
<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h2>Key Takeaways</h2>
<ul><li><b>A 5,000-region milestone</b>: 23andMe can now connect members to more than 5,000 geographic regions, ethnolinguistic groups and communities around the world, giving you the most comprehensive genetic ancestry breakdown on the market.</li>
<li><b>163 new Genetic Groups</b>: This update spans Egypt, the Arabian Peninsula and North Africa, from Coptic communities along the Nile to Amazigh peoples of the Atlas and Rif mountains.</li>
<li><b>More specific ancestry insights</b>: The vast majority of members with roots in this part of the world will see at least one new Genetic Group in their Ancestry Composition report.</li>
</ul>
</td></tr></tbody></table></figure>



<p class="wp-block-paragraph">Five thousand. That is how many geographic regions, ethnolinguistic groups and cultural communities 23andMe can now connect you to. We reached that milestone today with the release of 163 new Genetic Groups across North Africa, Egypt and the Arabian Peninsula. When we last marked a milestone in early 2025, that number stood at <a href="https://www.23andme.org/blog/articles/ancestry-composition-4000-regions/" target="_blank" rel="noreferrer noopener">4,000</a>.</p>



<p class="wp-block-paragraph">These new Genetic Groups span some of the most storied landscapes on Earth: the Nile Valley, the oases and highlands of Arabia and the mountains of the Maghreb, the region of northwestern Africa stretching from Morocco to Libya. If your family has roots in any of these places, your Ancestry Composition report may now tell a more detailed version of your story.</p>



<h2 class="wp-block-heading"><strong>What Are Genetic Groups?</strong></h2>



<p class="wp-block-paragraph"><a href="https://customercare.23andme.com/hc/en-us/articles/360003184973-Country-Matches-and-Genetic-Groups" target="_blank" rel="noreferrer noopener">Genetic Groups</a> are clusters of people who share more recent DNA with one another than with the broader population, usually because their families lived in the same region or community for many generations. They are part of 23andMe’s Ancestry Composition report.</p>



<p class="wp-block-paragraph">By analyzing shared DNA patterns among consented 23andMe members and looking at the information about their families that they choose to share, our scientists can identify genetic signatures more specific than a single label like “North African” can capture. <a href="https://www.23andme.org/shop/premium-ancestry/" target="_blank" rel="noreferrer noopener">23andMe Premium</a> members can also explore any <a href="https://www.23andme.org/blog/articles/discover-distant-genetic-groups-with-23andme-premium" target="_blank" rel="noreferrer noopener">Distant Genetic Group</a> connections they may have to these regions.</p>



<h2 class="wp-block-heading"><strong>Which Communities Are Part of This Update?</strong></h2>



<p class="wp-block-paragraph">This update includes Genetic Groups for communities across Egypt, Saudi Arabia, Yemen, the Gulf states, Morocco, Algeria, Tunisia and Libya. Each group reflects a community&#8217;s history, and a few show how migration, faith and geography have shaped DNA in this region.</p>



<figure class="wp-block-image size-large"><img loading="lazy" decoding="async" width="1024" height="466" src="https://blogcms.23andme.org/wp-content/uploads/2026/09/north_africa_genetic_groups-1024x466.png" alt="" class="wp-image-35617" srcset="https://blogcms.23andme.org/wp-content/uploads/2026/09/north_africa_genetic_groups-1024x466.png 1024w, https://blogcms.23andme.org/wp-content/uploads/2026/09/north_africa_genetic_groups-300x137.png 300w, https://blogcms.23andme.org/wp-content/uploads/2026/09/north_africa_genetic_groups-768x350.png 768w, https://blogcms.23andme.org/wp-content/uploads/2026/09/north_africa_genetic_groups-880x401.png 880w, https://blogcms.23andme.org/wp-content/uploads/2026/09/north_africa_genetic_groups-1180x537.png 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



<h3 class="wp-block-heading"><strong>Coptic Communities Along the Nile</strong></h3>



<p class="wp-block-paragraph">Coptic communities trace one of the longest continuous histories in Egypt. The Coptic Christian church <a href="https://en.wikipedia.org/wiki/Copts" target="_blank" rel="noreferrer noopener">traces its roots to the first century CE</a> and still uses Coptic as its liturgical language. Coptic was <a href="https://en.wikipedia.org/wiki/Coptic_language" target="_blank" rel="noreferrer noopener">the final stage of the ancient Egyptian language</a> that gradually gave way to Arabic in everyday life after the Arab conquest of Egypt.</p>



<p class="wp-block-paragraph">New Genetic Groups now distinguish Coptic communities up and down the Nile, from Upper Egypt to the Faiyum Oasis. Alongside them are other communities from the Nile Delta, plus a group for Egyptian Nubian peoples <a href="https://en.wikipedia.org/wiki/Nubians" target="_blank" rel="noreferrer noopener">who have long lived along the Nile</a> in southern Egypt and northern Sudan.</p>



<h3 class="wp-block-heading"><strong>From the Gulf Coast to the Yemeni Highlands</strong></h3>



<p class="wp-block-paragraph">On the Arabian Peninsula, the new Genetic Groups trace communities from the Persian Gulf to the Red Sea. Members can now see connections to communities from Bahrain or <a href="https://en.wikipedia.org/wiki/Najd" target="_blank" rel="noreferrer noopener">the Najd</a>, the vast plateau of central Saudi Arabia, or from <a href="https://en.wikipedia.org/wiki/Hejaz" target="_blank" rel="noreferrer noopener">the Hijaz</a>, home to Mecca and Medina, which have drawn pilgrims and settlers for centuries.</p>



<p class="wp-block-paragraph">Farther south, Genetic Groups in the Yemeni Highlands trace to terraced mountain slopes where <a href="https://www.smithsonianmag.com/smart-news/your-mocha-named-after-birthplace-coffee-trade-180965016/" target="_blank" rel="noreferrer noopener">coffee was first cultivated commercially</a> before merchants shipped it to the world through the port of Mocha.</p>



<h3 class="wp-block-heading"><strong>Amazigh Peoples of the Maghreb</strong></h3>



<p class="wp-block-paragraph">Many of the new North African Genetic Groups connect to Amazigh peoples, one of the indigenous peoples of North Africa. Members can now see connections to people from Kabylia, a mountainous region of northern Algeria, the Rif mountains along Morocco’s Mediterranean coast and the Nafusa Mountains of northwestern Libya.</p>



<h2 class="wp-block-heading"><strong>How Did 23andMe Reach 5,000 Ancestry Regions?</strong></h2>



<p class="wp-block-paragraph">23andMe reached 5,000 ancestry regions by steadily adding Genetic Groups as more members chose to participate and tell us about their family story. Since passing 4,000, recent updates have added new Genetic Groups across <a href="https://www.23andme.org/blog/articles/new-genetic-groups-across-oceania/" target="_blank" rel="noreferrer noopener">Oceania</a>, <a href="https://www.23andme.org/blog/articles/discover-new-filipino-genetic-groups-with-23andme/" target="_blank" rel="noreferrer noopener">the Philippines</a> and <a href="https://www.23andme.org/blog/articles/new-genetic-groups-across-southeast-asia/" target="_blank" rel="noreferrer noopener">Southeast Asia and Madagascar</a>. This update brings that same level of detail to North Africa, Egypt and the Arabian Peninsula.</p>



<p class="wp-block-paragraph">People of Western Asian and North African descent remain underrepresented in genetic research and this update is one step toward reflecting these communities more fully. None of it would be possible without the 23andMe members who share their family stories and consent to take part in research.</p>



<p class="wp-block-paragraph">Already a 23andMe member? <a href="https://you.23andme.com/" target="_blank" rel="noreferrer noopener">Sign in</a> to see if you have connections to these new Genetic Groups in your Ancestry Composition report. New to 23andMe? Explore how <a href="https://www.23andme.org/shop/compare-dna-tests/" target="_blank" rel="noreferrer noopener">23andMe</a> can help you discover your roots.</p>



<p class="wp-block-paragraph">With this update there are now:</p>



<ul class="wp-block-list">
<li>33 Genetic Groups in Algeria</li>



<li>24 Genetic Groups in Egypt</li>



<li>5 Genetic Groups in Libya</li>



<li>40 Genetic Groups in Morocco</li>



<li>15 Genetic Groups in Saudi Arabia</li>



<li>13 Genetic Groups in Tunisia</li>



<li>6 Genetic Groups in Yemen</li>



<li>17 Genetic Groups for Jewish communities in the region</li>



<li>10 additional Genetic Groups throughout the region</li>
</ul>



<p class="wp-block-paragraph"></p>


Sr. Manager, Product Science

Alisa Lehman

23andMe Reaches 5,000 Ancestry Regions With 163 New Genetic Groups Across North Africa, Egypt and the Arabian Peninsula


<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h2>Key Takeaways</h2>
<ul><li>In Crohn&#8217;s disease, the immune system mistakenly attacks harmless bacteria in the digestive tract. This causes inflammation that can lead to symptoms like abdominal pain, diarrhea and unintended weight loss.</li>
<li>Genetics play an important role in Crohn&#8217;s disease. 23andMe&#8217;s new polygenic risk score (PRS) report incorporates more than 2,000 genetic variants to estimate an individual&#8217;s likelihood of developing the condition.</li>
<li>Other factors also impact risk for Crohn&#8217;s, including family history, age, ancestry, geography and tobacco exposure.</li>
</ul>
</td></tr></tbody></table></figure>



<p class="wp-block-paragraph">About <a href="https://www.niddk.nih.gov/health-information/digestive-diseases/crohns-disease/definition-facts" target="_blank" rel="noreferrer noopener">one million people</a> in the U.S. have Crohn&#8217;s disease, one of the two main types of inflammatory bowel disease (IBD). But Crohn&#8217;s disease can be <a href="https://pubmed.ncbi.nlm.nih.gov/39351057/" target="_blank" rel="noreferrer noopener">hard to recognize</a> at first, because early symptoms overlap with more common conditions and often come and go over time.&nbsp;</p>



<p class="wp-block-paragraph">Our new Crohn&#8217;s Disease Polygenic Risk Score report*, now available for 23andMe <a href="https://www.23andme.org/shop/premium-ancestry-health/" target="_blank" rel="noreferrer noopener">Premium Ancestry + Health</a> members, can help you understand how your DNA impacts your likelihood of developing Crohn&#8217;s. It also provides information about common symptoms and non-genetic risk factors.</p>



<h2 class="wp-block-heading">What is Crohn&#8217;s disease?</h2>



<p class="wp-block-paragraph"><a href="https://my.clevelandclinic.org/health/diseases/9357-crohns-disease" target="_blank" rel="noreferrer noopener">Crohn&#8217;s disease</a> is a type of IBD, a group of conditions in which the immune system mistakenly attacks harmless bacteria in the gut, leading to chronic inflammation (see sidebar). Most people with Crohn&#8217;s are diagnosed between the ages of 15 and 35, but symptoms can develop at any age.</p>



