
<p><em><br>The Maryland Dove docked at Historic St. Mary’s City, Maryland. This ship is a reconstruction of the Dove, a 17th-century trading vessel that, alongside the passenger ship the Ark, carried colonists to found Maryland in 1634.<strong> </strong>Image credit: Jenn Dorsey, Historic St. Mary&#8217;s City</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>By analyzing the DNA of 49 individuals buried in St. Mary’s City, Maryland 300–400 years ago, scientists were able to link 1.3 million 23andMe participants to some of the individuals from Maryland&#8217;s first capital.</li>
<li>For the first time, ancient DNA combined with modern genealogy was used to propose the identities of unknown historical figures, including Maryland’s second governor, Thomas Greene.</li>
<li>The study showed the genetic impact of a documented historical migration, showing a clear genetic link between the original 17th-century Maryland settlers and modern-day populations in Kentucky.</li></ul>
</td></tr></tbody></table></figure>



<p>Nearly four centuries ago, a small group of English and Irish settlers stepped ashore on the southern tip of Maryland and founded a colony they called St. Mary&#8217;s City. Many came seeking religious freedom, others arrived as indentured servants. Over the years, a significant number of these early colonists were buried at the site of the 17th-century Brick Chapel, but their names have since been lost to time.</p>



<p>Now, a new study published in <em><a href="https://www.cell.com/current-biology/fulltext/S0960-9822(26)00516-6" target="_blank" rel="noreferrer noopener">Current Biology</a></em> and co-led by researchers at the 23andMe Research Institute, Harvard Medical School, and the Smithsonian Institution’s National Museum of Natural History is helping restore their stories. With the support of Historic St. Mary&#8217;s City, the researchers analyzed the genomes of 49 individuals buried in St. Mary&#8217;s City&#8217;s Chapel Field. By comparing their DNA to more than 11.5 million consenting 23andMe research participants, the team traced where these colonists came from, mapped how their descendants spread across America, and, for the first time, proposed possible identities for three previously unknown individuals, including the colony&#8217;s second governor.</p>



<figure class="wp-block-embed is-type-video is-provider-youtube wp-block-embed-youtube wp-embed-aspect-16-9 wp-has-aspect-ratio"><div class="wp-block-embed__wrapper">
<iframe loading="lazy" title="Genetic legacy of St. Mary&#039;s City / Curr. Biol., May 14, 2026 (Vol. 36, Issue 11)" width="500" height="281" src="https://www.youtube.com/embed/fRbf3AkLXtY?feature=oembed" frameborder="0" allow="accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture; web-share" referrerpolicy="strict-origin-when-cross-origin" allowfullscreen></iframe>
</div></figure>



<h2 class="wp-block-heading" id="h-a-short-lived-colonial-capital">A short lived colonial capital</h2>



<p>Established in 1634, St. Mary&#8217;s City was the founding English settlement in the colony of Maryland. It was envisioned by George Calvert, the first Baron Baltimore, as both an expansion of the King&#8217;s realm and a place of religious freedom, particularly for persecuted Catholics. The first settlers departed from the Isle of Wight aboard two ships, the <em>Ark </em>and the <em>Dove </em>in late 1633, and arrived at Maryland&#8217;s southern shore the following year.</p>



<p>Though its role as a capital city was short-lived (the seat of government moved to present-day Annapolis in 1695), St. Mary&#8217;s City left a lasting mark on American history. The Chapel Field cemetery, located at the site of the colony&#8217;s Brick Chapel, served as the primary burial ground for nearly a century. Despite existing written records and the ability of many present-day Americans to trace their ancestry to the historic city, many gaps remain in our knowledge of this founding population.</p>



<figure class="wp-block-image size-large"><img loading="lazy" decoding="async" width="1024" height="733" src="https://blogcms.23andme.com/wp-content/uploads/2026/05/brick_chapel_reconstruction-1024x733.png" alt="" class="wp-image-35277" srcset="https://blogcms.23andme.com/wp-content/uploads/2026/05/brick_chapel_reconstruction-1024x733.png 1024w, https://blogcms.23andme.com/wp-content/uploads/2026/05/brick_chapel_reconstruction-300x215.png 300w, https://blogcms.23andme.com/wp-content/uploads/2026/05/brick_chapel_reconstruction-768x550.png 768w, https://blogcms.23andme.com/wp-content/uploads/2026/05/brick_chapel_reconstruction-880x630.png 880w, https://blogcms.23andme.com/wp-content/uploads/2026/05/brick_chapel_reconstruction-1180x844.png 1180w, https://blogcms.23andme.com/wp-content/uploads/2026/05/brick_chapel_reconstruction.png 1280w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /><figcaption class="wp-element-caption"><em>2010 image of the exterior of the reconstructed 1667 Brick Chapel at Historic St. Mary&#8217;s City. Image credit: Donald Winter, Historic St. Mary&#8217;s City</em></figcaption></figure>



<h2 class="wp-block-heading" id="h-ancient-dna-meets-the-world-s-largest-genetics-database">Ancient DNA meets the world&#8217;s largest genetics database</h2>



<p>Researchers extracted ancient DNA from the bones of individuals buried at the site, then used an identity-by-descent approach to find genetic matches among living 23andMe customers who consented to research.</p>



<p>More than 1.3 million consented research participants share DNA with one or more of the St. Mary&#8217;s individuals. DNA sharing occurred at particularly high rates among participants with ancestry from western England and Wales. Several individuals in the study showed stronger genetic connections to Ireland, lending weight to accounts of Irish settlers among the earliest colonists.</p>



<h2 class="wp-block-heading" id="h-tracking-a-documented-migration-in-dna">Tracking a documented migration in DNA</h2>



<p>One of the study&#8217;s most compelling findings is the detection of a clear genetic signal corresponding to a migration previously known only from historical records. Following the Revolutionary War, many Catholic families from St. Mary&#8217;s County faced economic hardship and growing religious discrimination. This prompted a wave of emigration to Kentucky primarily between 1780 and 1820. These settlers established themselves mainly in what are now Nelson and Washington counties.&nbsp;</p>



<p>When the research team mapped which 23andMe participants shared the closest genetic connections to the St. Mary&#8217;s individuals, they found enrichment around Louisville, Kentucky, highlighting the power of this approach.</p>



<h2 class="wp-block-heading" id="h-expanding-the-calvert-family-tree">Expanding the Calvert family tree</h2>



<p>Among the 49 individuals studied, three of the burials were already known: Philip Calvert, the colony&#8217;s fifth governor, his first wife Anne Wolseley Calvert, and an infant, who was confirmed using DNA to be Philip Calvert&#8217;s son, likely from his second marriage. All three were buried in unusual lead coffins beneath the chapel floor.&nbsp;</p>



<p>By comparing their DNA to the remaining individuals in the study, the researchers identified three additional members of the extended Calvert family. The team also identified five other family groupings among the burials, including one that spanned three generations. Given the extraordinarily high mortality rates of the early colonial period, finding a multigenerational family within a single cemetery was a notable finding.</p>



<h2 class="wp-block-heading" id="h-a-new-approach-to-identifying-the-nameless-dead">A new approach to identifying the nameless dead</h2>



<p>Perhaps the most novel aspect of the study is what it demonstrates about using wide-ranging disciplines—from genetics and genealogy to archaeology, history, and osteology—to propose identities for otherwise unknown burials.</p>



<p>The study team invited consented 23andMe research participants who shared the strongest genetic connections to the St. Mary&#8217;s burials to contribute details from their own family trees. Researchers then searched for names that appeared across multiple genealogies and combined those findings with other anthropological evidence. Focusing on three closely related individuals, they found overlaps pointing to a single colonial family: Governor Thomas Greene, the second governor of the Maryland colony, his first wife Anne, and their son Leonard. This marks the first time ancient DNA has been used to propose identities for unknown historical individuals without any prior knowledge of who they might be, a significant milestone for the field.</p>



<h2 class="wp-block-heading" id="h-research-built-with-community">Research built with community</h2>



<p>Cutting-edge science wasn&#8217;t the only key to the success of this study. The early Maryland descendant community, including those who trace their lineage to the original <em>Ark</em> and <em>Dove</em> voyage, provided active support of the project.</p>



<figure class="wp-block-image size-large is-resized"><img loading="lazy" decoding="async" width="683" height="1024" src="https://blogcms.23andme.com/wp-content/uploads/2026/05/reenactor_woman_sewing_small-683x1024.png" alt="" class="wp-image-35280" style="width:257px;height:auto" srcset="https://blogcms.23andme.com/wp-content/uploads/2026/05/reenactor_woman_sewing_small-683x1024.png 683w, https://blogcms.23andme.com/wp-content/uploads/2026/05/reenactor_woman_sewing_small-200x300.png 200w, https://blogcms.23andme.com/wp-content/uploads/2026/05/reenactor_woman_sewing_small-768x1152.png 768w, https://blogcms.23andme.com/wp-content/uploads/2026/05/reenactor_woman_sewing_small-587x880.png 587w, https://blogcms.23andme.com/wp-content/uploads/2026/05/reenactor_woman_sewing_small-787x1180.png 787w, https://blogcms.23andme.com/wp-content/uploads/2026/05/reenactor_woman_sewing_small.png 1101w" sizes="auto, (max-width: 683px) 100vw, 683px" /><figcaption class="wp-element-caption"><em>St. Mary’s City historical interpreter portraying a seamstress. Image credit: Chip Clark, Smithsonian institution</em></figcaption></figure>



<p>The study also depended on the millions of 23andMe members who chose to participate in research. Participants who reported genealogical ties to 17th-century St. Mary&#8217;s City were significantly more likely to share DNA with the colonial individuals than those who did not, underscoring the real-world meaning of those genetic connections.</p>



<h2 class="wp-block-heading" id="h-what-this-means-for-the-future-of-ancient-dna-research">What this means for the future of ancient DNA research</h2>



<p>The St. Mary&#8217;s City study represents something genuinely new: a framework that combines ancient DNA, archaeology, genealogical records, and a large modern genetics database to answer questions that written history could not resolve alone. The approach, particularly the method for proposing identities for unknown individuals, opens a door to similar work at countless other historical sites.</p>



