uncovered in various parts of the Neanderthal homeland, from Siberia to Spain. &nbsp; The researchers then took physical measurements of the skeletons themselves. Finally, they developed and ran complex computer simulations based on the genetic and skeletal data, in an attempt to discover the most likely scenario for how Neanderthals evolved and spread across much of Eurasia.
The authors concluded that the most likely scenario for how the Neanderthals populated Europe and Western Asia involves three Neanderthal sub-groups: one centered in Western Europe, another in Southern Europe, and the final group in the Levant/Western Asia. &nbsp; They propose that the Neanderthals within each of these sub-groups were more genetically – and perhaps physically – similar to each other than they were to members of another sub-group. &nbsp; This is contrary to the idea that the Neanderthals were a single, uniform population.
This result begs the question of cultural distinctions between the sub-groups. &nbsp; After all, if they were genetically and physically different from one another, it is entirely plausible that cultural differences, such as tool technologies, between the sub-groups also existed. &nbsp; The authors hope to understand cultural differences between Neanderthal sub-groups in the same way as they&#8217;ve understood genetic and physical differences. &nbsp; And, as more fossils are found and more DNA extracted, we will hopefully develop – with even more confidence – a clear picture on the origins and movements of Neanderthals.

There’s More to Neanderthals than Meets the Eye

By Anne Wojcicki
After discussion with officials from the Food and Drug Administration today, 23andMe will comply with the FDA’s directive and stop offering new consumers access to health-related genetic tests while the company moves forward with the agency’s regulatory review <img loading="lazy" decoding="async" class="alignright size-medium wp-image-6586" src="https://blog-api.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog-300x300.jpg" alt="23andMe_Logo_blog" width="300" height="300" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog-300x300.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog-150x150.jpg 150w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog-271x271.jpg 271w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog.jpg 350w" sizes="auto, (max-width: 300px) 100vw, 300px" />processes.
23andMe has been giving consumers access to health information for six years and is committed to finding the right regulatory path for our customers.  I am highly disappointed that we have reached this point and will work hard to make sure consumers have direct access to health information in the near future.  Our goal is to work cooperatively with the FDA to provide that opportunity.
We also want to make clear that we stand behind the data we have generated for customers. Our lab partner adheres to strict quality standards that are part of the <a href="https://www.fda.gov/MedicalDevices/DeviceRegulationandGuidance/IVDRegulatoryAssistance/ucm124105.htm">Clinical Laboratory Improvement Amendments of 1988</a> – known as CLIA. These are the same standards used in the majority of other health and disease-related tests. We decided several years ago to comply with CLIA guidelines to be consistent with other types of laboratory testing and to assure customers about the quality of data.
As we work with the FDA to get clearance, there will be some significant changes to the site.  Customers who purchased kits on or after the FDA’s warning letter of November 22nd will not have access to health-related results. Those customers will have access to ancestry-related genetic information and their raw data without 23andMe’s interpretation of that data. They may receive health-related results in the future, depending on FDA marketing authorization.
Customers who purchased kits before November 22, 2013 will continue to have access to all the reports they’ve always had.
This is clearly a much different service than in the past, so we are offering customers who purchased kits on or after November 22, 2013 a full refund if they wish. Those customers will get an email from 23andMe with details on the refund policy. Eligible customers who do not receive an email are encouraged to check their spam email folders for the email with their personalized instructions or contact our Customer Care Team.
Research is and will continue to be a significant priority for the company.  The 500,000+ customers we have today have given us more than 250 million survey data points.  You, our customer, have powered an incredibly important crowd-sourced research database that I believe can have a significant impact on the pace of discoveries and cures. We will continue our Parkinson’s, sarcoma, MPN and African American research projects and plan to launch more communities in 2014.
23andMe will also continue educational efforts to consumers, physicians and other health providers as we believe genetics will be an increasingly important part of all of our lives.
Finally, I want to say thank you to our customers for your support and your stories.  Many of you have written in about how 23andMe has changed your life.  It is rewarding for me and all the employees at 23andMe to serve our customers.  I am committed to 23andMe and committed to being a pioneer in the genetics revolution.