<div style="float: right; text-align: justified; width: 400px; background-color: #eee; padding: 15px; margin-left: 10px;">
<strong>Crohn&#8217;s disease, ulcerative colitis and irritable bowel syndrome</strong>
<p>Crohn&#8217;s disease is one of two main types of inflammatory bowel disease (IBD), alongside ulcerative colitis (UC). There are <a href="https://www.crohnscolitisfoundation.org/patientsandcaregivers/what-is-crohns-disease/overview" target="_blank" rel="noreferrer noopener">a few key differences</a>:</p>
<ul><li>Crohn&#8217;s disease can affect any part of the digestive tract from the mouth to the anus, whereas UC only affects the colon and rectum.</li>
<li>In Crohn&#8217;s, patches of inflammation alternate with healthy sections of tissue, whereas UC usually impacts continuous stretches, starting at the rectum.</li>
<li>Crohn&#8217;s disease impacts all layers of the intestinal wall, whereas UC only affects the innermost lining.</li></ul>
<p>IBD is also different from irritable bowel syndrome (IBS), which can cause uncomfortable symptoms but doesn&#8217;t involve inflammation or cause damage to the digestive tract.</p>
</div>



<p class="wp-block-paragraph"></p>



<p class="wp-block-paragraph"><a href="https://www.mayoclinic.org/diseases-conditions/crohns-disease/symptoms-causes/syc-20353304" target="_blank" rel="noreferrer noopener">Common symptoms</a> of Crohn&#8217;s disease include abdominal pain, diarrhea, fatigue, reduced appetite and unintended weight loss, which sometimes come and go over time. Most people can manage their symptoms with ongoing medical treatment, which may include medication to reduce inflammation and calm an overactive immune response, and they lead full, active lives. But over time, chronic inflammation can lead to serious complications, including scarring and blockages in the intestine, abnormal tunnels called fistulas and an increased risk for colorectal cancer.</p>



<p class="wp-block-paragraph">Crohn&#8217;s disease can also take an emotional toll. Flares can be unpredictable, which can make it hard to plan ahead for work, school, travel or social events. And needing frequent bathroom access can make everyday activities feel stressful. The <a href="https://www.crohnscolitisfoundation.org/patientsandcaregivers/community-support" target="_blank" rel="noreferrer noopener">Crohn&#8217;s &amp; Colitis Foundation</a> offers support to people experiencing the challenges of Crohn&#8217;s disease.</p>



<h2 class="wp-block-heading">What causes Crohn&#8217;s disease?</h2>



<p class="wp-block-paragraph">The exact cause of Crohn&#8217;s disease isn&#8217;t fully understood. But scientists believe it involves an <a href="https://www.crohnsandcolitis.com/crohns/causes" target="_blank" rel="noreferrer noopener">overactive immune response</a>, where the immune system mistakenly attacks some of the trillions of harmless bacteria that normally live in our guts. This leads to ongoing inflammation that can cause damage over time.</p>



<p class="wp-block-paragraph">Research suggests a strong genetic component to Crohn&#8217;s disease: an estimated <a href="https://pubmed.ncbi.nlm.nih.gov/42018767/" target="_blank" rel="noreferrer noopener">78% of the difference in risk</a> between different people may be explained by DNA. Scientists have discovered hundreds of genetic variants associated with Crohn&#8217;s, including variants in <a href="https://medlineplus.gov/genetics/condition/crohns-disease/#causes" target="_blank" rel="noreferrer noopener">genes like</a> <em>NOD2</em> (which helps sense bacteria inside our bodies), <em>ATG16L1</em> (which helps cells engulf and destroy harmful microbes) and <em>IL23</em> (which helps immune cells communicate with each other).</p>



<figure class="wp-block-image aligncenter size-full is-resized"><img loading="lazy" decoding="async" width="612" height="252" src="https://blogcms.23andme.org/wp-content/uploads/2026/09/PRS-hero-crohns.png" alt="" class="wp-image-35606" style="width:263px;height:auto" srcset="https://blogcms.23andme.org/wp-content/uploads/2026/09/PRS-hero-crohns.png 612w, https://blogcms.23andme.org/wp-content/uploads/2026/09/PRS-hero-crohns-300x124.png 300w" sizes="auto, (max-width: 612px) 100vw, 612px" /></figure>



<p class="wp-block-paragraph">Besides genetics, many other factors can influence a person&#8217;s chances of developing Crohn&#8217;s disease. For example, people with a close family member with Crohn&#8217;s or another type of IBD are more likely to develop Crohn&#8217;s, as are people with Ashkenazi Jewish ancestry or who live in industrialized and urban environments. Smoking cigarettes can also increase risk. Some studies suggest that a healthy diet and regular exercise is associated with <em>lower</em> risk for Crohn&#8217;s.</p>



<h2 class="wp-block-heading">Ways to Take Action</h2>



<p class="wp-block-paragraph">There&#8217;s no sure way to prevent Crohn&#8217;s disease. But for those experiencing symptoms, learning about your genetics may help reduce the time it takes to get a diagnosis.</p>



<p class="wp-block-paragraph">For those who do develop Crohn&#8217;s, most need medication, and some may also need surgery or nutritional support. But certain lifestyle habits can also help manage symptoms and reduce the frequency of symptom flares. For example:</p>



<ul class="wp-block-list">
<li>Certain foods and drinks may trigger symptoms, such as spicy foods, dairy, caffeine and carbonated drinks. Keeping a food diary can help you identify potential triggers&nbsp;to avoid. It may also be helpful to keep an eye on medications like NSAIDs that can irritate the gut.</li>



<li>Eating smaller, more frequent meals can be easier on the digestive system, and drinking lots of water throughout the day can help counter fluid loss from diarrhea.&nbsp;</li>



<li>Stress can sometimes worsen Crohn&#8217;s symptoms, so staying active, getting plenty of sleep and practicing relaxation techniques may help.</li>



<li>Smoking cigarettes is linked to more frequent and severe flares. If you need help quitting, <a href="http://smokefree.gov" target="_blank" rel="noreferrer noopener">smokefree.gov</a> offers support and resources.</li>
</ul>



<p class="wp-block-paragraph">People with Crohn&#8217;s disease also have a higher risk of developing colorectal cancer, so experts recommend getting earlier and more frequent screening colonoscopies to catch potential cancers and pre-cancers.</p>



<h2 class="wp-block-heading">Learn About Your Genetics</h2>



<p class="wp-block-paragraph">The Crohn&#8217;s Disease PRS report was made possible thanks to millions of 23andMe customers who have consented to participate in research. Their contributions help our scientists make genetic discoveries that benefit the entire research community and allow us to develop new reports and features for our members.</p>



<p class="wp-block-paragraph">If you&#8217;re a 23andMe <a href="https://www.23andme.org/shop/premium-ancestry-health/" target="_blank" rel="noreferrer noopener">Premium Ancestry + Health</a> member, you can now access the new Crohn&#8217;s Disease PRS report (along with your other Health Predisposition reports) to see how your genetics may influence your chances of developing Crohn&#8217;s disease.</p>



<p class="wp-block-paragraph"><em>Note: Due to limited data, the PRS powering this report failed to meet our performance standards for members of East and Southeast Asian descent. Members with these ancestries are not able to receive a personalized genetic result at this time. We hope with additional data and research we may be able to provide these members a result in the future.</em></p>



<p class="wp-block-paragraph"><em>* The 23andMe Crohn&#8217;s Disease PRS report is based on a genetic model that includes data and insights from 23andMe consented research participants and incorporates more than 2,000 genetic variants to provide information on the likelihood of being diagnosed with Crohn&#8217;s disease. 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 Crohn&#8217;s Disease 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.</em></p>



<p class="wp-block-paragraph"></p>


Senior Product Scientist

Ruth Tennen

How Your DNA Can Influence Your Risk for Crohn’s Disease


<p class="wp-block-paragraph"><em>By Steven Micheletti, Ph.D. and Stella Aslibekyan, Ph.D.</em></p>



<p class="wp-block-paragraph">Cover image courtesy of <em>Science</em></p>



<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h2>Key Takeaways</h2>
<ul><li>The <i>EGFR</i> T790M variant confers a significantly elevated risk for lung cancer, increasing the odds by over 25 times for carriers.</li>
<li>This variant, while still rare, was found at a frequency approximately ten times higher than what had been previously reported.</li>
<li>The higher frequency of the variant in people of British and Irish descent in the Southeastern United States was traced to early European settlers in this region.</li>
<li>This highlights the important reality that factors beyond exposure to tobacco smoke may increase someone’s risk for lung cancer.</li>
</ul>
</td></tr></tbody></table></figure>



<p class="wp-block-paragraph">Anyone with lungs can get lung cancer. And while many people think exposure to tobacco smoke is the only risk factor, tens of thousands of Americans <a href="https://www.cdc.gov/lung-cancer/nonsmokers/index.html" target="_blank" rel="noreferrer noopener"><em>without this risk factor </em></a>are diagnosed with lung cancer every year, showing that smoking is by no means the whole story of lung cancer risk. For many people with lung cancer the question of why has had no good answer. For some, a new study is starting to change that.</p>



<p class="wp-block-paragraph">A collaboration between the 23andMe Research Institute and <a href="https://www.dana-farber.org/" target="_blank" rel="noreferrer noopener">Dana-Farber Cancer Institute</a>, one of the world’s leading centers of cancer research and treatment, has shown that a specific, rare genetic variant in the <em>EGFR</em> gene, the T790M variant, is the largest known single genetic risk factor for lung cancer. <a href="https://www.science.org/doi/10.1126/science.aec0473" target="_blank" rel="noreferrer noopener">This research</a>, published today in <em>Science</em>, is a crucial step for clinical genetics, potentially transforming lung cancer screening efforts. It is also a fascinating detective story, tracing the variant&#8217;s origins back to the colonial history of the American Southeast.</p>



<h2 class="wp-block-heading">Unmasking of a Powerful Lung Cancer Risk Variant</h2>



<p class="wp-block-paragraph">Not all <em>EGFR</em> T790M changes are the same. This variant is well-known as a mutation that occurs within a tumor and helps lung cancers <a href="https://pubmed.ncbi.nlm.nih.gov/27071706/" target="_blank" rel="noreferrer noopener">resist treatments</a>. This study looked at something different: people who inherit this genetic variant and have it in each of their cells since birth.&nbsp;</p>



<p class="wp-block-paragraph">This inherited version of the <em>EGFR</em> T790M variant has <a href="https://pubmed.ncbi.nlm.nih.gov/37579253" target="_blank" rel="noreferrer noopener">been reported before</a> in small studies of families with multiple cases of lung cancer. However, the inherited form of this genetic variant is so rare that researchers have struggled to establish precise estimates for how it impacts lung cancer risk or even understand how common this variant really is. The scale of research participation at the 23andMe Research Institute changed this entirely.</p>