<p>As the United States approaches its 250th anniversary, this research underscores the enduring connections between the nation&#8217;s earliest European settlers and millions of living Americans.</p>


Sr. Scientist I, Population Genetics R&D

Éadaoin Harney

Ancient DNA and 23andMe Are Rewriting the Story of Some of America’s Earliest Colonists


<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 scientists and collaborators have shown that asthma, hay fever and eczema share many underlying genetic associations, pointing to a common immune-system foundation.</li>
<li>Including diverse populations in genetic research helped uncover additional genetic variants associated with eczema.</li>
<li>Insights from large genome-wide studies have shaped the science behind 23andMe&#8217;s five allergy and asthma reports.</li></ul>
</td></tr></tbody></table></figure>



<p>If you have ever spent a May morning sneezing your way through a pollen cloud, or watched a child scratch at itchy patches of eczema, you are not alone. May is Asthma and Allergy Awareness Month, and according to the <a href="https://aafa.org/allergies/allergy-facts/" target="_blank" rel="noreferrer noopener">Asthma and Allergy Foundation of America</a>, more than 100 million people in the United States experience some form of allergy each year. Behind those numbers sits a deep and tangled biology, one that 23andMe scientists and their academic collaborators have been working to untangle for more than a decade.</p>



<h2 class="wp-block-heading" id="h-a-decade-plus-of-allergy-and-asthma-genetic-research">A decade-plus of allergy and asthma genetic research</h2>



<p><a href="https://pubmed.ncbi.nlm.nih.gov/23817569/" target="_blank" rel="noreferrer noopener">In 2013</a>, 23andMe researchers led a genome-wide association study (a GWAS, which looks across the genome for genetic variants more common in people with a given trait) of nearly 54,000 people with self-reported allergies. That early study identified <a href="https://blog.23andme.com/articles/new-genetic-associations-found-for-allergies-and-asthma" target="_blank" rel="noreferrer noopener">16 genetic variants</a> associated with cat, dust-mite and pollen allergies, eight of which overlapped with asthma. In the years that followed, 23andMe contributed to more than a dozen additional publications.</p>



<p>A 2017 paper in <a href="https://pubmed.ncbi.nlm.nih.gov/29083406/" target="_blank" rel="noreferrer noopener"><em>Nature Genetics</em></a> analyzed about 360,000 people and identified 136 genetic variants associated with asthma, hay fever or eczema. This showed that these conditions may have a common genetic foundation rooted in immune regulation. Follow-up work in <a href="https://pubmed.ncbi.nlm.nih.gov/29679657/" target="_blank" rel="noreferrer noopener">2019</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/32603359/" target="_blank" rel="noreferrer noopener">2020</a> pushed further, surfacing <a href="https://blog.23andme.com/articles/the-shared-genetics-of-allergies-hay-fever-and-eczema" target="_blank" rel="noreferrer noopener">eleven additional variants in or near nine genes</a> associated with allergies, and finding additional genetic variants associated with developing allergies, asthma and eczema <a href="https://blog.23andme.com/articles/researchers-identify-new-genetic-associations-for-allergies-asthma-and-eczema" target="_blank" rel="noreferrer noopener">at a very early age</a>.</p>



<p>Digging more into age of onset, a <a href="https://pubmed.ncbi.nlm.nih.gov/30929738/" target="_blank" rel="noreferrer noopener">2019 analysis</a> using UK Biobank data, and then replicated with 23andMe data, found that around 30% of the genetic variants associated with asthma were shared between childhood-onset and adult-onset asthma, but most genetic variants were distinct.</p>



<p>A <a href="https://pubmed.ncbi.nlm.nih.gov/37794016/" target="_blank" rel="noreferrer noopener">2023 multi-ancestry analysis</a> that included more than 3 million consented 23andMe research participants identified new genetic variants associated with eczema. Importantly, this work included a diverse set of participants that enabled the discovery of two genetic variants that may be associated with eczema specifically in people of Japanese ancestry. It&#8217;s a reminder that studying diverse populations matters for finding new genetic associations.</p>



<h2 class="wp-block-heading" id="h-insights-don-t-stop-at-the-journal-page">Insights don&#8217;t stop at the journal page</h2>



<p>Discoveries from the 23andMe Research Institute don&#8217;t sit on a shelf. Many of them flow directly into the reports you can see in your <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ account, including five that are especially relevant this month: <a href="https://www.23andme.com/topics/health-predispositions/asthma/" target="_blank" rel="noreferrer noopener">Asthma</a> and <a href="https://www.23andme.com/topics/health-predispositions/eczema/" target="_blank" rel="noreferrer noopener">Eczema (Atopic Dermatitis)</a>, which can be found with other Health Predisposition reports, and <a href="https://www.23andme.com/topics/wellness/cat-allergy/" target="_blank" rel="noreferrer noopener">Cat Allergy</a>, <a href="https://www.23andme.com/topics/wellness/dog-allergy/" target="_blank" rel="noreferrer noopener">Dog Allergy</a>, and <a href="https://www.23andme.com/topics/wellness/seasonal-allergies/" target="_blank" rel="noreferrer noopener">Seasonal Allergies</a>*, which can be found with other Wellness reports.</p>



<p>Each of these reports uses a polygenic score, a calculation that adds up the small effects of many genetic variants to estimate your likelihood of developing a condition. This information, alongside other factors like family history and environment, may help you understand and manage these conditions.&nbsp;</p>



<p>The genetic variants drawn on by these reports trace back to research like that above, which is to say, they trace back in part to consented 23andMe research participants who answered survey questions about their own allergies and asthma. The more people contribute, the better the science gets, and the better the reports become for the next generation of 23andMe members.</p>



<h2 class="wp-block-heading" id="h-what-you-can-do-this-allergy-season">What you can do this allergy season</h2>



<p>Genetics is only one piece of why asthma or allergies show up in your life, and there is plenty you can do regardless of what your genes say.</p>



<ul class="wp-block-list">
<li>Track your triggers. Keeping a simple log of when symptoms flare can help you and your clinician spot patterns, whether the culprit is tree pollen, a particular pet or an indoor mold.&nbsp;</li>



<li>For those with asthma, recognize the warning signs of an asthma attack and create a plan for action. Catching an asthma attack early can prevent severe symptoms.</li>



<li>Check your reports. Your 23andMe Asthma, Eczema (Atopic Dermatitis) and allergy-related reports can give you a sense of your genetic likelihood, which may be useful context to share with a healthcare professional.</li>



<li>Talk to a clinician. If symptoms are persistent or affecting daily life, allergists and dermatologists have a growing toolkit of treatments.</li>
</ul>



<p>The science that built today&#8217;s reports were powered by people willing to share a little about their own health. 23andMe research participants are helping to shape new discoveries. The next finding might just turn into the next report.</p>



<p>*<em>The 23andMe Asthma, Eczema (Atopic Dermatitis), Cat Allergy, Dog Allergy, and Seasonal Allergies PRS reports are based on a genetic model that includes data and insights from 23andMe consented research participants and incorporates many genetic variants to provide information on the likelihood of experiencing these conditions. These reports do not describe a person’s overall likelihood, do not account for lifestyle or family history and have not been reviewed by the US Food and Drug Administration. These 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>


Sr. Manager, Product Science

Alisa Lehman

The Genetics of Asthma and Allergies: More Than a Decade of 23andMe Research


<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>Around one in five Americans will develop some form of skin cancer by age 70. Melanoma, basal cell carcinoma, and squamous cell carcinoma account for the vast majority of these skin cancers.</li>
<li>23andMe research has identified dozens of genetic markers associated with skin cancer over the last decade, helping scientists to potentially improve screening and understand complex genetic connections.</li>
<li>While genetics play a part, your sun exposure history, skin type, and family history all matter. Understanding these factors allows you to take control through regular screening and small daily habits that can meaningfully reduce your risk.</li></ul>
</td></tr></tbody></table></figure>



<p>Here&#8217;s a sobering number to sit with: roughly <a href="https://www.skincancer.org/skin-cancer-information/skin-cancer-facts/" target="_blank" rel="noreferrer noopener">one in five</a> Americans will develop some form of skin cancer by age 70, making it the <a href="https://www.skincancer.org/skin-cancer-information/skin-cancer-facts/" target="_blank" rel="noreferrer noopener">most common cancer</a> in the United States. May is Skin Cancer Awareness Month, a good moment to talk about how the sun, your skin, and your DNA come together to shape your personal risk.</p>



<h2 class="wp-block-heading" id="h-the-genetic-story-behind-skin-cancer">The Genetic Story Behind Skin Cancer</h2>



<p>Skin cancer isn&#8217;t one disease but <a href="https://www.aad.org/public/diseases/skin-cancer/types/common" target="_blank" rel="noreferrer noopener">several</a>. Melanoma, though less common, is often more dangerous because it&#8217;s more likely to spread to other organs. Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), together called non-melanoma skin cancers, are far more common and usually less aggressive, though SCC can spread if left untreated.</p>



<h3 class="wp-block-heading" id="h-23andme-research-on-skin-cancer">23andMe Research on Skin Cancer</h3>



<p>Over the last decade, scientists at the 23andMe Research Institute have worked alongside collaborators and with hundreds of thousands of consented participants to map the DNA markers associated with these cancers. This research helps scientists worldwide hunt for better treatments and identify those who may need more aggressive screening.</p>



<p>Key milestones from our research community include:</p>



<ul class="wp-block-list">
<li>A <a href="https://www.nature.com/articles/ncomms12510" target="_blank" rel="noreferrer noopener">2016 study</a> that found 14 new genetic variants associated with BCC.</li>



<li>A <a href="https://www.nature.com/articles/s41467-022-35345-8" target="_blank" rel="noreferrer noopener">2022 study</a> that identified 19 additional BCC genetic variants and 15 SCC-associated genetic variants.</li>



<li><a href="https://www.nature.com/articles/s42003-023-05753-7" target="_blank" rel="noreferrer noopener">Most recently</a>, a study that was able to identify 36 new BCC genetic variants, 33 of which also showed associations with SCC risk.</li>
</ul>