23andMe’s Updates Regarding FDA’s Review

<img loading="lazy" decoding="async" class="alignright wp-image-6586 size-medium" title="23andMe_Logo_blog" src="http://35.88.189.111/wp-content/uploads/2010/05/23andMe_Logo_blog-300x300.jpg" alt="An image of the 23andMe logo." width="300" height="300" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog-300x300.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog-150x150.jpg 150w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog-271x271.jpg 271w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog.jpg 350w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Today 23andMe <a href="https://www.23andme.com/about/press/fda_application/">announced</a> that we’ve submitted our first round of 510(k) documentation to the U.S. Food and Drug Administration (FDA). The application provides a detailed description of our Personal Genome Service ®, extensive data supporting the performance of our technology, and comprehensive discussions of the science supporting the information we present to customers about their genetics and its impact on health.
Not too long ago personal genomics was a new idea. Consumer personal genomics was even more novel &#8212; the idea that everyone, not just doctors and researchers or those with special health needs, could know what was in their DNA. What wasn’t new was the desire to improve our knowledge of what all that DNA means and for that knowledge to make a difference in people’s lives.
We started 23andMe six years ago with those goals in mind and since then more than 150,000 people have joined us to learn more about what&#8217;s in their bodies and to contribute to our innovative research platform. Already our growing research community has made discoveries in many diverse topics, including the photic sneeze reflex, male pattern baldness, and Parkinson’s disease.
As with anything new and potentially disruptive, there have also been concerns. The FDA responded to some of these concerns by indicating that direct-to-consumer genetic testing services require regulatory review to remain on the market. We remain strong in our belief that consumers have a fundamental right to their personal genetic data. We believe personal genetic data will power a revolution in healthcare. But we also recognize that appropriate oversight of this industry can be a stepping stone on the path to realizing that revolution.
For the last three years we have worked with FDA to apply their regulatory approach to direct-to-consumer genetic testing. It is important to us that a regulatory framework for genetic testing reflect the dynamic nature of genetic science and protect individual access. What we know about the genome changes every day. If we want our genetic information to be current, there needs to be a way for us to update that information quickly.
We are confident that our initial application to the FDA is complete and comprehensive. Being the first in the industry to announce we are actively working toward FDA clearance of our direct-to-consumer service demonstrates our commitment to make personal genetics an integral part of routine healthcare without sacrificing people’s right to access information about themselves. Our goal is to remain the world’s trusted source of genetic information &#8212; not just for people with a doctor’s order, but for everyone regardless of why or how they choose to learn about their DNA. DNA is fascinating, but it’s even more fascinating when it’s about you.

23andMe Takes First Step Toward FDA Clearance

<img decoding="async" class="alignright size-medium wp-image-6586" title="23andMe_Logo_blog" src="https://blog-api.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog-300x299.jpg" alt="" width="250" />
In March earlier this year, <a href="https://blog.23andme.com/articles/23andme-presents-at-fda-advisory-panel-meeting-on-direct-to-consumer-genetic-tests/" target="_blank" rel="noopener">23andMe presented its views</a> on possible federal regulation of the direct-to-consumer (DTC) genetic testing industry at an Advisory Committee meeting convened by the FDA. We reiterated our belief that individuals have a right to access their own genetic information without physician involvement, and suggested components of a regulatory framework that would ensure the high quality of that genetic information while maintaining direct-to-consumer access to personal genetic testing and enabling innovation.
Despite compelling arguments for DTC genetic testing the panel concluded that access to most types of health-related genetic tests should require a physician’s approval. At 23andMe, we encourage individuals to discuss their genetic test results with their health care providers and involve them fully in decision-making about their health. But we also contend that individuals should be allowed direct access to this information. We continue to work with FDA to develop a reasonable path forward.
In the months before and following the meeting, many of you responded to our call and submitted public comments to the FDA supporting as well as arguing against direct-to-consumer genetic testing. More open and honest debate about this issue can only be beneficial for the industry over the long run.
On September 22, 2011, Bay area citizens will have another chance to make their voices heard. FDA’s Center for Devices and Radiological Health (CDRH) will be holding the third of its 2011 public town hall discussions where individuals can present their views directly to senior CDRH officials, including the Center Director, the Deputy Director for Science, and the head of the Office of In Vitro Diagnostics, which regulates DTC genetic testing. The September town hall will be held at the Embassy Suites Hotel near the San Francisco international airport.
For more information about the town hall, see the official FDA announcement. Note that while anyone in attendance can ask questions during the Q&amp;A session, individuals must register and specifically request to speak if they would like to make comments during the public presentation period.
If you have strong opinions on whether individuals should have direct access to their genetic information, we encourage you to continue making your views known to FDA, whether through in-person meetings such as the town hall in September, or through letters and other correspondence. After all, we believe that having more information is a good thing!