<h2 class="wp-block-heading">More Common and More Impactful Than Expected</h2>



<p class="wp-block-paragraph">Out of over 10 million consented research participants, 641 carried the <em>EGFR</em> T790M variant. While still rare, this is approximately ten times higher than that reported in public databases like <a href="https://gnomad.broadinstitute.org/" target="_blank" rel="noreferrer noopener">gnomAD</a>.&nbsp;</p>



<p class="wp-block-paragraph">Overall, people with this variant had 25x higher odds of developing lung cancer. To put this into perspective, this relative risk is equal to or higher than that of other well-established inherited cancer risk genetic variants, such as those in the BRCA1 and BRCA2 genes for breast and ovarian cancer. And while exposure to tobacco smoke is still the number one risk factor for lung cancer, in the study this variant put people at even higher risk than having a history of smoking.</p>



<p class="wp-block-paragraph">The study also highlighted a rare phenomenon: the risk associated with the <em>EGFR</em> T790M variant is specific to lung cancer alone. Often genetic variants that dramatically increase the risk of one cancer also increase the risk of other cancers, but for people with the <em>EGFR</em> T790M variant there were no significant associations with other frequent cancers, including breast, prostate or colorectal cancer. This finding could help people with this variant know the specific, targeted screening they may need.</p>



<h2 class="wp-block-heading">A Genetic Ancestry Detective Story</h2>



<p class="wp-block-paragraph">One of the greatest strengths of the 23andMe Research Institute is the ability to combine different scientific disciplines to deeply understand genetics, health and history. In this case, 23andMe scientists were able to analyze geographic data and genetic relatedness among those with the <em>EGFR</em> T790M variant to uncover a distinct historical pattern and trace the origin and spread of this rare variant.</p>



<p class="wp-block-paragraph">People who have the <em>EGFR</em> T790M variant (or &#8220;carriers&#8221;) disproportionately traced their ancestry to the Southern U.S., particularly Tennessee, Alabama, and Georgia. Using sophisticated genetic dating methods, 23andMe researchers estimated that carriers of the <em>EGFR</em> T790M variant in the Southern Appalachian region shared an ancestor who lived in the early 19th century. Around this time was when early European settlers expanded into the Southern Appalachian region forming smaller tight-knit communities prior to the Civil War.</p>



<p class="wp-block-paragraph">The data supports that the <em>EGFR</em> T790M variant, likely originating in Europe, was carried by early settlers of British and Irish descent to the Southeastern United States. During the late 18th century, regional expansion and demographic isolation led to a founder effect, where a small group is genetically separated from a larger population. This genetic bottleneck significantly increased how common the <em>EGFR</em> T790M variant is within this specific subpopulation, with researchers finding that people with ancestry from the Southern United States are six times more likely to carry the variant than those from other regions. This is one of the most recent founder events of a medically important variant. This may enable doctors and researchers to identify potential carriers based on where their ancestors were from.</p>



<h2 class="wp-block-heading">The Power of the 23andMe Research Institute</h2>



<p class="wp-block-paragraph">This research stands out precisely because it would have been extremely difficult using traditional methods. The study highlights the strength of the 23andMe Research Institute, which combines two crucial elements:</p>



<ol class="wp-block-list">
<li><strong>Large-Scale Data:</strong> The sheer size of the research community (over 11 million consented research participants) provided the necessary power to detect the 641 <em>EGFR</em> T790M carriers and characterize the risk from this rare genetic variant. For comparison, the <a href="https://www.ukbiobank.ac.uk/" target="_blank" rel="noreferrer noopener">UK Biobank</a> and <a href="https://allofus.nih.gov/" target="_blank" rel="noreferrer noopener">All of Us</a> databases, while large, contained only 2 and 19 carriers, respectively, making a robust risk assessment impossible with those databases.</li>



<li><strong>Wide Variety of Genetics Expertise:</strong> This collaboration of researchers, spanning epidemiology, oncology, statistical genetics, and population genetics, was able to go beyond a simple association. They used self-reported data, deep ancestry analysis, and complex genetic dating to not only better understand the magnitude of the lung cancer association but also to contextualize the variant in history.</li>
</ol>



<p class="wp-block-paragraph">By bringing together a large number of consented research participants and diverse expertise, 23andMe has been able to help shine a light on the most significant single genetic risk factor for lung cancer to date, and link it directly to an important moment in American history. This discovery underscores the power of large-scale genetic studies to transform our understanding of rare, high-risk genetic variants and potentially reshape clinical screening and public health efforts.</p>



<p class="wp-block-paragraph">Data analyzed in this study includes participants in the <a href="https://www.23andme.org/lung-cancer/" target="_blank" rel="noreferrer noopener">Lung Cancer Genetics Study</a>, an initiative funded by the <a href="https://susanwfoundation.org/" target="_blank" rel="noreferrer noopener">Susan Wojcicki Foundation</a> and powered by 23andMe in collaboration with 22 lung cancer advocacy organizations. By uniting the stakeholders that support the patients and families living with this critically underfunded disease, the Lung Cancer Genetics Study hopes to help contribute to more discoveries like this in the future.</p>



<p class="wp-block-paragraph">Additional data came from participants in the <a href="https://inheritstudy.org/" target="_blank" rel="noreferrer noopener">INHERIT (Investigating Hereditary Risk in Thoracic Cancers) Study</a>, led by the Dana-Farber Cancer Institute in partnership with <a href="https://go2.org/" target="_blank" rel="noreferrer noopener">GO2 for Lung Cancer</a> (GO2) and the <a href="https://alcmi.org/" target="_blank" rel="noreferrer noopener">Addario Lung Cancer Medical Institute</a> (ALCMI), which aims to to further understand the genetic risk and predispositions for developing lung cancer.</p>



<p class="wp-block-paragraph">Learn more about the <a href="https://www.23andme.org/lung-cancer/" target="_blank" rel="noreferrer noopener">Lung Cancer Genetics Study</a> and <a href="https://inheritstudy.org/" target="_blank" rel="noreferrer noopener">INHERIT</a>.</p>



<div style="width: 100%; margin: 0 auto; text-align: justify; background-color: #eee; padding: 15px;">
<h4>About the Authors</h4>
<p><strong>Steven Micheletti</strong>, Ph.D. — Sr. Machine Learning Scientist I, Population Genetic R&#038;D
</p>
<p> 
Dr. Steven Micheletti is a Population Geneticist specializing in the intersection of large-scale genomics and human history. As an architect of models connecting individuals to Genetic Groups, his work provides high-resolution insights into ancestral origins. His research investigates how historical events, such as the Transatlantic Slave Trade, have shaped the genetic landscape of present-day populations and influenced the distribution of health-related variants.
</p>
<p><strong>Stella Aslibekyan</strong>, Ph.D. — Principal Scientist, Genetic Epidemiology
</p>
<p> 
Stella is a Principal Scientist at the 23andMe Research Institute and is the scientific lead for the Lung Cancer Genetics Study. She leads the Real World Evidence team that helps ensure our health data (including surveys, EHRs, and wearables) are of high research quality. The team also conducts original studies that deepen our understanding of conditions like Parkinson’s disease and lung cancer.
</p>
</div>


Landmark Study Reveals a Powerful Inherited Lung Cancer Risk Variant and its Colonial American Roots


<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h2>Key Takeaways</h2>
<ul><li>Through 23andMe&#8217;s Historical Matches® feature, 23andMe Premium members can now find out if their DNA connects them to the Shaman of Bad Dürrenberg, a Mesolithic woman from what is now central Germany whose richly furnished grave has fascinated researchers for nearly a century.</li>
<li>A 2022 study resequenced her genome, then used her DNA as a benchmark to measure if her hunter-gatherer ancestry was present in the farming communities that settled the region roughly 2,000 years later.</li>
<li>From the same study 15 members of that farming community have been added to Historical Matches, descendants of migrants who carried agriculture out of Anatolia and into Europe, part of one of the most significant demographic shifts in the continent&#8217;s history.</li>
</ul>
</td></tr></tbody></table></figure>



<p class="wp-block-paragraph">Did you know that many of the historical and ancient individuals we feature in <a href="https://www.23andme.org/blog/articles/23andmes-historic-matches/" target="_blank" rel="noreferrer noopener">Historical Matches</a> were discovered by accident during construction work? For instance, in 1903, workmen digging a drainage trench in England&#8217;s Gough&#8217;s Cave stumbled on the skeleton of Cheddar Man, one of the oldest near-complete human skeletons ever found in Britain. In 1954, construction crews building a fire station in Hungary uncovered a hilltop site that turned out to be the long-lost monastery and burial ground of an 11th-century Hungarian king, Sámuel Aba, and his descendants. And in 2012, workers in Blihun Hanben, Taiwan, uncovered burials dating to the Iron Age while they were constructing a highway.&nbsp;</p>



<p class="wp-block-paragraph">This September 14–18th is National Construction Appreciation Week, so we thought it was the perfect opportunity to highlight the unexpected role that construction work (and construction workers) often play in the historical and ancient stories you love learning about. This month, we&#8217;re adding one of the most interesting burials construction workers have ever uncovered to Historical Matches: the Shaman of Bad Dürrenberg.</p>



<h2 class="wp-block-heading">Found During a Water Pipe Job</h2>



<p class="wp-block-paragraph">In 1934, construction crews digging a trench through a spa garden near Bad Dürrenberg, in what is now the German state of Saxony-Anhalt, uncovered a grave dating to the Mesolithic Period, roughly 9,000 years ago. Inside was a woman, seated in a flexed position in a small pit lined with red ochre, buried alongside an infant. Around her lay hundreds of objects, including a pair of roe deer antlers likely worn as a headdress, pierced teeth from wild boar and aurochs, tortoise-shell containers and a bone tool researchers think was once used to apply pigment.</p>



<p class="wp-block-paragraph">Researchers also noticed an indentation at the base of her skull, once mistaken for evidence that she had been decapitated. It&#8217;s now understood to be a congenital condition of her first two vertebrae that may have caused symptoms like dizziness or unusual bodily sensations during her life. Between the richness of her grave and this anatomical quirk, archaeologists have interpreted her burial as that of a woman who held a distinctive spiritual or social role in her community, which is how she came to be known as the Shaman of Bad Dürrenberg.</p>



<p class="wp-block-paragraph">Her fame has only grown since. A reconstruction by artist Karol Schauer has been on permanent display at the <a href="https://www.landesmuseum-vorgeschichte.de/en/permanent-exhibition/human-succession/the-shaman-from-bad-duerrenberg" target="_blank" rel="noreferrer noopener">State Museum of Prehistory</a> in Halle, Germany, for years, and in March 2026 the museum opened a dedicated exhibition on her life and burial, with loans from collections across Europe and the Near East. And ongoing studies of the artifacts she was buried with keep yielding new details. For instance, researchers recently identified microscopic traces of feathers, including goose feathers, suggesting her headdress may have been more elaborate than anyone initially realized.</p>