<h3 class="wp-block-heading" id="h-connecting-the-dots-polygenic-risk-scores">Connecting the Dots: Polygenic Risk Scores</h3>



<p>To make sense of all these different genetic variants, which individually have small overall effects on skin cancer risk, scientists combine them into disease risk scores, also called polygenic risk scores, that summarize the contribution of many genetic variants at once.&nbsp;</p>



<p><a href="https://www.nature.com/articles/s41467-020-20246-5" target="_blank" rel="noreferrer noopener">In 2021</a> 23andMe researchers combined genetic variants and non-genetic factors (including things like age, pigmentation traits, mole counts, sun exposure history, and family history) to create scores that predict the likelihood of developing BCC, SCC, and melanoma. These risk scores also predicted earlier age of skin cancer diagnosis.</p>



<h3 class="wp-block-heading" id="h-an-unexpected-connection">An Unexpected Connection</h3>



<p>One of the more <a href="https://www.jidonline.org/article/S0022-202X(18)31749-4/fulltext" target="_blank" rel="noreferrer noopener">intriguing findings</a>: genes that protect against vitiligo (the autoimmune condition that causes patches of skin to lose pigment) appear to <em>increase</em> skin cancer risk. This suggests that the same genetic &#8220;wiring&#8221; that tells your immune system how to interact with your skin’s pigment cells may also play a role in defending against skin cancer.</p>



<h2 class="wp-block-heading" id="h-the-23andme-skin-cancer-reports">The 23andMe Skin Cancer Reports</h2>



<p>At 23andMe, our goal is to not only make new genetic discoveries, but to transform these scientific discoveries into personalized insights that empower members to take action. To translate this science into something personal we created two reports: the <a href="https://www.23andme.com/topics/health-predispositions/melanoma/" target="_blank" rel="noreferrer noopener">Skin Cancer (Melanoma)</a>* and <a href="https://www.23andme.com/topics/health-predispositions/basal-and-squamous-cell-skin-cancers/" target="_blank" rel="noreferrer noopener">Skin Cancer (Basal and Squamous Cell Carcinomas)</a>** PRS reports, which estimate your likelihood of developing skin cancers based on many genetic variants. Both reports are powered by polygenic risk scores and are available to <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members.</p>



<p>These reports can&#8217;t tell you whether you will get skin cancer, but they do give you one more piece of information to weigh alongside your skin type, sun exposure history, and family history when thinking about prevention and screening.</p>



<h3 class="wp-block-heading" id="h-the-gap-in-genetic-research">The Gap in Genetic Research</h3>



<p>Skin cancer affects people of every background, but the conversation around it has historically centered on lighter-skinned populations. People with darker skin have a lower overall incidence of skin cancer, yet they often face worse outcomes in part because melanomas in people of color more often appear in less sun-exposed places like the palms, soles, and under the nails, where they can go unnoticed until later stages.&nbsp;</p>



<p>Much of the foundational genetic research on skin cancer has also been conducted primarily in people of European descent, which limits how well polygenic risk scores perform for people of other ancestries. In fact, the polygenic risk score behind the 23andMe Skin Cancer (Melanoma) and Skin Cancer (Basal and Squamous Cell Carcinomas) reports did not perform well enough to deliver results to people of all backgrounds, and unfortunately these members are not able to receive their personalized genetic results for these topics. The Skin Cancer (Melanoma) genetic results are not available for individuals of East/Southeast Asian, South Asian, or Sub-Saharan African/African American descent, and the Skin Cancer (Basal and Squamous Cell Carcinomas) genetic results are not available for individuals of East/Southeast Asian or South Asian descent.</p>



<p>This is precisely why expanding who participates in genetic research is so important. The more people of all ancestries, backgrounds, and ethnicities participate in research, the stronger and more inclusive these insights become. 23andMe research participants are on the forefront of helping change this, for themselves and for future generations. Learn more <a href="https://www.23andme.com/research/" target="_blank" rel="noreferrer noopener">here</a>.</p>



<h2 class="wp-block-heading" id="h-what-you-can-do">What You Can Do</h2>



<p>Genetics is one part of the story you can&#8217;t change, but almost everything else about skin cancer prevention is in your hands:</p>



<ul class="wp-block-list">
<li>Wear broad-spectrum sunscreen (SPF 30 or higher) daily, even when it&#8217;s cloudy, and reapply every two hours outdoors.</li>



<li>Seek shade, especially between 10 a.m. and 4 p.m., when UV radiation is strongest.</li>



<li>Skip tanning beds. Their UV exposure can contribute to melanoma and other skin cancers.</li>



<li>Do a monthly <a href="https://www.cancer.org/cancer/risk-prevention/sun-and-uv/skin-exams.html" target="_blank" rel="noreferrer noopener">self-check</a>. Look for new or changing moles, sores that bleed or don’t heal, and anything that’s new or changing in size, shape, or color.</li>



<li>See a dermatologist for a full-body skin exam, especially if you have a personal or family history of skin cancer.</li>
</ul>



<p>Catching skin cancer early dramatically improves outcomes. Most skin cancers, when found early, are highly treatable.</p>



<p>If you&#8217;re a 23andMe+ Premium member, take a few minutes this Skin Cancer Awareness Month to review your Skin Cancer (Melanoma) and Skin Cancer (Basal and Squamous Cell Carcinomas) reports, and then put sunscreen on tomorrow morning.</p>



<p><em>* The 23andMe Skin Cancer (Melanoma) PRS report is based on a genetic model that includes data and insights from 23andMe consented research participants and incorporates more than 1,800 genetic variants to provide information on the likelihood of experiencing melanoma. 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 Skin Cancer (Melanoma) 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><em>** The 23andMe Skin Cancer (Basal and Squamous Cell Carcinomas) PRS report is based on a genetic model that includes data and insights from 23andMe consented research participants and incorporates more than 11,000 genetic variants to provide information on the likelihood of experiencing basal and squamous cell carcinomas. 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 Skin Cancer (Basal and Squamous Cell Carcinomas) 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>


More Than Skin Deep: What DNA Can Reveal About Skin Cancer Risk


<p><em>By Matthew J. Kmiecik, Ph.D.</em></p>



<p>April is Parkinson’s Awareness Month, a time dedicated to increasing education about the condition and highlighting the incredible progress being made in research. At the 23andMe Research Institute, this month holds a special significance. Since 2009, we have been committed to uncovering the genetic underpinnings of Parkinson’s disease to help pave the way for future breakthroughs.</p>



<h2 class="wp-block-heading" id="h-understanding-parkinson-s-disease">Understanding Parkinson’s Disease</h2>



<p>Parkinson’s disease is a neurodegenerative condition characterized by tremors, muscle stiffness, and challenges with movement and balance. Motor symptoms can be just the tip of the iceberg, as many non-motor symptoms also occur, including sleep disturbances, loss of smell, and constipation. While it typically develops after the age of 55, the journey for every individual is unique.</p>



<p>About 1–2% of people develop Parkinson’s during their lifetime. While we are still learning why some people develop the condition and others don’t, we know that a combination of factors is at play:</p>



<ul class="wp-block-list">
<li>Age: Risk increases as we get older.</li>



<li>Sex: Males have a higher likelihood of developing Parkinson’s than females.</li>



<li>Environment: Exposure to certain chemicals, such as pesticides and chemicals used for metal degreasing or dry cleaning, can increase risk.</li>



<li>Family History: Having a first-degree relative (parents, siblings, and children) with the condition can increase your own chances.</li>



<li>Head Injury: Some studies suggest that head injury, in particular those that result in prolonged loss of consciousness, can increase the risk of developing Parkinson&#8217;s disease later in life.</li>
</ul>



<h3 class="wp-block-heading" id="h-the-genetic-connection">The Genetic Connection</h3>



<p>For some people, DNA plays an important role in their chances of developing Parkinson&#8217;s. Two of the most well-studied genes associated with Parkinson’s are <em>LRRK2</em> and <em>GBA</em> (also known as <em>GBA1</em>). 23andMe offers the <a href="https://www.23andme.com/topics/health-predispositions/parkinsons-disease/" target="_blank" rel="noreferrer noopener">Parkinson’s Disease Genetic Health Risk report</a>* that specifically looks at two genetic variants: one in each of these genes associated with an increased risk of developing Parkinson&#8217;s disease. The chance that someone carrying these variants actually develops Parkinson’s is different depending on what variant they carry. Estimates range from roughly 24% to over 50% for <em>LRRK2</em> G2019S carriers<sup>[1][2]</sup>, and from about 10% to 30% for <em>GBA1</em> N409S carriers (formerly known as N370S)<sup>[3][4]</sup>, depending on the study and genetic ancestry.</p>



<h3 class="wp-block-heading" id="h-what-our-research-adds">What Our Research Adds</h3>



<p>While most people who have these variants will not develop Parkinson’s, <a href="https://doi.org/10.1002/acn3.70176" target="_blank" rel="noreferrer noopener">recent research</a> from the 23andMe Research Institute and collaborators has helped us better understand the nuances of the condition and why it affects every individual differently.</p>



<ul class="wp-block-list">
<li>The researchers found that a person&#8217;s overall genetic background can &#8220;dial&#8221; their risk up or down. Among <em>GBA1</em> carriers, those with a low-risk genetic background had roughly the same chance of developing Parkinson’s as non-carriers. But <em>GBA1</em> carriers with a high-risk genetic background were about five times more likely to develop the disease. The takeaway: carrying one variant is only part of the picture, as many other genes and variants across the genome can nudge the risk up or down.<br></li>



<li>For carriers of both <em>LRRK2</em> and <em>GBA1</em> carriers, the risk was even higher. This research showed that these &#8220;dual carriers&#8221; face a much higher risk of developing Parkinson’s—about a 30% chance by the age of 80, compared to just 2% in people without either genetic variant.<br></li>



<li>Genetics don&#8217;t just influence whether someone develops Parkinson&#8217;s; it also impacts how the disease progresses. The researchers found that in those already living with PD, carrying <em>APOE</em> E4—commonly associated with Alzheimer’s disease—increases the risk of experiencing hallucinations, memory challenges, and concentration issues. In fact, each additional copy of the <em>APOE</em> E4 raised the risk of these symptoms by 11% to 35%.</li>
</ul>