FDA to Hold Public Town Hall Discussion in San Francisco

<img decoding="async" class="alignright size-medium wp-image-8732" title="DNA-chains" src="https://blog-api.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog.jpg" alt="" width="300" />
On March 8th, the FDA convened a two-day advisory panel meeting to discuss questions related to direct-to-consumer genetic tests. The questions focused on the benefits and risks of providing consumers with direct access to these tests, potential strategies for communication and education to mitigate any risks, and regulatory standards for ensuring that the tests are accurate and reliable. As one of the leading companies in this area, we felt it was important to outline our perspectives and broad requests on these topics, and were pleased to see many other companies from the industry join us in expressing similar views. Updated meeting materials are now available  on the FDA website, and both presentations that 23andMe gave at this meeting are available <a href="https://blog.23andme.com/articles/23andme-presents-at-fda-advisory-panel-meeting-on-direct-to-consumer-genetic-tests/" target="_blank" rel="noopener">here</a>.
In the several years since the direct-to-consumer genetic testing industry made its debut, it has seen all manner of reaction. Many are fascinated by our newfound ability to peek into our genomes, to add another source of data to the ones we already collect, and to leverage it to know more about our connections to the world, whether that be literally through known and predicted relatives or through the relationship between genetics and our health and traits. Others may not be interested or may not want to know what their genetics might tell them.  But some feel that all genetic tests and/or their interpretations should be available only through a physician.
For our part, 23andMe was founded on the belief that individuals have a right to access their own genetic information, and this conviction is still as firmly held as ever.
While the debate is clearly no longer academic &#8212; many more people are aware of and using these tests and the FDA is taking an active role in learning about and devising guidelines for this industry as a result &#8212; it is clear that challenges remain. Some observers fear that the panel’s recommendations will severely curtail direct access to genetic testing, but we agree with <a href="http://www.genomicslawreport.com/index.php/2011/03/11/the-fda-and-dtc-genetic-testing-setting-the-record-straight/" target="_blank" rel="noopener">Dan Vorhaus</a> of Genomics Law Report that the FDA will take a reasoned approach to integrating the feedback it received from its panel with other information pertinent to the issue.
The advisory panel meeting was in many ways a microcosm of the ongoing debate, with one exception. Although the panel had an individual representing the consumer and the patient, the panel did not have the opportunity to hear directly from consumers and others who have first-hand experience with the information provided by direct-access genetic testing services.
Fortunately, there are many channels through which you can make your voices heard. The FDA has reopened the public docket on this topic for the submission of additional comments (until May 2, 2011) and we strongly encourage those of you with an opinion or perspective on the questions posed by the FDA regarding DTC genetic tests to send in a comment. Regardless of the content of those comments, we believe that a larger number and a wider variety of comments will be beneficial for helping the FDA to guide its regulatory policies in this area.
<ul>
<li>Electronic comments can be submitted at <a href="http://www.regulations.gov/" target="_blank" rel="noopener">http://www.regulations.gov/</a>, referencing docket ID FDA-2011-N-0066.</li>
<li>Written comments, referencing docket ID FDA-2011-N-0066 in the header, can be sent to: 
Division of Dockets Management (HFA-305) 
Food and Drug Administration 
5630 Fishers Lane, Rm 1061 
Rockville, MD 20852</li>
</ul>
You can also post comments to the <a href="https://www.facebook.com/FDA" target="_blank" rel="noopener">FDA Facebook page</a>, or attend one of several FDA (Center for Devices and Radiological Health, or CDRH) town hall meetings. The next town hall meeting will be held in May in Orlando, FL, and there is also one planned for San Francisco at a place and time to be announced.
Finally, it may be helpful to make your congressional representatives aware of your views on this issue. You may contact members of the <a href="https://en.wikipedia.org/wiki/United_States_House_Committee_on_Energy_and_Commerce" target="_blank" rel="noopener">House Committee on Energy and Commerce</a>, or find contact information online for your own House representative or <a href="http://www.senate.gov/general/contact_information/senators_cfm.cfm" target="_blank" rel="noopener">Senator</a>.