<h2 class="wp-block-heading">An Old Genome Gets an Upgrade</h2>



<p class="wp-block-paragraph">The Shaman of Bad Dürrenberg&#8217;s DNA has been studied several times. Mitochondrial DNA extracted from her remains <a href="https://pubmed.ncbi.nlm.nih.gov/19729620/" target="_blank" rel="noreferrer noopener">in 2009</a>, and a full genome sequenced <a href="https://pubmed.ncbi.nlm.nih.gov/32523989/" target="_blank" rel="noreferrer noopener">in 2020</a>, already placed her ancestry firmly among Europe&#8217;s Mesolithic hunter-gatherers. This was enough information for researchers who were interested in studying her physical appearance to predict that she likely had dark skin and light eyes, a combination common among hunter-gatherers across Europe at the time.</p>



<p class="wp-block-paragraph"><a href="https://pubmed.ncbi.nlm.nih.gov/35578825/" target="_blank" rel="noreferrer noopener">In 2022</a>, researchers sequenced her genome again, this time to a much higher quality, as part of a study of Neolithic farmers who settled the same general region around 2,000 years after she lived. Her high-quality genome gave them a detailed benchmark for local hunter-gatherer ancestry, which they used to measure exactly how much of it was present in the incoming farming population. The answer: very little. These farmers did carry hunter-gatherer ancestry, but this ancestry was likely acquired earlier, as farming populations expanded through southeastern Europe.</p>



<h2 class="wp-block-heading">Neighbors, Two Thousand Years Later</h2>



<p class="wp-block-paragraph">The same 2022 study analyzed the genomes of 32 individuals from a Linear Pottery culture cemetery near Derenburg, in the same general region the Shaman once called home. These farmers descended from migrants who carried agriculture out of Anatolia and into Europe, part of one of the most significant demographic shifts in the continent&#8217;s history. Their DNA showed that farming spread through Europe primarily via the movement of people themselves, not just the exchange of ideas and technology, and that very little hunter-gatherer ancestry, like the Shaman&#8217;s, made it into this new farming population. Fifteen of these individuals are also joining the Shaman in the Historical Matches feature.</p>



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



<p class="wp-block-paragraph">Curious whether your DNA connects you to the Shaman of Bad Dürrenberg, one of the Neolithic farmers who came after her or any of the hundreds of other historical figures in our database? <a href="https://www.23andme.org/shop/premium-ancestry/" target="_blank" rel="noreferrer noopener">23andMe Premium</a> members can explore the Historical Matches feature to find out.</p>


Sr. Scientist I, Population Genetics R&D

Éadaoin Harney

New Historical Matches Could Connect You to the Shaman of Bad Dürrenberg and the Early Farmers Who Lived in Central Germany After Her


<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h2>Key Takeaways</h2>
<ul><li>About 1 in 8 men will be diagnosed with prostate cancer during their lifetime, making it the second most frequently diagnosed cancer among men in the United States.</li>
<li>Risk can be impacted by both rare, high-impact variants and the cumulative effect of thousands of common variants.</li>
<li>Guidelines vary, but screening may begin at age 50, or as early as 40 or 45 for men who are African American, have a family history or have an increased genetic likelihood.</li>
</ul>
</td></tr></tbody></table></figure>



<p class="wp-block-paragraph">September is Prostate Cancer Awareness Month, which makes this a good moment to sit with a number: about 1 in 8 men are expected to be diagnosed with prostate cancer at some point in their lives. That makes it one of the <a href="https://seer.cancer.gov/statfacts/html/common.html" target="_blank" rel="noreferrer noopener">most commonly diagnosed cancers</a> among men in the United States. Prostate cancer risk varies significantly from person to person, driven in part by genetic factors. To help more people learn about their genetics, 23andMe is now making its Hereditary Prostate Cancer (HOXB13-Related) Genetic Health Risk report* available to all members who have health reports, including those with the Health+Ancestry service.</p>



<h2 class="wp-block-heading">Key Factors Shaping Prostate Cancer Risk</h2>



<p class="wp-block-paragraph">Age is one of the strongest prostate cancer risk factors. Prostate cancer is <a href="https://www.cancer.org/cancer/types/prostate-cancer/causes-risks-prevention/risk-factors.html" target="_blank" rel="noreferrer noopener">rare in men younger than 40</a>, but the chance of developing it climbs quickly after age 50, and roughly 6 in 10 cases are found in men older than 65.</p>



<p class="wp-block-paragraph">Ancestry matters too. African American men are <a href="https://www.cancer.org/cancer/types/prostate-cancer/causes-risks-prevention/risk-factors.html" target="_blank" rel="noreferrer noopener">more likely to develop prostate cancer</a>, tend to be diagnosed at younger ages and are more likely to develop aggressive forms of the disease. In the U.S., more than 1 in 6 African American men develops prostate cancer by age 80, compared with about 1 in 8 men of European descent. Researchers are still working out how much of that difference reflects genetics, environment or unequal access to screening and care.</p>



<p class="wp-block-paragraph">Family history is a third factor. Having a close relative with prostate cancer, or with certain other cancers, raises your own likelihood.</p>



<div style="float: right; text-align: justified; background-color: #eee; padding: 15px; margin-left: 10px; margin-right: 10px; margin-bottom: 35px;">
<p> 
<strong>Prostate Cancer Isn&#8217;t the Only Cancer That Matters in Your Family History</strong></p>
<p>When you think about family history, it&#8217;s natural to look for prostate cancer. But a family history of other cancers can also indicate an increased risk for prostate cancer.</p>
<p>Cancers worth noting on both sides of your family:</p>
<ul><li>Prostate cancer</li>
<li>Breast cancer, including male breast cancer</li>
<li>Ovarian cancer</li>
<li>Pancreatic cancer</li>
<li>Colorectal cancer</li>
<li>Uterine cancer</li></ul>
<p>If any of these run in your family, mention them at your next appointment.</p>
</div>



<h2 class="wp-block-heading">The Genetic Spectrum: From Rare to Common Variants</h2>



<p class="wp-block-paragraph">Your genetics can influence prostate cancer risk in two ways.</p>



<p class="wp-block-paragraph">The first involves rare genetic variants that cause a large impact. An example is a variant called G84E in the <a href="https://www.23andme.org/blog/articles/23andmes-new-hereditary-prostate-cancer-hoxb13-related-report/" target="_blank" rel="noreferrer noopener"><em>HOXB13</em> gene</a>. Men who have this variant have a <a href="https://pubmed.ncbi.nlm.nih.gov/22841674/" target="_blank" rel="noreferrer noopener">33</a> to <a href="https://pubmed.ncbi.nlm.nih.gov/30527799/" target="_blank" rel="noreferrer noopener">53 percent chance</a> of developing prostate cancer by age 80, and they tend to develop prostate cancer earlier than those without the variant. Another example are variants in the <a href="https://www.23andme.org/shop/brca/" target="_blank" rel="noreferrer noopener"><em>BRCA</em> genes, particularly <em>BRCA2</em>.</a> While these variants are mostly known for increasing the risk of breast and ovarian cancer, they can also increase the risk of prostate cancer. Genetic variants like these are uncommon, and they account for only a small share of all prostate cancer cases, but for the people who have them the effect is meaningful.</p>



<p class="wp-block-paragraph">The second route involves thousands of common genetic variants, each shifting the likelihood of prostate cancer by a tiny amount. Any one of these variants doesn&#8217;t make much of an impact on their own, but together they can move a person&#8217;s likelihood noticeably. Scientists capture this combined effect in a <a href="https://www.23andme.org/blog/articles/three-new-prs-cancer-reports/" target="_blank" rel="noreferrer noopener">polygenic risk score</a>, a single number that sums up the influence of many small genetic contributions at once.</p>



<p class="wp-block-paragraph">That second approach comes with an important limitation. Many of the variants linked to prostate cancer, and the <a href="https://pubmed.ncbi.nlm.nih.gov/36353656/" target="_blank" rel="noreferrer noopener">risk models built from them</a>, were identified mostly in men of European descent and may be less informative for men of other ancestries. This same research gap may contribute to worse outcomes in the communities that already carry more of the burden. Closing it depends on genetic studies that include far more people from underrepresented backgrounds.</p>



<h2 class="wp-block-heading">What Your 23andMe Results Can (and Can’t) Tell You</h2>



<p class="wp-block-paragraph">23andMe offers three reports that approach prostate cancer from these two different angles.</p>



<p class="wp-block-paragraph">The Hereditary Prostate Cancer (HOXB13-Related) report looks specifically for the G84E variant in the <em>HOXB13</em> gene. It is the first and only direct-to-consumer test cleared by the FDA to provide genetic health risk information for HOXB13-related hereditary prostate cancer. And now, this report is available to all members with health reports including Premium Ancestry + Health, Health + Ancestry and Health Only members. The 23andMe BRCA1/BRCA2 (Selected Variants) report* is also available to all of these members.&nbsp;</p>



<p class="wp-block-paragraph">The Prostate Cancer Polygenic Risk Score report* uses more than a thousand common variants to estimate your likelihood of developing prostate cancer. It is available to 23andMe Premium Ancestry + Health members who reported their birth sex as male.</p>



<p class="wp-block-paragraph">If you were assigned female at birth, you likely do not have a prostate and are not at risk for prostate cancer, but the Hereditary Prostate Cancer (HOXB13-Related) report is still available to you. If you have a variant detected this result is information worth sharing with your male relatives, who may carry the same variant.</p>



<h2 class="wp-block-heading">What You Can Do</h2>



<p class="wp-block-paragraph">Both reports can inform a more specific conversation with your healthcare provider. If you have a prostate, a few things are worth acting on regardless of your results:</p>



<ul class="wp-block-list">
<li>Talk with a healthcare professional about the benefits and risks of prostate cancer screening. Guidelines vary, but screening may be recommended starting at 50, or as early as 40 or 45 if you are African American, have an increased genetic likelihood or have a family history.</li>



<li>Maintain a healthy weight. Some studies have found that men who are overweight are more likely to develop aggressive forms of prostate cancer.</li>



<li>If you smoke, you can find resources and support for quitting. Smoking is associated with an increased risk of dying from prostate cancer.</li>



<li>Learn and write down your family health history, including cancers on both sides of your family. It is one of the most useful things you can bring to a screening conversation.</li>
</ul>