<h2 class="wp-block-heading" id="h-power-in-numbers-17-years-of-research">Power in Numbers: 17 Years of Research</h2>



<p>Since launching our Parkinson’s research community in 2009, the 23andMe Research Institute has grown one of the largest genetic studies of Parkinson’s disease in the world. Our study has included more than 30,000 consented research participants with Parkinson’s. Their ongoing contribution has led to more than <a href="https://research.23andme.com/publications/" target="_blank" rel="noreferrer noopener">30 publications</a> on Parkinson&#8217;s disease, most recently a <a href="https://pubmed.ncbi.nlm.nih.gov/41667488/" target="_blank" rel="noreferrer noopener">paper</a> exploring other biological factors that might influence Parkinson&#8217;s disease risk or progression.&nbsp;</p>



<p>This progress is only possible because of this community who make up one of the world’s largest genetic studies of Parkinson’s disease. A large study size is what allows scientists to zoom in on tiny DNA clues that would be impossible to spot in just a small handful of people.</p>



<h2 class="wp-block-heading" id="h-how-you-can-get-involved">How You Can Get Involved</h2>



<p>Awareness is the first step toward action. This Parkinson’s Awareness Month you can:</p>



<ul class="wp-block-list">
<li>Share the facts about PD symptoms and risks with your loved ones.</li>



<li>If you are a 23andMe member, you can opt-in and view your <a href="https://www.23andme.com/topics/health-predispositions/parkinsons-disease/" target="_blank" rel="noreferrer noopener">Parkinson’s Disease Genetic Health Risk report</a>.</li>



<li>If you or a loved one are living with Parkinson’s or you&#8217;re just interested in this research, consider joining our <a href="https://www.23andme.com/pd/" target="_blank" rel="noreferrer noopener">research community</a>.&nbsp;</li>
</ul>



<p>This April, consider taking a step toward greater awareness for yourself, and for the millions of people living with Parkinson&#8217;s disease around the world.</p>



<div style="width: 100%; margin: 0 auto; text-align: justify; background-color: #eee; padding: 15px;">
<h4>About the Author</h4>
<p><strong>Matthew J. Kmiecik</strong>, Ph.D. — Scientist I, Parkinson’s Disease Research
</p>
<p> 
Dr. Matthew Kmiecik is a cognitive neuroscientist whose research has long focused on how the brain processes information under conditions of injury and disease. With over a decade of research experience, Dr. Kmiecik is a Scientist at the 23andMe Research Institute, where his work is supported by The Michael J. Fox Foundation for Parkinson&#8217;s Research. His current research focuses on identifying genetic and biological markers of Parkinson&#8217;s disease risk and progression, including cognitive assessments, sensory measurements, and wearable-based tools to better understand how the disease unfolds over time.</p>
</div>



<p>* 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 Parkinson’s Disease genetic health risk report is indicated for reporting of the G2019S variant in the LRRK2 gene, and the N409S variant (formerly known as N370S) in the GBA gene and describes if a person has variants associated with an increased risk of developing Parkinson’s disease. The variants included in this report are most common and best studied in&nbsp; people of European, Ashkenazi Jewish, and North African Berber descent.</p>



<h5 class="wp-block-heading">References</h5>



<p>[1] Clark, L. N., Wang, Y., Karlins, E., Saito, L., Mejia-Santana, H., Harris, J., Louis, E. D., Cote, L. J., Andrews, H., Fahn, S., Waters, C., Ford, B., Frucht, S., Ottman, R., &amp; Marder, K. (2006). Frequency of LRRK2 mutations in early- and late-onset Parkinson disease. Neurology, 67(10), 1786–1791. <a href="https://doi.org/10.1212/01.wnl.0000244345.49809.36" target="_blank" rel="noreferrer noopener">https://doi.org/10.1212/01.wnl.0000244345.49809.36</a>&nbsp;</p>



<p>[2] Kmiecik, M. J., Micheletti, S., Coker, D., Heilbron, K., Shi, J., Stagaman, K., Filshtein Sonmez, T., Fontanillas, P., Shringarpure, S., Wetzel, M., Rowbotham, H. M., Cannon, P., Shelton, J. F., Hinds, D. A., Tung, J. Y., 23andMe Research Team, Holmes, M. V., Aslibekyan, S., &amp; Norcliffe-Kaufmann, L. (2024). Genetic analysis and natural history of Parkinson’s disease due to the LRRK2 G2019S variant. Brain, 147(6), 1996–2008. <a href="https://doi.org/10.1093/brain/awae073" target="_blank" rel="noreferrer noopener">https://doi.org/10.1093/brain/awae073</a>&nbsp;</p>



<p>[3] Rana, H. Q., Balwani, M., Bier, L., &amp; Alcalay, R. N. (2013). Age-specific Parkinson disease risk in GBA mutation carriers: Information for genetic counseling. Genetics in Medicine, 15(2), 146–149. <a href="https://doi.org/10.1038/gim.2012.107" target="_blank" rel="noreferrer noopener">https://doi.org/10.1038/gim.2012.107</a>&nbsp;</p>



<p>[4] Anheim, M., Elbaz, A., Lesage, S., Durr, A., Condroyer, C., Viallet, F., Pollak, P., Bonaïti, B., Bonaïti-Pellié, C., &amp; Brice, A. (2012). Penetrance of Parkinson disease in glucocerebrosidase gene mutation carriers. Neurology, 78(6), 417–420. <a href="https://doi.org/10.1212/WNL.0b013e318245f476" target="_blank" rel="noreferrer noopener">https://doi.org/10.1212/WNL.0b013e318245f476</a></p>



<p></p>


Parkinson’s Awareness Month: Genetics, Awareness, and Research


<p><em>By James Ashenhurst, PhD.</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>New work from the 23andMe Research Institute has identified specific variants in the <i>GLP1R</i> and <i>GIPR</i> genes that influence how individuals respond to GLP-1 medications, affecting weight loss outcomes and the risk of side effects like nausea.</li>
<li>Utilizing data from over 27,000 consented research participants, 23andMe conducted a landmark genome-wide association study (GWAS) to uncover the genetics behind why these medications impact people in such distinct ways.</li>
<li>23andMe Total Health™ members can now access an exclusive interactive tool that combines an individual’s genetic results with their medical history to help doctors and patients move toward data-driven, personalized weight management decisions.</li></ul>
</td></tr></tbody></table></figure>



<p>GLP-1 medications, such as semaglutide (Ozempic®, Wegovy®) and tirzepatide (Mounjaro®, Zepbound®), have transformed the clinical approach to weight management. In fact, an estimated 1 in 8 adults in the U.S. have used a GLP-1 medication in recent years.<sup>[1]</sup>&nbsp;</p>



<p>Yet, if you or someone you know has taken one, you might have noticed that not everyone has the same experience on these drugs. While GLP-1 medications are commonly prescribed to help control blood sugar and to assist in weight loss, there is substantial variation in how well they work for different people. Some individuals lose as little as 5% of their body weight, whereas others lose more than 20%.<sup>[2][3]</sup> Similarly, while gastrointestinal side effects such as nausea and vomiting are common, some people experience moderate to severe forms, whereas others report no nausea at all.<sup>[4]</sup>&nbsp;</p>



<p>While lifestyle characteristics like diet patterns and exercise may certainly explain some of these differences, potential genetic causes of this variation have been unclear, until today. <strong>Scientists at the 23andMe Research Institute published a study in </strong><a href="https://www.nature.com/articles/s41586-026-10330-z" target="_blank" rel="noreferrer noopener"><strong><em>Nature</em></strong></a><strong> that has identified genetic variants associated with weight loss and side effects among those who have taken GLP-1 medications.</strong></p>



<h2 class="wp-block-heading" id="h-the-mystery-of-medication-response">The Mystery of Medication Response</h2>



<p>When people begin a GLP-1 journey, they may start with uncertainty about efficacy and possible side effects. While the market is crowded with weight loss support and medications, few resources offer personalized insight into the simple question: “What can I expect?”.</p>



<p>To find answers, we turned to our incredible community of 23andMe research participants. Over 27,000 consented participants made this research possible by sharing their experiences with GLP-1 medications through an ongoing research survey. Using 23andMe’s unique crowdsourced approach to research, we were able to conduct the first large-scale genome-wide association study (GWAS) just seven months after starting the study, a very rapid rate for a study of this kind. In simple terms, a GWAS is like scanning a massive library of DNA to find specific &#8220;spelling differences&#8221; (genetic variants) that are more common in people who share a specific trait. In this case, scientists wanted to understand if there were genetic differences that were associated with how participants&#8217; bodies responded to GLP-1 medications.&nbsp;</p>



<h2 class="wp-block-heading" id="h-discovering-the-genetic-links">Discovering the Genetic Links</h2>



<p>23andMe Research Institute scientists uncovered fascinating genetic associations for response to GLP-1 medications, including a person&#8217;s potential for weight loss and their risk of experiencing nausea or vomiting.</p>



<p>First, the study identified a genetic variant that is associated with both weight loss and nausea for the two major classes of GLP1 medications: semaglutide and tirzepatide. This variant is located in the <em>GLP1R</em> gene, which codes for the receptor protein that is the target of GLP-1 medications.</p>



<p>Second, the study identified another genetic variant that is associated with side-effects, specifically nausea and vomiting, while using tirzepatide (Mounjaro® or Zepbound®). You might wonder why this second variant only affects tirzepatide users. It comes down to how the drugs are designed: while semaglutide acts only on GLP-1 receptors, tirzepatide is a dual-target drug that also acts on GIP receptors (GIP, or gastric inhibitory polypeptide, is another hormone like GLP-1 that helps regulate insulin and blood sugar). Our team discovered that this second variant is located in the <em>GIPR</em> gene, which explains why it impacts tirzepatide response but not semaglutide.</p>