DTC Genetic Tests and the Future of Regulation: Make Your Voices Heard

Editor&#8217;s note: This post has been altered from the original. The slides from the presentation have been removed.
23andMe, like many others, believes that individuals have a right to access their own genetic information and that personal genetics will pave the way for significant advances in healthcare. These beliefs fueled the development of our direct access <a href="https://www.23andme.com/howitworks/" target="_blank" rel="noopener">Personal Genome Service</a> ® &nbsp;and <a href="https://www.23andme.com/research/" target="_blank" rel="noopener">23andWe</a>, our web-based, participant-driven research platform. As for any other new industry
<img decoding="async" class="alignright size-full wp-image-6586" title="23andMe_Logo_blog" src="https://blog-api.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog.jpg" alt="" width="300" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog.jpg 350w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog-150x150.jpg 150w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog-300x300.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/05/23andMe_Logo_blog-271x271.jpg 271w" sizes="(max-width: 350px) 100vw, 350px" />
or technology, however, there are concerns about the validity, accuracy, and applicability of the services and information that companies in the direct-to-consumer genetic testing industry provide. 23andMe supports thoughtful regulation that ensures consumers receive high quality information and enables, rather than inhibits, innovation.
Over the next two days, the FDA is hosting an Advisory Panel Meeting to address a number of questions related to clinical genetic tests that are marketed and provided directly to consumers. The FDA will be hearing the ideas and perspectives primarily of the Molecular and Clinical Genetics Panel of the Medical Devices Advisory Committee, which include voting members and temporary members added for this meeting. In addition, the FDA has invited several speakers to present background information and their views on this topic, and has provided for one hour each day for public comment.
It is during the public comment period that 23andMe will be giving two presentations. This afternoon, 23andMe’s General Counsel Ashley Gould will speak about our position on the subject matter the panel will be addressing as well as our broad requests for the panel’s consideration. 23andMe’s Senior Director of Regulatory Affairs &amp; Quality Assurance, Rose Romeo, will present tomorrow afternoon on considerations for risk mitigation and thoughts on regulatory frameworks moving forward. Slides from both of their presentations can be viewed below. The agenda and other background material are available at the FDA website, including <a href="http://www.regulations.gov/#!docketDetail;dct=PS+N;rpp=10;po=0;D=FDA-2011-N-0066" target="_blank" rel="noopener">public comments</a>.
Much of the complexity in discussing regulation of genetic testing stems from the brisk evolution of technologies in this area. The first draft sequence of the human genome was first published only 10 years ago, and companies are now sequencing full genomes on demand at increasingly affordable prices. In our presentations, we take the position that all genetic testing services, whether ordered by a physician or offered through direct access, should adhere to the same standards. We simultaneously request that the FDA consider redefining and establishing regulatory standards, including some fundamental definitions, to accommodate large-scale genetic testing and support innovation of its technologies and applications. We also request that regulation be based upon evidence and not fear of potential harm to individuals which, to date, has not been demonstrated. In fact, growing numbers of participating individuals and independent studies focused on this issue provide preliminary evidence that the vast majority of people understand the information presented and experience no significant negative effects.
23andMe has been proactively collaborating with the FDA and remains committed to finding a path forward that benefits everyone. The addition of Rose Romeo to our team, who has extensive regulatory experience and is eager to help us forge that path, attests to the strength of that commitment. We look forward to working together with a wide variety of agencies, organizations, and the medical community at large to establish the regulatory and functional frameworks that will ensure consumers and healthcare professionals have access to genetic information that is clear, useful, and engaging.

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