<p class="wp-block-paragraph">Take a few minutes this month to check your genetic results and, if anything stands out, bring it to your next appointment. If you have learned you carry a HOXB13 variant and want help figuring out what comes next, <a href="https://customercare.23andme.com/hc/en-us/articles/12279139459735-Learning-You-Have-A-HOXB13-Variant-Finding-Support-And-Resources" target="_blank" rel="noreferrer noopener">start here</a>.</p>



<p class="wp-block-paragraph">* <em>The 23andMe PGS test includes health predisposition and carrier status reports. Health predisposition reports include both reports that meet FDA requirements for genetic health risks and PRS reports which are based on a statistical model that includes data and insights from 23andMe consented research participants, and have not been reviewed by the FDA. The test uses qualitative genotyping to detect select clinically relevant variants in the genomic DNA of adults from saliva for the purpose of reporting and interpreting genetic health risks and reporting carrier status. It is not intended to diagnose any disease. Your ethnicity may affect the relevance of each report and how your genetic health risk results are interpreted. Each genetic health risk report describes if a person has variants associated with a higher risk of developing a disease, but does not describe a person’s overall risk of developing the disease. Each PRS report describes if a person has a certain likelihood of developing a condition, but does not describe a person’s overall likelihood. The test is not intended to tell you anything about your current state of health, or to be used to make medical decisions, including whether or not you should take a medication, how much of a medication you should take, or determine any treatment. 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. For certain conditions, we provide a single report that includes information on both carrier status and genetic health risk.</em></p>



<p class="wp-block-paragraph"><em>Warnings &amp; Limitations:</em></p>



<p class="wp-block-paragraph"><em>The Hereditary Prostate Cancer (HOXB13-Related) Genetic Health Risk report is indicated for reporting the G84E variant in the HOXB13 gene. The report describes if a person has the G84E variant and if a male is at increased risk for prostate cancer. The variant included in this report is most common in people of European descent, especially in people of Northern European descent. The 23andMe PGS Genetic Health Risk Report for BRCA1/BRCA2 (Selected Variants) is indicated for reporting of 44 variants in the BRCA1 and BRCA2 genes. The report describes if a person&#8217;s genetic result is associated with an increased risk of developing breast cancer and ovarian cancer and may be associated with an increased risk for prostate cancer, pancreatic cancer, and potentially other cancers. The variants included in this report do not represent the majority of the BRCA1/BRCA2 variants people of most ethnicities.</em></p>



<p class="wp-block-paragraph"><em>These reports do not include variants in other genes linked to hereditary cancers and the absence of variants included in this report does not rule out the presence of other genetic variants that may impact cancer risk. These reports are for over-the-counter use by adults, and provide genetic information to inform discussions with a healthcare professional. The PGS test is not a substitute for visits to a healthcare professional for recommended screenings or appropriate follow-up. Results should be confirmed by an independent genetic test prescribed by your own healthcare provider before taking any medical action.  For important information and limitations regarding genetic health risk reports, visit</em> <a href="https://www.23andme.org/test-info" target="_blank" rel="noreferrer noopener"><em>https://www.23andme.org/test-info</em></a><em>.</em></p>


What Your DNA Can Tell You About Prostate Cancer Risk


<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h2>Key Takeaways</h2>
<ul><li>High cholesterol has more than one cause. For most people it reflects thousands of small genetic effects plus lifestyle and age, but for about 1 in 250 people a single inherited variant is doing most of the work.</li>
<li>Familial hypercholesterolemia (FH) is common and often missed. FH raises LDL cholesterol often from birth and rarely responds to diet and exercise alone, yet as many as 70% of people who have it have never been diagnosed.</li>
<li>Genetic results are a starting point for a discussion with your healthcare professional about screening, treatment and testing your relatives.</li>
</ul>
</td></tr></tbody></table></figure>



<p class="wp-block-paragraph">September is National Cholesterol Education Month, and September 24 is <a href="https://world-heart-federation.org/events/familial-hypercholesterolemia-fh-awareness-day/" target="_blank" rel="noreferrer noopener">Familial Hypercholesterolemia (FH) Awareness Day</a>. Together they make this a good time to ask a question that standard cholesterol testing does not answer: why is your number the way it is?</p>



<h2 class="wp-block-heading">Same Number, Two Very Different Stories</h2>



<p class="wp-block-paragraph">A standard lipid panel measures how much cholesterol is circulating in your blood right now. It is a snapshot, and a useful one. About <a href="https://www.23andme.org/genetics/health-predispositions/ldl-cholesterol/" target="_blank" rel="noreferrer noopener">55% of people in the U.S.</a> will develop high cholesterol by their 70s, and high LDL (sometimes called &#8220;bad cholesterol&#8221;) raises the risk for heart disease, stroke and peripheral artery disease. Because high LDL usually causes no symptoms at first, regular screening matters.</p>



<p class="wp-block-paragraph">What your lab results cannot tell you is the reason behind your number. For most people with high cholesterol, the cause is complex. Thousands of common genetic variants each nudge LDL levels slightly upward, and those small effects combine with diet, activity, age, weight, pregnancy, other health conditions and certain medications leading to your LDL level. Change the modifiable parts of that equation and your LDL often responds.</p>



<p class="wp-block-paragraph">For a smaller group, the cause is monogenic, meaning a single genetic variant is responsible for most of their LDL level. That is a fundamentally different situation, and it calls for a different response.</p>



<h2 class="wp-block-heading">When One Gene Does the Heavy Lifting</h2>



<p class="wp-block-paragraph">FH is very high cholesterol that runs in families. Variants in genes including <em>LDLR</em>, <em>APOB</em> and <em>PCSK9</em> reduce the liver&#8217;s ability to clear LDL from the bloodstream. In people with a variant in one of these genes, LDL levels can be elevated from birth rather than creeping up as you age.</p>



<p class="wp-block-paragraph">That lifetime exposure is what makes FH serious. <a href="https://www.23andme.org/genetics/health-predispositions/fh/" target="_blank" rel="noreferrer noopener">About 1 in 250 people worldwide have FH</a>, and according to the <a href="https://familyheart.org/13-annual-fh-awareness-day" target="_blank" rel="noreferrer noopener">Family Heart Foundation</a> as many as 70% of them have not been diagnosed. Left untreated, men with FH have roughly a 50% risk of a heart attack by age 50, and women roughly a 30% risk by age 60. Sometimes a heart attack is the first sign of elevated LDL.</p>



<p class="wp-block-paragraph">Healthy habits still matter for people with FH, but they are usually not enough to lower LDL on their own. Effective treatment typically requires cholesterol-lowering medication alongside lifestyle changes, and starting earlier substantially reduces cardiovascular risk.</p>



<p class="wp-block-paragraph">FH also travels through families. Each first-degree relative (parents, siblings or children) of someone with FH has at least a 50% chance of having inherited the same variant, often with no outward signs. This is why genetic counselors recommend cascade testing: once one person is diagnosed, close relatives get tested too. It is one of the most effective ways to catch FH early.</p>



<h2 class="wp-block-heading">What Your Genetics Can Add</h2>



<p class="wp-block-paragraph">23andMe offers a few different windows into cholesterol-related genetics.</p>



<ul class="wp-block-list">
<li>The Familial Hypercholesterolemia Genetic Health Risk report* looks for 24 variants, one in the <em>APOB</em> gene and 23 in the <em>LDLR</em> gene. It does not cover all of the more than 1,000 known FH variants, so a negative result does not rule FH out.</li>



<li>If you do not have an FH variant, the LDL Cholesterol PRS report* uses a polygenic score built from more than 2,000 genetic markers to estimate your likelihood of developing high LDL cholesterol. This covers more typical, common genetic changes that, combined with diet and lifestyle, can lead to high LDL cholesterol.</li>



<li>The SLCO1B1 Drug Transport report** covers a variant that affects a protein responsible for transporting statins out of the bloodstream and into the liver. Statins are a commonly prescribed medication used to lower cholesterol. Certain genetic changes in the <em>SLCO1B1</em> gene are associated with higher chances of experiencing side effects.</li>
</ul>



<p class="wp-block-paragraph">None of these diagnose a condition or tell you your cholesterol level today. They can give you and your clinician more context for a conversation.</p>



<h2 class="wp-block-heading">What You Can Do This Month</h2>



<ul class="wp-block-list">
<li>Get a baseline lipid panel if you have not had one recently. Most guidelines recommend adults start in their twenties and repeat every few years.</li>



<li>Ask your relatives about early heart disease, heart attacks before age 55 in men or 65 in women, or cholesterol that has been high for as long as anyone can remember. These are red flags worth mentioning to your doctor.</li>



<li>If your numbers stay high despite doing everything right, ask why. A genetic counselor can help you figure out whether genetic testing makes sense.</li>



<li>Ask about Lp(a) testing. Lipoprotein(a) is a cholesterol-carrying particle that can significantly raise your risk for heart disease. It&#8217;s often skipped in routine lab tests. Your Lp(a) levels are largely set by your genetics and stay fairly stable for life, so a single test may be all you need.</li>
</ul>



<p class="wp-block-paragraph">Curious what your DNA says about your cholesterol? Review your Familial Hypercholesterolemia Genetic Health Risk report and your LDL Cholesterol PRS report. And if you want to go deeper on how monogenic and complex conditions differ, our <a href="https://www.23andme.org/education" target="_blank" rel="noreferrer noopener">Genetics Learning Hub</a> is free and open to everyone.</p>



<p class="wp-block-paragraph"><em>* The 23andMe PGS test includes health predisposition and carrier status reports. Health predisposition reports include both reports that meet FDA requirements for genetic health risks and PRS reports which are based on a statistical model that includes data and insights from 23andMe consented research participants, and have not been reviewed by the FDA. The test uses qualitative genotyping to detect select clinically relevant variants in the genomic DNA of adults from saliva for the purpose of reporting and interpreting genetic health risks and reporting carrier status. It is not intended to diagnose any disease. Your ethnicity may affect the relevance of each report and how your genetic health risk results are interpreted. Each genetic health risk report describes if a person has variants associated with a higher risk of developing a disease, but does not describe a person’s overall risk of developing the disease. Each PRS report describes if a person has a certain likelihood of developing a condition, but does not describe a person’s overall likelihood. The test is not intended to tell you anything about your current state of health, or to be used to make medical decisions, including whether or not you should take a medication, how much of a medication you should take, or determine any treatment. 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. For certain conditions, we provide a single report that includes information on both carrier status and genetic health risk. The Familial Hypercholesterolemia genetic health risk report is indicated for reporting of one variant in the APOB gene and 23 variants in the LDLR gene and describes if a person has variants associated with an increased risk of developing very high LDL cholesterol, which can lead to heart disease.&nbsp; The majority of the variants included in this report have been most studied in people of European and Lebanese descent, as well as in the Old Order Amish. For important information and limitations regarding each genetic health risk report, visit</em> <a href="http://23andme.org/shop/test-info/" target="_blank" rel="noreferrer noopener"><em>23andme.org/shop/test-info/</em></a><em>&nbsp;&nbsp;</em></p>