<figure class="wp-block-image size-large"><img loading="lazy" decoding="async" width="649" height="1024" src="/wp-content/uploads/2026/04/image-649x1024.png" alt="" class="wp-image-35199" srcset="https://blogcms.23andme.com/wp-content/uploads/2026/04/image-649x1024.png 649w, https://blogcms.23andme.com/wp-content/uploads/2026/04/image-190x300.png 190w, https://blogcms.23andme.com/wp-content/uploads/2026/04/image-768x1212.png 768w, https://blogcms.23andme.com/wp-content/uploads/2026/04/image-558x880.png 558w, https://blogcms.23andme.com/wp-content/uploads/2026/04/image.png 1014w" sizes="auto, (max-width: 649px) 100vw, 649px" /></figure>



<p>Describing the impact of the study, Dr. Adam Auton, Vice President of Human Genetics at the 23andMe Research Institute said, <strong><em>&#8220;Identifying these variants in the GLP1R and GIPR genes provides an important new insight into why these medications impact people in distinct ways. It’s a great example of how our large-scale, participant-engaged research program can clarify the biological mechanisms behind drug response, and moves us closer to a future where &#8216;precision medicine&#8217; isn&#8217;t just an aspiration.&#8221;</em></strong></p>



<h2 class="wp-block-heading">Translating Emerging Science into Personalized Insights</h2>



<p>Discovering these variants is a massive step forward, but our ultimate goal is to meet the need for more personalized insight into GLP-1 medication responses.</p>



<p>That is why a new report and interactive tool related to GLP-1 medications is now available exclusively through the 23andMe+ <a href="https://www.23andme.com/total-health/wl-mrr?utm_source=23andme&amp;utm_medium=blog&amp;utm_campaign=wlmrr_april_2026" target="_blank" rel="noreferrer noopener">Total Health</a>™ service. This interactive tool combines an individual’s genetic results for these two variants with demographics and medical history to estimate both weight loss and nausea likelihood based on data from 23andMe research participants. All these factors combined can result in significant variability in the likelihood of weight loss or side effects. In fact, the estimates for weight loss can vary between -6% to -20% of baseline weight after one year. Likewise, the estimated risk of nausea and vomiting can range between 5% to 78% risk for experiencing these side effects.</p>



<h2 class="wp-block-heading">What You Need to Know About the New Report</h2>



<p>The science of genetics is always evolving and the 23andMe Research Institute strives to be on the forefront of genetics research, powered by the participation of our members. Our mission is also to help people benefit from genetics research, which is why we are thrilled to provide this new report to our Total Health members. This report is designed to be reviewed in consultation with a clinician and is intended for use in a supervised clinical context, which is why it is exclusively available through the physician-supervised Total Health service.</p>



<p>The shift toward personalized care enabled by this report is echoed by Dr. Noura Abul-Husn, Chief Medical Officer of the 23andMe Research Institute, who views the data as a catalyst for better patient-doctor relationships: <strong><em>&#8220;For healthcare professionals, the true value of this data lies in its potential to transform weight loss discussions from a trial-and-error approach into data-driven, shared decision-making with patients. Integrating genetic markers, such as those we’ve identified in the GLP1R and GIPR genes, with clinical factors provides a clearer picture of how a patient’s unique biology may interact with a specific therapy, allowing both patients and their doctors to proactively manage expectations and tailor care with greater precision from day one.&#8221;</em></strong></p>



<h2 class="wp-block-heading">A Sincere Thank You to Our Participants</h2>



<p>The GLP-1 Study is ongoing, and our survey is designed to allow participants to share their journey over time so we can continue to investigate how these medications are associated with genetics and health. Discoveries like this simply would not exist without our research participants. Current 23andMe members can choose to contribute answers and to fuel new discoveries.</p>



<p><a href="https://you.23andme.com/research/" target="_blank" rel="noreferrer noopener">Participate in the next discovery</a></p>



<div style="width: 100%; margin: 0 auto; text-align: justify; background-color: #eee; padding: 15px;">
<h4>About the Author</h4>
<p><strong>James Ashenhurst</strong>, Ph.D. — Sr. Scientist I, Product R&#038;D
</p>
<p>Dr. Ashenhurst is a Senior Scientist at the 23andMe Research Institute who studies how health history, lifestyle, and genetics combine to predict risk for health conditions and differences in medication response.</p>
</div>



<h6 class="wp-block-heading"><strong>References</strong></h6>



<p>1. Montero, A., Sparks, G., Presiado, M. &amp; Hamel, L. <a href="https://www.kff.org/health-costs/kff-health-tracking-poll-may-2024-the-publics-use-and-views-of-glp-1-drugs/" target="_blank" rel="noreferrer noopener">KFF Health Tracking Poll May 2024: The Public’s Use and Views of GLP-1 Drugs</a> | KFF. </p>



<p>2. Wilding, J. P. H. <em>et al.</em> Once-Weekly Semaglutide in Adults with Overweight or Obesity. <em>New Engl J Med</em> <strong>384</strong>, 989–1002 (2021). <a href="https://pubmed.ncbi.nlm.nih.gov/33567185/" target="_blank" rel="noreferrer noopener">https://pubmed.ncbi.nlm.nih.gov/33567185/</a></p>



<p>3. Ryan, D. H. <em>et al.</em> Long-term weight loss effects of semaglutide in obesity without diabetes in the SELECT trial. <em>Nat Med</em> <strong>30</strong>, 2049–2057 (2024). <a href="https://pubmed.ncbi.nlm.nih.gov/38740993/" target="_blank" rel="noreferrer noopener">https://pubmed.ncbi.nlm.nih.gov/38740993/</a></p>



<p>4. Joy, Bethany, et al. Exploring the rates of Gastrointestinal adverse effects among five GLP-1 receptor agonists: A systematic review and Meta-Analysis of randomized controlled trials. <em>Endocrine</em> <strong>91</strong>(1), 23 (2026). <a href="https://pubmed.ncbi.nlm.nih.gov/41489846/" target="_blank" rel="noreferrer noopener">https://pubmed.ncbi.nlm.nih.gov/41489846/</a></p>



<p></p>


Sr. Scientist I, Product R&D

James Ashenhurst

Unlocking the Genetics of GLP-1 Medications: Why Your DNA Matters


<p><em>By Bertram Koelsch, Ph.D.</em></p>



<p>The more we learn about genetics, the more we realize how beautifully complex the story of human variation truly is. For many of us, our first introduction to genetics is in the classroom. As genomic science leaps forward, it is vital that science education keeps pace. A <a href="https://www.tandfonline.com/eprint/S9WVJXKE2DBYWHZGBIFV/full" target="_blank" rel="noreferrer noopener">recently published paper</a> in the <em>Journal of Science Teacher Education</em> highlights both the challenges and the exciting opportunities in updating how science is taught in order to reflect the complexity of modern genetics.</p>



<p>The 23andMe Research Institute is committed to more than just internal discovery; we aim to support and collaborate with professional educators in developing their own expertise in these complex principles. We were honored to have played a supporting role for these educators, and would like to share their work.</p>



<h2 class="wp-block-heading" id="h-the-challenge-teaching-complexity">The Challenge: Teaching Complexity</h2>



<p>The paper explores a fundamental shift in genetics education: moving from a &#8220;one-gene, one-trait&#8221; <a href="https://www.genome.gov/genetics-glossary/Mendelian-Inheritance" target="_blank" rel="noreferrer noopener">Mendelian model</a> to an understanding of complex traits that are influenced by hundreds or thousands of genetic variants working in tandem with environmental factors.</p>



<p>Teaching this complexity isn&#8217;t easy. This case study followed a &#8220;co-design process&#8221; involving a middle school science teacher and educators from the University of North Carolina at Greensboro and the <a href="https://www.exploratorium.edu/" target="_blank" rel="noreferrer noopener">Exploratorium</a> Museum in San Francisco working together to create professional activities for other science teachers to update how they teach more complex genetics.</p>



<p>Throughout this process the middle school teacher identified several challenges to teaching these complex topics, including:</p>



<ul class="wp-block-list">
<li>A lack of real-world examples tailored to hook students’ interest.</li>



<li>Nuanced word choices that can be confusing when describing the relationship between genes and a trait.</li>



<li>How and when to introduce core ideas and activities to help students build their understanding step-by-step.</li>
</ul>



<h2 class="wp-block-heading" id="h-a-collaborative-solution">A Collaborative Solution</h2>



<p>In order to find interesting examples to capture students&#8217; interest and to support further understanding of complex genetics, the co-design team was able to call on 23andMe Research Institute scientists to share data and real-world examples from research studies of complex traits. In the end the co-design team developed a <a href="https://www.exploratorium.edu/file/inheritance-its-more-complicated" target="_blank" rel="noreferrer noopener">classroom activity</a>, using height as a relevant example, to demonstrate the impact of multiple genetic variants on a trait.</p>



<figure class="wp-block-image size-large"><img loading="lazy" decoding="async" width="1024" height="578" src="/wp-content/uploads/2026/04/Figure2-Principles-of-a-polygenic-score-1024x578.png" alt="" class="wp-image-35182" srcset="https://blogcms.23andme.com/wp-content/uploads/2026/04/Figure2-Principles-of-a-polygenic-score-1024x578.png 1024w, https://blogcms.23andme.com/wp-content/uploads/2026/04/Figure2-Principles-of-a-polygenic-score-300x169.png 300w, https://blogcms.23andme.com/wp-content/uploads/2026/04/Figure2-Principles-of-a-polygenic-score-768x434.png 768w, https://blogcms.23andme.com/wp-content/uploads/2026/04/Figure2-Principles-of-a-polygenic-score-880x497.png 880w, https://blogcms.23andme.com/wp-content/uploads/2026/04/Figure2-Principles-of-a-polygenic-score-1180x666.png 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /><figcaption class="wp-element-caption"><em>Example of materials shared by 23andMe with the co-design team.</em></figcaption></figure>



<p><strong>&#8220;By providing a space for teachers to work directly with scientists, we create opportunities for them to engage with authentic data and nuanced examples of complex inheritance,&#8221;</strong> said Hilleary Osheroff, of the Teacher Institute at the Exploratorium, one of the authors of this study.&nbsp;</p>