<p class="wp-block-paragraph"><em>** 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</em> <a href="http://23andme.org/shop/test-info/pharmacogenetics/" target="_blank" rel="noreferrer noopener"><em>23andme.org/shop/test-info/pharmacogenetics/</em></a>&nbsp;</p>



<p class="wp-block-paragraph"></p>


Same Cholesterol Number, Different Genetic Story


<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h2>Key Takeaways</h2>
<ul><li>SuperAgers are adults aged 80 and older whose memory matches that of people decades younger.</li>
<li>Different variants in the APOE gene can impact the likelihood of Alzheimer’s. The e4 variant is associated with higher likelihood while the e2 variant is associated with lower likelihood and is more common in people who reach very old age.</li>
<li>There&#8217;s much we still don&#8217;t know about healthy aging. A 2026 study found SuperAgers were no more likely to have the APOE e2 variant, and their Alzheimer’s polygenic risk scores looked essentially the same as cognitively healthy peers.</li>
</ul>
</td></tr></tbody></table></figure>



<p class="wp-block-paragraph">Imagine hearing a list of 15 unrelated words, spending the next 20 minutes on something else, then recalling nine or more of them. That is a strong performance for someone in their late 50s. Now imagine doing it in your 80s. A small group of older adults can, and researchers call them SuperAgers. Are these people simply genetically lucky? <a href="https://pubmed.ncbi.nlm.nih.gov/42493810/" target="_blank" rel="noreferrer noopener">A study published in July 2026</a> suggests the answer is more complicated than that.</p>



<h2 class="wp-block-heading">How Does the APOE Gene Affect Alzheimer’s Risk?</h2>



<p class="wp-block-paragraph">The <a href="https://www.nia.nih.gov/health/alzheimers-causes-and-risk-factors/alzheimers-disease-genetics-fact-sheet" target="_blank" rel="noreferrer noopener">APOE gene</a> is the strongest common genetic influence on late-onset Alzheimer’s disease, and it typically comes in three versions that push risk in different directions. </p>



<p class="wp-block-paragraph">The e3 version is the most common and is considered neutral. The e4 version increases the likelihood of developing Alzheimer’s and is linked to an earlier age of onset. <a href="https://www.nia.nih.gov/health/alzheimers-causes-and-risk-factors/alzheimers-disease-genetics-fact-sheet" target="_blank" rel="noreferrer noopener">About 25%</a> of people carry one copy of e4 and 2–3% carry two copies. People with two copies have been estimated to have up to a 60% chance of developing Alzheimer’s by age 85 compared to a risk of <a href="https://www.23andme.org/genetics/health-predispositions/late-onset-alzheimers/" target="_blank" rel="noreferrer noopener">about 10%</a> in the general population.</p>



<p class="wp-block-paragraph">The e2 version is the least common, but it has been associated with a lower likelihood of developing Alzheimer’s. It also shows up more often in people who live exceptionally long lives. In an <a href="https://pubmed.ncbi.nlm.nih.gov/30060062/" target="_blank" rel="noreferrer noopener">analysis</a> of 28,297 participants across seven studies of aging, carrying a single copy of e2 was associated with greater odds of reaching extreme old age.</p>



<p class="wp-block-paragraph">One important caveat runs through all of this. Most genetic studies and risk estimates for Alzheimer&#8217;s disease come from studies of people of European descent. How well those numbers transfer to people of other ancestries remains an open question, even as Alzheimer’s <a href="https://www.alz.org/getmedia/ef8f48f9-ad36-48ea-87f9-b74034635c1e/alzheimers-facts-and-figures.pdf" target="_blank" rel="noreferrer noopener">disproportionately affects</a> Black and Hispanic Americans.</p>



<h2 class="wp-block-heading">How Might APOE e2 Protect Neurons?</h2>



<p class="wp-block-paragraph"><a href="https://pubmed.ncbi.nlm.nih.gov/42103698/" target="_blank" rel="noreferrer noopener">New laboratory research</a> suggests e2 may help neurons protect their own DNA. Researchers grew human neurons from stem cells that were genetically identical except at the APOE gene, then compared them. Neurons carrying the e2 variant showed lower levels of DNA damage and were more resistant to becoming senescent, a state in which cells stop functioning normally but do not die, after being exposed to stress compared to neurons carrying the e4 variant. The team saw similar patterns in the brains of aged mice carrying human e2 and e4 variants of the APOE gene.</p>



<p class="wp-block-paragraph">Notably, adding purified e2 APOE protein to neurons that had the e4 genetic variant reduced DNA damage signaling, which hints that some of the protection may come from the APOE protein itself. It&#8217;s important to remember this was observed in cells and mice. It is not a treatment, and the researchers are clear that the precise molecular steps still need to be worked out.</p>



<h2 class="wp-block-heading">Do SuperAgers Have More Protective Genetics?</h2>



<p class="wp-block-paragraph">Here is where the story turns. If e2 lowers the chances of Alzheimer&#8217;s and e4 raises it, you might expect more SuperAgers to have the e2 variant and few would have e4. That&#8217;s not what researchers found.</p>



<p class="wp-block-paragraph">They compared the DNA of 142 SuperAgers and 89 cognitively healthy adults of similar age. 12.7% of SuperAgers and 13.1% of controls had at least one copy of the e2 variant. The proportion carrying at least one e4 variant was 15.7% and 19.0%. Neither difference was statistically significant.&nbsp;</p>



<p class="wp-block-paragraph">Researchers also calculated three different Alzheimer’s polygenic risk scores, which combine the small effects of many common variants into a single estimate of genetic likelihood, and found no meaningful difference between the groups. A handful of SuperAgers even carried two copies of e4 or had high polygenic risk scores and still had youthful memory.</p>



<p class="wp-block-paragraph">In other words, genetic variants that impact your chances of getting Alzheimer&#8217;s, including e2, e4 and other common genetic risk factors, don&#8217;t change your chance of having the memory of a 60-year-old at age 85.&nbsp;</p>



<h2 class="wp-block-heading">What This Study Cannot Tell Us Yet</h2>



<p class="wp-block-paragraph">Does this mean that APOE doesn&#8217;t actually matter? No. The APOE e4 variant remains the strongest common genetic influence on late-onset Alzheimer&#8217;s that researchers have found, and nothing in this study challenges that. What the study asked was a narrower question: whether APOE and other common variants explain why some people keep exceptional memory into their 80s.&nbsp;</p>



<p class="wp-block-paragraph">This was a small study, and that is not a flaw so much as a reality of the field. People who live well into their 80s with the memory of a 60-year-old are rare, which makes them hard to recruit in large numbers. The SuperAging analysis was also a snapshot in time rather than a study that followed people as they aged, and it did not measure vascular health, physical activity, sleep or other lifestyle factors that may matter a great deal.&nbsp;</p>



<p class="wp-block-paragraph">So the question remains open: what influences your chances of healthy aging? Other genetic factors, lifestyle, environment and probably some combination of all three. Answering this question will require more research and participation from larger and more diverse groups of individuals.</p>



<p class="wp-block-paragraph">Curious about your own APOE variants? 23andMe&#8217;s Late-Onset Alzheimer’s Disease Genetic Health Risk report* can tell you if you carry the e4 variant, and <a href="https://www.23andme.org/shop/total-health/" target="_blank" rel="noreferrer noopener">Premium Ancestry + Total Health</a> members can see if they carry other APOE variants through exome sequencing. </p>



<p class="wp-block-paragraph"><em>* The 23andMe PGS test uses qualitative genotyping to detect select clinically relevant variants in the genomic DNA of adults from saliva for the purpose of reporting and interpreting genetic health risks. It is not intended to diagnose any disease. Your ethnicity may affect the relevance of each report and how your genetic health risk results are interpreted. Each genetic health risk report describes if a person has variants associated with a higher risk of developing a disease, but does not describe a person’s overall risk of developing the disease. The test is&nbsp; not intended to tell you anything about your current state of health, or to be used to make medical decisions, including whether or not you should take a medication, how much of a medication you should take, or determine any treatment.&nbsp;&nbsp;</em></p>



<p class="wp-block-paragraph"><em>The Late-Onset Alzheimer’s Disease genetic health risk report is indicated for reporting of the e4 variant in the APOE gene and describes if a person has a variant associated with an increased risk of developing late-onset Alzheimer’s disease. The e4 variant included in this report is found and has been studied in many ethnicities. Detailed risk estimates have been studied the most in people of European descent.</em></p>



<p class="wp-block-paragraph"></p>


What We Know, and Don’t Know, About Genetics, Alzheimer’s and Aging


<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h2>Key Takeaways</h2>
<ul><li>A comprehensive exam can potentially catch early signs of glaucoma, diabetic retinopathy and other conditions before you notice any symptoms.</li>
<li>Type 2 diabetes, glaucoma and nearsightedness are each shaped by hundreds or thousands of genetic variants rather than a single gene.</li>
<li>Your DNA, family history, ethnicity, age and lifestyle all can shape your actual chances of developing these conditions.</li>
</ul>
</td></tr></tbody></table></figure>



<p class="wp-block-paragraph">August is National Eye Exam Month, a yearly nudge to finally book the appointment you may have been meaning to schedule since spring. It&#8217;s tempting to treat that visit as a quick read of the eye chart and potentially a refreshed glasses prescription, but a comprehensive eye exam looks much deeper into the eye, and what a doctor finds there can say something about your broader health, and sometimes about your genes.</p>



<h2 class="wp-block-heading" id="h-what-your-eye-doctor-is-really-looking-for">What Your Eye Doctor Is Really Looking For</h2>



<p class="wp-block-paragraph">An estimated <a href="https://www.cdc.gov/vision-health/about-eye-disorders/why-eye-exams-are-important.html" target="_blank" rel="noreferrer noopener">11 million Americans</a> over age 12 need some form of vision correction. During a comprehensive exam, an eye doctor isn&#8217;t only checking how well you see, they&#8217;re also looking for early signs of conditions like <a href="https://my.clevelandclinic.org/health/diseases/8589-cataracts-age-related" target="_blank" rel="noreferrer noopener">cataracts</a>, <a href="https://www.mayoclinic.org/diseases-conditions/diabetic-retinopathy/symptoms-causes/syc-20371611" target="_blank" rel="noreferrer noopener">diabetic retinopathy</a>, <a href="https://my.clevelandclinic.org/health/diseases/15246-macular-degeneration" target="_blank" rel="noreferrer noopener">age-related macular degeneration</a> and <a href="https://my.clevelandclinic.org/health/diseases/4212-glaucoma" target="_blank" rel="noreferrer noopener">glaucoma</a>, ideally before those conditions cause any noticeable vision loss.</p>



<h2 class="wp-block-heading" id="h-the-genetics-behind-eye-conditions">The Genetics Behind Eye Conditions</h2>