<p>Co-author Sara Porter, from the Teacher Education and Higher Education Department at University of North Carolina at Greensboro added, <strong>&#8220;This collaboration allows educators to bridge the gap between abstract theory and classroom practice without the need for extensive time in the laboratory, ultimately empowering them to bring the most current genomic science to their students.&#8221;</strong></p>



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



<p>The importance of robust science education throughout the K-12 years cannot be overstated. By providing students with a more accurate framework for how genetics works, we empower the next generation to better understand their own health and the diversity of the human experience.</p>



<p><strong>“At the 23andMe Research Institute, we believe that genetic literacy is a fundamental tool,”</strong> says Anne Greb, Director of Genomics Education at 23andMe. <strong>“Engaging in community projects like this that support early science education is a priority for us. By supporting teachers today, we are ensuring that the scientists, healthcare providers, and informed citizens of tomorrow have a clear-eyed understanding of the science that connects us all, from understanding their own traits and disease risks to recognizing the genetic relatedness that connects people.”</strong></p>



<p>The responsive nature of the co-design process described in the paper shows that when scientists and teachers work together, they create a &#8220;resource-rich&#8221; environment. We are proud to have played a role in this research and remain dedicated to helping bridge the gap between the lab and the classroom.</p>



<p><strong>Interested in helping a young person in your life learn more about genetics? Check out more educational activities from the </strong><a href="https://www.exploratorium.edu/education/teacher-institute/phenomenal-genome-project" target="_blank" rel="noreferrer noopener"><strong>Exploratorium</strong></a><strong> and the 23andMe </strong><a href="https://education.23andme.com/" target="_blank" rel="noreferrer noopener"><strong>Genetics Learning Hub</strong></a><strong>.</strong></p>



<div style="width: 100%; margin: 0 auto; text-align: justify; background-color: #eee; padding: 15px;">
<h4>About the Author</h4>
<p><strong>Bertram Koelsch</strong>, Ph.D. — Director, Product Research &#038; Development
</p>
<p> 
Dr. Bertram Koelsch leads a team of R&#038;D scientists at 23andMe whose work spans the full breadth of the 23andMe experience — from genetic ancestry and relative matching to consumer health insights. Drawing on machine learning and the insights unlocked by 23andMe&#8217;s vast base of research-consented participants, his team builds models that deepen what customers can learn about themselves. With a Ph.D. in Bioengineering from UC Berkeley and UCSF, he brings a rigorous scientific foundation to the challenge of making genetics meaningful and actionable for everyone. At heart, Dr. Koelsch thinks of himself as an engineer — someone driven not just by scientific discovery, but by the desire to build things that tangibly improve people&#8217;s lives. That ethos runs through everything his team does, for example, ensuring polygenic risk scores can empower consumers to take a more proactive role in their own health.</p>
</div>


Bertram Koelsch

Teaching Complex Genetics to Kids: What a New Study Says Works


<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>Proactive Risk Detection: 82% of participants were unaware of their genetic risks prior to testing, showing that direct-to-consumer genetic testing identifies high-impact health risks often missed by traditional clinical screening.</li>
<li>High Medical Follow-Through: When members shared results with healthcare professionals, it led to 86% of them receiving at least one medical recommendation, ranging from screenings all the way up to preventive surgeries, with an impressive 88% patient adherence rate.</li>
<li>Bridging the Gap: There is a significant opportunity to better educate healthcare professionals, particularly primary care providers, and encourage the 54% of members who haven&#8217;t yet shared their results to do so.</li></ul>
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<p>Every day, people turn to 23andMe to better understand how their genetics can impact their health. While our DNA kits offer a wealth of information, for many, the most critical discovery is a high-impact health result that can be addressed through personalized medical action.</p>



<p>To understand how these insights translate into real-world care, researchers at 23andMe recently studied over 1,000 consenting participants who received results for medically actionable conditions, such as hereditary cancers and cardiovascular diseases. We wanted to know: are people turning this data into action? The short answer is yes.</p>



<p><a href="https://www.sciencedirect.com/science/article/pii/S2949774426009003" target="_blank" rel="noreferrer noopener">Our results</a>, recently published in <em><a href="https://www.sciencedirect.com/journal/genetics-in-medicine-open" target="_blank" rel="noreferrer noopener">Genetics in Medicine Open</a></em>, demonstrate that these high-impact findings are serving as a catalyst for proactive health management. Here are the key takeaways from the study.</p>



<h2 class="wp-block-heading" id="h-people-are-finding-unknown-health-risks">People are finding unknown health risks</h2>



<p>This study found that most individuals who had a medically actionable genetic variant identified through 23andMe were unaware of their genetic risk beforehand. In fact, 82% of them had no prior clinical genetic testing for that variant, even though most (68%) reported a personal or family history of a related health condition.</p>



<p>These findings are a reminder that most genetic testing is only ordered to help diagnose those who are already sick or those with a strong family history of a condition. And even then, people who do qualify for genetic testing are often missed by the healthcare system<sup>[1][2]</sup>. The findings of this study are important because it shows that direct-to-consumer genetic testing can identify people who might otherwise go undetected through traditional healthcare channels.</p>



<h2 class="wp-block-heading" id="h-genetic-results-drive-real-medical-action">Genetic results drive real medical action</h2>



<p>The most exciting finding? Genetic results don’t just provide new insights, they spur real-world change. When people took their genetic results to a healthcare professional, it often led to important, personalized health actions. Almost 1,500 medical recommendations, including follow-up blood testing, cancer screenings, starting medications and preventive surgery, were made by healthcare professionals based on individuals’ genetic results.</p>



<p>And once those recommendations were given, people followed them! The overall adherence to medical recommendations was high at 88%. Whether it was a recommendation for earlier screenings, medication, or even prophylactic surgery, people followed their doctor’s medical advice and took action based on their genetic results.</p>



<h2 class="wp-block-heading" id="h-there-are-opportunities-for-an-even-greater-benefit">There are opportunities for an even greater benefit</h2>



<p>While the findings are overwhelmingly positive, the study also identified a few specific ways we can help more people turn high-impact results into meaningful health actions.</p>



<ul class="wp-block-list">
<li><strong>Sharing results with doctors:</strong> Less than half of the research participants (46%) in this study reported sharing their results with a healthcare professional. The good news is that for those who did share, 86% received at least one medical recommendation. This means there is a big opportunity to encourage more people to share genetic results with their doctors and for us to make it easier to do so.</li>



<li><strong>Educating healthcare professionals on genetic testing:</strong> We found a gap in how participants felt about their interactions with different types of healthcare professionals. Those who shared results with a specialist were more likely to say that specialists (such as oncologists or cardiologists) were knowledgeable about their results compared to those who shared results with their primary care provider. This highlights a need for more education about genetic testing, especially for frontline primary care providers. Good news, this is exactly what we plan to do. Building on years of engagement with healthcare professionals, the 23andMe Research Institute plans to continue to develop and expand our education and clinical support resources to empower healthcare professionals to turn genetic data into better patient care.</li>



<li><strong>Addressing health inequity:</strong> This study also uncovered a potential disparity. Individuals with variants in the <em>TTR</em> gene, which were more common in non-White individuals, had the lowest rates of prior genetic testing and were less likely to receive medical recommendations after sharing their results with a healthcare professional. This is a critical insight that informs how direct-to-consumer genetic testing could help uncover and address health inequities, especially for conditions that are more common in historically underserved communities.</li>
</ul>



<h2 class="wp-block-heading" id="h-the-takeaway">The takeaway</h2>



<p>This study provides powerful evidence that direct-to-consumer genetic testing can make meaningful differences in the healthcare actions taken by individuals and their doctors. High-impact genetic results that are easily accessible and understandable can empower individuals with critical health insights, which, when shared with a healthcare professional, can personalize their care and lead to life-changing preventive actions!</p>



<h3 class="wp-block-heading" id="h-references">References:</h3>



<p>[1] Childers CP et al. (2017). “National Estimates of Genetic Testing in Women With a History of Breast or Ovarian Cancer.” J Clin Oncol. <a href="https://pubmed.ncbi.nlm.nih.gov/28820644/">https://pubmed.ncbi.nlm.nih.gov/28820644/</a>&nbsp;</p>



<p>[2] Manickam K et al. (2018). “Exome Sequencing-Based Screening for BRCA1/2 Expected Pathogenic Variants Among Adult Biobank Participants.” JAMA Netw Open. <a href="https://pubmed.ncbi.nlm.nih.gov/30646163/">https://pubmed.ncbi.nlm.nih.gov/30646163/</a></p>



<p></p>


A photo of a doctor showing a patient information on a digital tablet.

Stacey Detweiler

New Research Demonstrates: 23andMe Members are Taking Action on Their Health


<p>Since 2014, a powerful collaboration between <a href="https://palmerlab.org/" target="_blank" rel="noreferrer noopener">Abraham Palmer, Ph.D.</a> and <a href="https://www.sanchezroigelab.org/" target="_blank" rel="noreferrer noopener">Sandra Sanchez-Roige, Ph.D.</a> at the University of California San Diego (UCSD) and 23andMe has been at the forefront of understanding how our DNA influences complex human behaviors. This enduring partnership has yielded groundbreaking insights published in high-impact journals such as <em>Nature Neuroscience</em>, the <em>American Journal of Psychiatry</em>, and others. Some of these studies include the <a href="https://blog.23andme.com/articles/wait-new-genetic-research-impulsivity" target="_blank" rel="noreferrer noopener">first-ever genome-wide association study of delay discounting</a> (the tendency to devalue larger future rewards in favor of smaller more immediate rewards), identification of more than a <a href="https://blog.23andme.com/articles/the-genetics-of-alcoholism" target="_blank" rel="noreferrer noopener">dozen variants associated with alcohol use disorder</a>, the discovery of the shared genetic associations between <a href="https://blog.23andme.com/articles/the-genetics-of-loneliness-and-its-impact-on-health" target="_blank" rel="noreferrer noopener">loneliness and other health conditions</a>, and one of the <a href="https://blog.23andme.com/articles/new-genetic-insights-into-cannabis-use" target="_blank" rel="noreferrer noopener">largest genetic studies on cannabis use</a>.&nbsp;</p>



<figure class="wp-block-image size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="761" src="/wp-content/uploads/2026/02/Palmer-and-Sanchez-Roige-1024x761.jpg" alt="" class="wp-image-34870" style="width:533px;height:auto" srcset="https://blogcms.23andme.com/wp-content/uploads/2026/02/Palmer-and-Sanchez-Roige-1024x761.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2026/02/Palmer-and-Sanchez-Roige-300x223.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2026/02/Palmer-and-Sanchez-Roige-768x571.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2026/02/Palmer-and-Sanchez-Roige-880x654.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2026/02/Palmer-and-Sanchez-Roige-1180x877.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2026/02/Palmer-and-Sanchez-Roige.jpg 2018w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



<h2 class="wp-block-heading" id="h-a-shared-pursuit-of-knowledge">A Shared Pursuit of Knowledge</h2>



<p>At its core, this collaboration is driven by a shared vision: to identify the genetic underpinnings of behaviors that significantly impact human health. The goal is not just academic; it&#8217;s about identifying novel insights that can lead to better prevention, intervention, and treatment strategies for individuals struggling with substance use disorders. By understanding the genetic factors that contribute to these complex traits, researchers can pave the way for more personalized and effective approaches.</p>



<h2 class="wp-block-heading" id="h-the-heart-of-the-research">The Heart of the Research</h2>



<p>These remarkable discoveries would be impossible without the generous contributions of 23andMe research participants. Millions of individuals have voluntarily consented to share their de-identified genetic and health data, providing the large sample sizes that are necessary to identify subtle yet significant genetic associations. This collective effort is the engine driving some of the largest behavioral genetic studies ever conducted.&nbsp;</p>



<h2 class="wp-block-heading" id="h-a-testament-to-enduring-science">A Testament to Enduring Science</h2>



<p>Science, by its very nature, takes time. New discoveries often lead to new questions, fueling further exploration. The 12-year span of this partnership is a testament to the dedication and long-term vision of both 23andMe and Drs. Palmer and Sanchez-Roige. It represents a sustained commitment to tackling some of the most challenging questions in human behavior, a commitment that continues to bear fruit.</p>



<h2 class="wp-block-heading" id="h-proven-through-peer-reviewed-science">Proven Through Peer-Reviewed Science</h2>



<p>The collaboration’s journey began when the first of three surveys was developed and deployed to 23andMe research participants in 2014. Just three years later, in 2017, the first <a href="https://pubmed.ncbi.nlm.nih.gov/29058377/" target="_blank" rel="noreferrer noopener">peer-reviewed publication</a> from this collaboration was published, showing that the online survey taken by 23andMe research participants can effectively be used to identify genetic factors underlying alcohol use disorder.&nbsp;</p>



<p>Since 2017, the momentum has only grown, with 16 additional papers already published and many more on the horizon. These papers represent a significant contribution to the global scientific community and stand as a direct result of the millions of research participants who have contributed their data and time.</p>



<h2 class="wp-block-heading">Trusted Partners</h2>



<p>From the perspective of Drs. Palmer and Sanchez-Roige, the decision to work with, and crucially, <em>continue</em> working with 23andMe for over a decade speaks volumes about the company&#8217;s rigorous research standards and commitment to scientific excellence.</p>



<p>&#8220;23andMe offers an unparalleled resource for genetic research,&#8221; says <a href="https://blog.23andme.com/articles/abraham-palmer-ucsd" target="_blank" rel="noreferrer noopener">Dr. Palmer</a>. &#8220;Their commitment to data privacy, ethical research, and the scale of their participant base makes them an ideal collaborator for tackling novel genetic questions that would be nearly impossible to answer elsewhere.&#8221;</p>



<p>&#8220;One of the reasons we’ve sustained this partnership for over a decade is 23andMe’s commitment to ethical oversight,&#8221; continues Dr. Palmer. &#8220;Every study we conduct is overseen by an independent Institutional Review Board (IRB), ensuring that participant privacy and informed consent are always the top priority. It allows us to focus on our research questions because we know 23andMe has systems in place to uphold the highest ethical standards.&#8221;</p>



<p>&#8220;What makes 23andMe a truly unique research environment is the strong engagement of the participants,&#8221; says Dr. Sanchez-Roige. &#8220;Unlike traditional studies that might take years to recruit a few hundred people, we can deploy a survey and receive thousands of thoughtful responses in a matter of days. This agility allows us to ask entirely new questions about behavior and environment, collecting the rich phenotypic data necessary to understand complex issues like aspects related to opioid use in ways we never could before.&#8221;</p>



<p>Dr. Sanchez-Roige continues, &#8220;working with the 23andMe Research Institute is more than just having access to a database; it has been a productive collaboration with outstanding colleagues. And the research participants are also devoted to contributing to science, meaning we aren&#8217;t just looking at static data; we are actively learning from millions of people who are as interested in these scientific answers as we are.&#8221;</p>



<h2 class="wp-block-heading">Looking Ahead</h2>



<p>As this research moves into the next phase of this partnership, the focus is expanding beyond genetics alone. Dr. Palmer says, &#8220;our recent work has demonstrated that answers to survey questions — even without genetic data — are powerful predictors for identifying individuals at risk for opioid use disorder.&#8221; Dr. Sanchez-Roige adds, &#8220;The data we’ve collected argues strongly for using a few questions to flag a small subset of individuals who are at high risk for opioid addiction before it&#8217;s too late. This project is ongoing, our survey on opioid use is still available for 23andMe research participants as we seek to obtain 500,000 completed responses.&#8221;</p>



<h3 class="wp-block-heading">A Heartfelt Thank You to Our Participants</h3>



<p>The true scale of this achievement is best measured in the time and dedication of research participants. &#8220;To put it in perspective, a single 15-minute survey that receives 500,000 responses represents the equivalent of 14.25 years of research participant time!&#8221; says Dr. Palmer. The ability to crowdsource data at this scale, in genotyped individuals, is what makes the 23andMe Research Institute a trusted research partner and a global leader in genetics and behavioral science.</p>



<p>The insights gained over the last 12 years are already reshaping how we understand the human experience. As we continue to ask new questions and uncover new associations, we move closer to a world where substance use disorders are met with better tools, deeper empathy, and more effective treatments.</p>



<p>Complete the <a href="https://you.23andme.com/research/surveys/opioid_pain_medication/" target="_blank" rel="noreferrer noopener">Opioid Pain Medication Survey</a> to help advance research efforts focused on the connection between genes and opioids.</p>



<p><em>Reference to UC San Diego does not imply endorsement or support of any product, service or company involved.</em></p>



<div style="max-width: 750px; width: 100%; margin: 0 auto; text-align: justify; background-color: #eee; padding: 15px;">
<h4>About the Collaborators</h4>
<p><strong>Abraham Palmer</strong>, Ph.D.
</p>
<p> 
Dr. Abraham Palmer is a Professor in the Department of Psychiatry at the University of California San Diego. His current research emphasizes leveraging large-scale human genetic datasets alongside powerful preclinical models to identify risk genes, map biological pathways, and translate genetic discoveries into a deeper mechanistic understanding of addiction and related psychiatric outcomes. He has been a member of 23andMe since 2012 and has completed more surveys than 99% of 23andMe research participants. He is an avid cyclist who lives in San Diego, California with his wife, two teenaged children, two cats and one dog.
<br><a href="https://palmerlab.org/" target="_blank" rel="noreferrer noopener">www.palmerlab.org</a></p>
<p><strong>Sandra Sanchez-Roige</strong>, Ph.D.
</p>
<p> 
Dr. Sandra Sanchez-Roige is an Associate Professor in the Department of Psychiatry at the University of California San Diego. Her research focuses on identifying the biological drivers that place people at risk for substance use disorders using genetics, genomics, medical bioinformatics, and cross-species translational approaches. She has been a member of 23andMe since 2016, is “likely to prefer chocolate over vanilla ice cream” and has a variant in the ACTN3 gene that means her “muscle composition is common in elite power athletes”, according to 23andMe reports. She co-leads the Sanchez-Roige Lab with Lisa, a talented British Shorthair cat, and Margot, a curious six-year-old girl, and Victor, a partner, slide beta-tester, and conference travel companion.
<br><a href="https://www.sanchezroigelab.org/" target="_blank" rel="noreferrer noopener">https://www.sanchezroigelab.org</a></p>
</div>