<p class="wp-block-paragraph"><a href="https://www.23andme.org/genetics/health-predispositions/amd/" target="_blank" rel="noreferrer noopener">Age-related macular degeneration</a>, or AMD, damages the macula, the part of the retina responsible for sharp central vision. It’s estimated that more than 10 million people in the U.S. have some form of AMD. AMD risk is associated with variants in many genes, most notably CFH and ARMS2. Other factors like age, smoking and family history can also influence risk. 23andMe has an Age-Related Macular Degeneration Genetic Health Risk report* that can tell you whether you may have an increased risk of developing AMD based on your genetics.</p>



<p class="wp-block-paragraph"><a href="https://www.23andme.org/genetics/health-predispositions/glaucoma/" target="_blank" rel="noreferrer noopener">Glaucoma</a> develops when the optic nerve, which carries visual signals from the eye to the brain, becomes damaged, often due to high pressure inside the eye. Vision loss from glaucoma can be so gradual that many people don&#8217;t notice it until it&#8217;s advanced, which is part of why regular screening matters. Many different genetic variants impact the likelihood of developing glaucoma, 23andMe&#8217;s Glaucoma PRS Report** uses more than 8,000 genetic markers to estimate a person&#8217;s likelihood. Other factors like age, family history and other health conditions can also influence your chances.</p>



<p class="wp-block-paragraph">Diabetic retinopathy, damage to the blood vessels in the retina caused by prolonged high blood sugar, is a leading cause of blindness in American adults and develops as a complication of diabetes. <a href="https://www.23andme.org/genetics/health-predispositions/type-2-diabetes/" target="_blank" rel="noreferrer noopener">Type 2 diabetes</a> is the most common form of diabetes, and many people with diabetes or prediabetes don’t know they have it. Because diabetic retinopathy follows from diabetes, an eye exam can sometimes be the first place these changes are caught. Thousands of genetic variants can contribute to your likelihood of type 2 diabetes along with other factors like diet, weight and lifestyle. For those curious about their genetics say, 23andMe offers a Type 2 Diabetes report**.</p>



<p class="wp-block-paragraph"><a href="https://www.23andme.org/genetics/wellness/nearsightedness/" target="_blank" rel="noreferrer noopener">Nearsightedness</a>, or myopia, is probably what you think of when you think of an eye exam. It affects an estimated 45 percent of U.S. adults and typically develops in childhood, when the eye grows just slightly too long for light to focus correctly on the retina. 23andMe&#8217;s Nearsightedness PRS Report** considers more than 2,700 genetic markers when estimating a person&#8217;s likelihood of being nearsighted, but other environmental factors like limited time spent outdoors during childhood can also contribute to your chances.</p>



<p class="wp-block-paragraph"><a href="https://www.23andme.org/genetics/health-predispositions/migraine/" target="_blank" rel="noreferrer noopener">Migraines</a> might seem like an outlier on this list, but they belong here too. Some people experience aura symptoms, which can include temporary visual disturbances, including flashes of light and blind spots, when they experience a migraine. A comprehensive eye exam is a useful way to rule out an underlying eye problem that could be contributing to head pain. The cause of migraines is still a mystery, but genetics, along with a family history of the condition, can increase likelihood of developing it. You can learn more about your genetics connected to migraines, with the 23andMe Migraine PRS report**.</p>



<h2 class="wp-block-heading" id="h-what-you-can-do-this-eye-exam-month">What You Can Do This Eye Exam Month</h2>



<ul class="wp-block-list">
<li>Book a comprehensive exam. Even if your vision feels fine, a dilated eye exam can catch changes to the retina and optic nerve well before you&#8217;d notice symptoms.</li>



<li>Know your family history. Glaucoma, AMD, migraine and diabetes all run in families, and sharing that history with your doctor helps them recommend the right screening schedule.</li>



<li>Ask about blood sugar and blood pressure. Since diabetic retinopathy and some AMD risk factors connect back to broader metabolic health, managing these numbers can support your eyes as well as the rest of your body.</li>



<li>Don&#8217;t ignore new visual symptoms. Experts agree sudden blind spots, flashes of light or eye pain warrant a prompt visit rather than a wait and see approach.</li>



<li>And if you have kids, encourage outdoor time for them. <a href="https://pubmed.ncbi.nlm.nih.gov/31937276/" target="_blank" rel="noreferrer noopener">More time spent outdoors during childhood</a> is linked to a lower likelihood of developing nearsightedness.</li>
</ul>



<p class="wp-block-paragraph">Curious what your own DNA suggests about your likelihood of developing AMD, glaucoma, nearsightedness or migraine? A <a href="https://www.23andme.org/shop/premium-ancestry-health/" target="_blank" rel="noreferrer noopener">23andMe Premium Ancestry + Health</a> membership unlocks these reports and many more, giving you one more part of the picture to bring to your next eye appointment.</p>



<p class="wp-block-paragraph"></p>



<p class="wp-block-paragraph"><em>* The 23andMe PGS test uses qualitative genotyping to detect select clinically relevant variants in the genomic DNA of adults from saliva for the purpose of reporting and interpreting genetic health risks. It is not intended to diagnose any disease. Your ethnicity may affect the relevance of each report and how your genetic health risk results are interpreted. Each genetic health risk report describes if a person has variants associated with a higher risk of developing a disease, but does not describe a person’s overall risk of developing the disease. The test is&nbsp; not intended to tell you anything about your current state of health, or to be used to make medical decisions, including whether or not you should take a medication, how much of a medication you should take, or determine any treatment. The Age-Related Macular Degeneration (AMD) genetic health risk report is indicated for reporting of the Y402H variant in the CFH gene, and the A69S in the ARMS2 gene and&nbsp; describes if a person has variants associated with an increased risk of developing AMD. The variants included in this report are common in many ethnicities, but are best studied in people of European descent.</em></p>



<p class="wp-block-paragraph"><em>** The 23andMe PRS reports are based on a genetic model that includes data and insights from 23andMe consented research and incorporate thousands of genetic variants to describe if a person has a certain likelihood of developing a condition, but does not describe a person’s overall likelihood. The PRS reports do not account for lifestyle or family history and have not been reviewed by the US Food and Drug Administration. The PRS reports are not intended to tell you anything about your current state of health, or to be used to make medical decisions or determine any treatment.</em></p>


Your Eye Exam and Your DNA: Two Lenses on the Same Picture


<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h2>Key Takeaways</h2>
<ul><li>Through the Historical Matches® feature, 23andMe Premium members can now discover whether their DNA connects them to 44 newly added Sarmatian and Hun-period individuals from the Carpathian Basin.</li>
<li>The Sarmatians once dominated a vast stretch of the Carpathian Basin for centuries, yet no nation claims them as their ancestors. New research reveals surprising genetic ties among them, stretching from Central Asia to Scandinavia, and even hints that their story may reach back further than historians realized.</li>
<li>We&#8217;ve also added five new individuals to our existing Hungarian Royalty group, including a long-unnamed medieval king and a murdered prince whose identity was only recently confirmed.</li>
</ul>
</td></tr></tbody></table></figure>



<p class="wp-block-paragraph">Some ancient peoples get to be famous. The Vikings have blockbuster shows. The Romans have, well, an empire&#8217;s worth of pop culture. The Sarmatians don&#8217;t get nearly as much attention, despite once dominating a vast stretch of Central Europe for centuries. In fact, many historians describe the Sarmatians as a &#8220;forgotten people,&#8221; a once-formidable presence on the edge of the Roman world not claimed as ancestors by any modern nation. This month, we&#8217;re helping to restore their legacy by adding 44 of them to <a href="https://www.23andme.org/blog/articles/23andmes-historic-matches/" target="_blank" rel="noreferrer noopener">Historical Matches</a>.</p>



<h2 class="wp-block-heading" id="h-who-were-the-sarmatians">Who Were the Sarmatians?</h2>



<p class="wp-block-paragraph">The Sarmatians were a nomadic people, who likely spoke an Iranian language. They originated in the southern Ural region of what is now western Russia more than two thousand years ago. From there, they moved west, eventually displacing the Scythians as the dominant power of the Pontic Steppe. By the 1st century CE, Sarmatian groups had settled the Carpathian Basin, a region spanning much of modern Hungary and Romania, ruling over the Celtic and Scythian populations who already lived there.</p>



<p class="wp-block-paragraph">Relations between the Sarmatians and the Roman Empire ran hot and cold, eventually boiling over into the Marcomannic-Sarmatian Wars in the late 2nd century CE. But despite these tensions the Sarmatians settled down, adopted farming, and formed lasting alliances with their Germanic neighbors.</p>



<h2 class="wp-block-heading" id="h-156-new-genomes-and-some-genuine-surprises">156 New Genomes, and Some Genuine Surprises</h2>



<p class="wp-block-paragraph">Last year, researchers published a study in <a href="https://pubmed.ncbi.nlm.nih.gov/40499540/" target="_blank" rel="noreferrer noopener"><em>Cell </em></a> sequencing 156 new ancient genomes from Sarmatian- and later Hun-period sites across the Carpathian Basin and the Romanian plains in order to learn about the genetics of the Sarmatians. </p>



<p class="wp-block-paragraph">Most of the individuals they sequenced carried a distinct steppe ancestry that linked them to their distant Sarmatian relatives who never left the Ural and Kazakh regions. This signal was strongest in the earliest generations and gradually diluted as later Sarmatians mixed with the region&#8217;s existing population.</p>



<p class="wp-block-paragraph">But a handful of individuals didn&#8217;t fit this pattern at all. Two men buried at the same cemetery in southern Hungary had ancestry that traced entirely to Scandinavia, thousands of kilometers to the north, suggesting a previously undetected wave of migration into this Sarmatian community. Others carried substantial East Asian-related ancestry, thousands of kilometers to the east.</p>



<h2 class="wp-block-heading" id="h-genetic-foreshadowing-of-a-migration-to-come-nbsp">Genetic Foreshadowing of a Migration to Come&nbsp;</h2>



<p class="wp-block-paragraph">Perhaps the most surprising discovery didn&#8217;t come from a Sarmatian burial at all. Two individuals from an even earlier Iron Age population in the Carpathian foothills, who lived centuries before the Sarmatians&#8217; documented arrival in the region, turned out to have ancestry that closely resembled the later Sarmatian populations that migrated into the region. It&#8217;s a hint that Sarmatians may have trickled into the region in small numbers long before their main migration, a genetic foreshadowing of a migration to come.</p>



<h2 class="wp-block-heading" id="h-a-much-more-well-known-genetic-group-also-gets-an-update">A Much More Well Known Genetic Group Also Gets an Update</h2>



<figure class="wp-block-image size-large is-resized"><img loading="lazy" decoding="async" width="669" height="1024" src="https://blogcms.23andme.org/wp-content/uploads/2026/08/Bela_II_Hungary-669x1024.jpg" alt="" class="wp-image-35508" style="width:314px;height:auto" srcset="https://blogcms.23andme.org/wp-content/uploads/2026/08/Bela_II_Hungary-669x1024.jpg 669w, https://blogcms.23andme.org/wp-content/uploads/2026/08/Bela_II_Hungary-196x300.jpg 196w, https://blogcms.23andme.org/wp-content/uploads/2026/08/Bela_II_Hungary-768x1176.jpg 768w, https://blogcms.23andme.org/wp-content/uploads/2026/08/Bela_II_Hungary-575x880.jpg 575w, https://blogcms.23andme.org/wp-content/uploads/2026/08/Bela_II_Hungary-771x1180.jpg 771w, https://blogcms.23andme.org/wp-content/uploads/2026/08/Bela_II_Hungary.jpg 1097w" sizes="auto, (max-width: 669px) 100vw, 669px" /></figure>



<p class="wp-block-paragraph">This month&#8217;s Historical Matches update isn&#8217;t only about a people history nearly forgot, though. We&#8217;ve also added five new individuals to our existing Hungarian Royalty group, including King Béla II, a medieval Hungarian ruler identified for the first time after going unnamed among royal remains for centuries. We also added Béla, Duke of Macsó, a prince murdered by rival noblemen in 1272 whose identity was only recently confirmed through DNA. Their genomes were recently sequenced as part of a large scale study of over 400 individuals who were buried in the Royal Basilica of Székesfehérvár, the traditional coronation and burial site of Hungarian monarchs.&nbsp;</p>



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



<p class="wp-block-paragraph">Want to see if your DNA connects you to the Sarmatians, Hungarian Royalty, or to hundreds of other historical individuals? <a href="https://www.23andme.org/shop/premium-ancestry/" target="_blank" rel="noreferrer noopener">23andMe Premium</a> members can explore these new additions through the Historical Matches feature.</p>


New Historical Matches Bring Back a Forgotten People


<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h2>Key Takeaways</h2>
<ul><li>23andMe’s new Premium Parental Inheritance feature allows members to see their Ancestry Composition split by Parent 1 and Parent 2.</li>
<li>Available to 23andMe Premium members, even if their parents haven&#8217;t taken a 23andMe DNA test.</li>
<li>The feature uses a new advanced Family Phasing algorithm to analyze shared DNA segments across distant relatives in the database to accurately determine parental inheritance.</li></ul>
</td></tr></tbody></table></figure>



<p class="wp-block-paragraph">Have you ever looked at your ancestry results and wondered, <em>&#8220;Where did this Scottish ancestry come from, my mom&#8217;s side or my dad&#8217;s?&#8221;</em> If you&#8217;re one of the millions of 23andMe members who haven&#8217;t connected with a parent who has tested with us, that question has been sitting unanswered.</p>



<p class="wp-block-paragraph">That changes today.</p>



<p class="wp-block-paragraph">We&#8217;re launching <strong>Premium Parental Inheritance</strong>, a feature that shows you which side of your family each ancestry region in your results came from regardless of whether or not a parent has ever taken a 23andMe test. Powering this expansion is a DNA analysis we call <strong>Family Phasing</strong>, a method that uses your existing DNA relatives to determine which side of your family your ancestry comes from. The feature is now available to all 23andMe Premium members.</p>



<h2 class="wp-block-heading" id="h-your-ancestry-has-two-sides-now-you-can-see-them">Your Ancestry Has Two Sides. Now You Can See Them.</h2>



<p class="wp-block-paragraph">Parental Inheritance has long let customers see their Ancestry Composition split by parent: how much of your Andalusian, Asturian &amp; Castilian ancestry came from one side, how much of your Nigerian ancestry came from the other. For people who had it, the reaction was often an &#8220;aha&#8221; moment. Suddenly your results became a story about blending two distinct family histories.</p>



<p class="wp-block-paragraph">But accessing it required connecting with a biological parent in the 23andMe database. If your parents had passed away, were unknown to you, or simply weren&#8217;t interested in testing, Parental Inheritance wasn&#8217;t available to you. That left many without a way to access a feature that helps answer so many questions.</p>



<p class="wp-block-paragraph">Family Phasing changes that for many people who have enough relatives in the dataset. Using these relatives, we can often confidently determine parental inheritance for large sections of your DNA.</p>



<p class="wp-block-paragraph">If you&#8217;re a 23andMe Premium member, you&#8217;ll now see your Ancestry Composition results split into Parent 1 and Parent 2 — showing how much of each ancestry region you inherited from each side.</p>



<p class="wp-block-paragraph">Some people won&#8217;t immediately know which labels map to their maternal or paternal sides. You can use your ancestry percentages as clues. If Parent 1 shows a high percentage of Irish ancestry and you know that Irish ancestry runs on your dad&#8217;s side, you can rename Parent 1 to &#8220;Paternal Side.&#8221; But if one of your parents has tested with 23andMe and is participating in DNA Relatives, you&#8217;ll see them connected to their corresponding side.</p>



<h2 class="wp-block-heading" id="h-the-science-how-family-phasing-works">The Science: How Family Phasing<strong> </strong>Works</h2>



<p class="wp-block-paragraph">To understand what&#8217;s new, it helps to understand how Parental Inheritance worked before.</p>



<p class="wp-block-paragraph">Your 23 chromosomes come in pairs: one chromosome in each pair comes from your mother, the other from your father. Figuring out which genetic information came from which parent is called phasing. Previously, 23andMe could perform a high-quality phasing by directly comparing your DNA to a connected biological parent&#8217;s.</p>



<p class="wp-block-paragraph">Without a connected parent, we relied on statistical, population-based phasing. These population-based phasing methods are typically good at determining which variant came from which parent over a short region of your genome. However, they fall short when trying to piece these short, well-phased regions together. As a result, they might phase your genome one way at one end of a chromosome, and the other way at the other end.</p>



<p class="wp-block-paragraph">Family Phasing solves this for portions of your genome by looking at the DNA relatives, even distant ones, you already have in the 23andMe database. The key insight: if you and a relative share a segment of DNA, and that relative is on your mother&#8217;s side, that shared segment probably came from your mother. Family Phasing uses these shared DNA segments across many of your relatives to build a confident picture of which portions of your ancestry came from each parent, no connected parent required.&nbsp;</p>



<figure class="wp-block-image aligncenter size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="903" src="https://blogcms.23andme.org/wp-content/uploads/2026/08/family-phasing-1024x903.png" alt="" class="wp-image-35500" style="width:403px;height:auto" srcset="https://blogcms.23andme.org/wp-content/uploads/2026/08/family-phasing-1024x903.png 1024w, https://blogcms.23andme.org/wp-content/uploads/2026/08/family-phasing-300x264.png 300w, https://blogcms.23andme.org/wp-content/uploads/2026/08/family-phasing-768x677.png 768w, https://blogcms.23andme.org/wp-content/uploads/2026/08/family-phasing-880x776.png 880w, https://blogcms.23andme.org/wp-content/uploads/2026/08/family-phasing-1180x1040.png 1180w, https://blogcms.23andme.org/wp-content/uploads/2026/08/family-phasing.png 1520w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



<p class="wp-block-paragraph">The more relatives you have in the database, and the more closely related to you they are, the more confidently we can determine which side each portion of your DNA came from. Your results include a general view that assigns every ancestry region to a parental side, plus a view of stricter confidence levels, where any lower confidence regions may show as inconclusive.</p>



<h2 class="wp-block-heading">Your Upgraded Path to Parental Inheritance</h2>



<p class="wp-block-paragraph">Thanks to our new Family Phasing technology, Parental Inheritance is getting a major upgrade and moving to 23andMe Premium. If your parents have never tested with 23andMe, this is what you&#8217;ve been waiting for. Premium members without parents connected can now explore their parental inheritance for the first time.</p>



<p class="wp-block-paragraph">If you&#8217;re a 23andMe Premium member and you previously had Parental Inheritance through a connected parent, your experience is evolving. The underlying science is now powered by Family Phasing.&nbsp;</p>



<p class="wp-block-paragraph">If you&#8217;re not already a 23andMe Premium member, your previous Parental Inheritance is no longer available. However, if you upgrade to a 23andMe Premium membership, your results will begin computing automatically, and you&#8217;ll receive a notification when your report is ready.</p>



<h2 class="wp-block-heading">What&#8217;s Coming Next</h2>



<p class="wp-block-paragraph">Parental Inheritance is more than a single feature — it&#8217;s a lens that can be applied across your entire genetic story. We&#8217;re exploring how to bring the same Parent 1 / Parent 2 view to other parts of your 23andMe experience, so you can understand not just <em>what</em> your DNA says, but <em>which side of your family</em> it came from.</p>



<p class="wp-block-paragraph">Your ancestry has always had two sides to it. Ready to see both? If you&#8217;re not currently a 23andMe Premium member, but interested in this feature, check out the <a href="https://www.23andme.org/membership/" target="_blank" rel="noreferrer noopener">23andMe Premium</a> membership to unlock Premium Parental Inheritance and find out which side of your family shaped the ancestry you carry.</p>



<p class="wp-block-paragraph"><em>Premium Parental Inheritance is available to 23andMe Premium subscribers in the US, Canada and UK. Results depend on the number and relatedness of your DNA relatives in our database. All users will receive a full partition of their ancestries into parental sides. However, users with more relative matches will typically receive more confident parental ancestry assignments.</em></p>



<p class="wp-block-paragraph"></p>


Group Product Manager

Sarabeth Hamberlin

You Asked Which Parent You Got It From. Now You Can Find Out.


<p class="wp-block-paragraph">23andMe&#8217;s blog offers genetics news, customers stories, and articles about research. </p>



<figure class="wp-block-image size-full"><img loading="lazy" decoding="async" width="600" height="333" src="http://35.88.189.111/wp-content/uploads/2018/03/Blog-Logo-e1521071249823.jpg" alt="" class="wp-image-26081" srcset="https://blogcms.23andme.org/wp-content/uploads/2018/03/Blog-Logo-e1521071249823.jpg 600w, https://blogcms.23andme.org/wp-content/uploads/2018/03/Blog-Logo-e1521071249823-300x167.jpg 300w, https://blogcms.23andme.org/wp-content/uploads/2018/03/Blog-Logo-e1521071249823-271x149.jpg 271w" sizes="auto, (max-width: 600px) 100vw, 600px" /></figure>



<h1 class="wp-block-heading" id="h-blog-insights">Blog Insights</h1>



<p class="wp-block-paragraph">23andMe is the only DTC DNA testing company with FDA authorization. Our blog gives readers a chance to learn more about genetic testing and science. Along with learning about science and research, we offer up tips and insights into the products and what you can learn by using 23andMe.</p>


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