<p></p>



<figure class="wp-block-table"><table class="has-fixed-layout" style="border:1px solid #000; border-collapse:collapse;"><tbody><tr><td>
<h3 class="wp-block-heading">Publications:</h3>
<ol>
<li>Sanchez-Roige, S et al. <a href="https://pubmed.ncbi.nlm.nih.gov/29058377/" target="_blank" rel="noreferrer noopener">“Genome-wide association study of alcohol use disorder identification test (AUDIT) scores in 20 328 research participants of European ancestry.”</a> <em>Addiction Biology</em> vol. 24,1 (2019): 121-131.</li>
<li>Sanchez-Roige, S et al. <a href="https://pubmed.ncbi.nlm.nih.gov/29230059/" target="_blank" rel="noreferrer noopener">“Genome-wide association study of delay discounting in 23,217 adult research participants of European ancestry.”</a> <em>Nature Neuroscience</em> vol. 21,1 (2018): 16-18.</li>
<li>Pasman, J A et al. <a href="https://pubmed.ncbi.nlm.nih.gov/30150663/" target="_blank" rel="noreferrer noopener">“GWAS of lifetime cannabis use reveals new risk loci, genetic overlap with psychiatric traits, and a causal influence of schizophrenia.”</a> <em>Nature Neuroscience</em> vol. 21,9 (2018): 1161-1170.</li>
<li>Sanchez-Roige, S et al. <a href="https://pubmed.ncbi.nlm.nih.gov/30336701/" target="_blank" rel="noreferrer noopener">“Genome-Wide Association Study Meta-Analysis of the Alcohol Use Disorders Identification Test (AUDIT) in Two Population-Based Cohorts.”</a> The <em>American Journal of Psychiatry</em> vol. 176,2 (2019): 107-118.</li>
<li>Sanchez-Roige, S et al. <a href="https://pubmed.ncbi.nlm.nih.gov/30718321/" target="_blank" rel="noreferrer noopener">“Genome-Wide Association Studies of Impulsive Personality Traits (BIS-11 and UPPS-P) and Drug Experimentation in up to 22,861 Adult Research Participants Identify Loci in the CACNA1I and CADM2 genes.”</a> <em>J Neurosci.</em> vol. 39,13 (2019): 2562-2572.</li>
<li>Karlsson Linnér, R et al. <a href="https://pubmed.ncbi.nlm.nih.gov/30643258/" target="_blank" rel="noreferrer noopener">“Genome-wide association analyses of risk tolerance and risky behaviors in over 1 million individuals identify hundreds of loci and shared genetic influences.”</a> <em>Nature Genetic</em>s vol. 51,2 (2019): 245-257.</li>
<li>Abdellaoui, A et al. <a href="https://pubmed.ncbi.nlm.nih.gov/31518406/" target="_blank" rel="noreferrer noopener">“Phenome-wide investigation of health outcomes associated with genetic predisposition to loneliness.”</a> <em>Human Molecular Genetics</em> vol. 28,22 (2019): 3853-3865.</li>
<li>Dennis, J et al. <a href="https://pubmed.ncbi.nlm.nih.gov/31796895/" target="_blank" rel="noreferrer noopener">“Genetic risk for major depressive disorder and loneliness in sex-specific associations with coronary artery disease.”</a> <em>Molecular Psychiatry</em> vol. 26,8 (2021): 4254-4264.</li>
<li>Gustavson, D E et al. <a href="https://pubmed.ncbi.nlm.nih.gov/32716714/" target="_blank" rel="noreferrer noopener">“The Latent Genetic Structure of Impulsivity and Its Relation to Internalizing Psychopathology.”</a> <em>Psychological Science</em> vol. 31,8 (2020): 1025-1035.</li>
<li>Sanchez-Roige, S et al. <a href="https://pubmed.ncbi.nlm.nih.gov/34728798/" target="_blank" rel="noreferrer noopener">“Genome-wide association study of problematic opioid prescription use in 132,113 23andMe research participants of European ancestry.”</a> <em>Molecular Psychiatry</em> vol. 26,11 (2021): 6209-6217.</li>
<li>Sanchez-Roige, S et al. <a href="https://pubmed.ncbi.nlm.nih.gov/37173343/" target="_blank" rel="noreferrer noopener">“CADM2 is implicated in impulsive personality and numerous other traits by genome- and phenome-wide association studies in humans and mice.”</a> <em>Translational Psychiatry</em> vol. 13,1 167 (2023).</li>
<li>Gustavson, D E et al. <a href="https://pubmed.ncbi.nlm.nih.gov/39323941/" target="_blank" rel="noreferrer noopener">“Executive Function and Impulsivity Predict Distinct Genetic Variance in Internalizing Problems, Externalizing Problems, Thought Disorders, and Compulsive Disorders: A Genomic Structural Equation Modeling Study.”</a> <em>Clin Psychol Sci.</em> vol. 12,5 (2024): 865-881.</li>
<li>Thorpe, H H A et al. <a href="https://pubmed.ncbi.nlm.nih.gov/38858598/" target="_blank" rel="noreferrer noopener">“Genome-wide association studies of coffee intake in UK/US participants of European ancestry uncover cohort-specific genetic associations.”</a> <em>Neuropsychopharmacology</em> vol. 49,10 (2024): 1609-1618.</li>
<li>Jennings, M V et al. <a href="https://pubmed.ncbi.nlm.nih.gov/38580523/" target="_blank" rel="noreferrer noopener">“A phenome-wide association and Mendelian randomisation study of alcohol use variants in a diverse cohort comprising over 3 million individuals.”</a> <em>EBioMedicine</em> vol. 103 (2024): 105086.</li>
<li>Mallard, T T et al. <a href="https://pubmed.ncbi.nlm.nih.gov/41152253/" target="_blank" rel="noreferrer noopener">“Characterizing the Pleiotropic Architecture of Impulsivity and Its Links to Psychopathology and Neurodevelopment.”</a> <em>The American Journal of Psychiatry</em> vol. 183,1 (2026): 31-47.</li>
<li>Thorpe, H H A et al. <a href="https://pubmed.ncbi.nlm.nih.gov/41077612/" target="_blank" rel="noreferrer noopener">“Genome-wide association studies of lifetime and frequency of cannabis use in 131,895 individuals.”</a> <em>Molecular Psychiatry</em> vol. 31,2 (2026): 1061-1073.</li>
<li>Thorpe, H H A et al. <a href="https://pubmed.ncbi.nlm.nih.gov/41286433/" target="_blank" rel="noreferrer noopener">“Genome-wide association study of delay discounting identifies 11 loci and reveals transdiagnostic associations across mental and physical health.”</a> <em>Molecular Psychiatry</em>, 10.1038/s41380-025-03356-8. (2025).</li>
</ol>
</td></tr></tbody></table></figure>



<p></p>


23andMe Blog

23andMe Blog Team

A Decade of Discovery: Unraveling the Genetics of Behavior with 23andMe and UCSD




<p>Black History Month is a time to honor the resilience and contributions of the Black community. At the 23andMe Research Institute, we recognize that our understanding of human health and genetics is deeply rooted in the participation of people of African descent, whose contributions are essential to shaping one of the most diverse genetic research cohorts in the world.</p>



<p>Despite decades of progress in genetics, people of African descent <a href="https://pubmed.ncbi.nlm.nih.gov/39694036/" target="_blank" rel="noreferrer noopener">remain vastly underrepresented in biomedical research</a>. That gap limits what science can uncover and who ultimately benefits from those discoveries. </p>



<p>Through member participation and programs aimed at <a href="https://www.23andme.com/global-genetics/" target="_blank" rel="noreferrer noopener">increasing research representation from certain global regions</a>, today, the 23andMe Research Institute is proud to host the world’s largest genetic research cohort of individuals with African ancestry reflecting the deep genetic diversity of African and African American communities and humanity as a whole. This diversity of research participants helps to drive discoveries that benefit all of us.</p>



<h2 class="wp-block-heading" id="h-from-participation-to-personal-insights">From Participation to Personal Insights</h2>



<p>It&#8217;s important that the new insights generated from our members&#8217; contributions to research are returned to you. The contributions of consented Black and African American research participants has led to significant enhancements in the member experience. For example:</p>



<ul class="wp-block-list">
<li><strong>Expanded Genetic Groups:</strong> Over 250 Genetic Groups in <a href="https://blog.23andme.com/articles/a-new-era-for-african-genetic-groups-at-23andme" target="_blank" rel="noreferrer noopener">Africa</a>, more than 200 <a href="https://blog.23andme.com/articles/new-23andme-update-connects-many-african-american-customers-to-southern-roots" target="_blank" rel="noreferrer noopener">African American</a> Genetic Groups, and 19 <a href="https://blog.23andme.com/articles/23andme-adds-more-detail-for-afro-caribbean-ancestry" target="_blank" rel="noreferrer noopener">Afro-Caribbean</a> Genetic Groups that have come as a direct result of more diverse data from 23andMe customers who have consented to participate in research.</li>



<li><strong>Targeted Health Reports:</strong> Through the years we have delivered insights into traits and conditions that disproportionately affect the Black and African American community, such as <a href="https://www.23andme.com/topics/carrier/sickle-cell-anemia/" target="_blank" rel="noreferrer noopener">sickle cell anemia</a>, <a href="https://www.23andme.com/topics/health-predispositions/g6pd-deficiency/" target="_blank" rel="noreferrer noopener">G6PD deficiency</a>, and <a href="https://blog.23andme.com/articles/the-duffy-antigen-gene-a-clue-behind-white-blood-cell-differences" target="_blank" rel="noreferrer noopener">Duffy antigen status</a>.</li>
</ul>



<p>But the impact of this research community extends far beyond individual reports and features for our members. It is fundamentally advancing what humanity knows about itself.</p>



<h2 class="wp-block-heading" id="h-global-impact-landmarks-in-research">Global Impact: Landmarks in Research</h2>



<p>By choosing to participate in our research program, our members are helping rewrite history books and shape the future of medicine. Here are a few ways our research cohort is making an impact:</p>



<h3 class="wp-block-heading" id="h-1-uncovering-lost-history">1. Uncovering Lost History</h3>



<p>23andMe researchers used DNA to connect living people to enslaved and free African Americans buried at the <a href="https://catoctinfurnace.org/ironworker/" target="_blank" rel="noreferrer noopener">Catoctin Furnace</a> historical site. This <a href="https://blog.23andme.com/articles/historical-dna-connection-to-early-enslaved-and-free-african-americans" target="_blank" rel="noreferrer noopener">landmark work</a> shows how DNA can be used to both restore some knowledge of the individuals buried at sites like this, as well as help bridge the gap left by missing historical records to living descendants, restoring stories that time and systemic erasure tried to hide.</p>



<p style="padding-left: 20pt">Harney, Éadaoin et al. “The genetic legacy of African Americans from Catoctin Furnace.” Science (New York, N.Y.) vol. 381,6657 (2023): eade4995. doi:10.1126/science.ade4995</p>



<h3 class="wp-block-heading" id="h-2-mapping-the-transatlantic-legacy">2. Mapping the Transatlantic Legacy</h3>



<p>Our large-scale study on the <a href="https://blog.23andme.com/articles/transatlantic-slave-trade" target="_blank" rel="noreferrer noopener">transatlantic slave trade</a> provided a deeper look into the genetic impact of the Middle Passage. By analyzing the genomes of over 50,000 research participants, we’ve been able to better understand the regional origins and the complex history of the African diaspora in the Americas. Ultimately, this research may empower participants to reconnect to histories that were severed by the transatlantic slave trade.</p>



<p style="padding-left: 20pt">Micheletti, Steven J et al. “Genetic Consequences of the Transatlantic Slave Trade in the Americas.” American journal of human genetics vol. 107,2 (2020): 265-277. doi:10.1016/j.ajhg.2020.06.012</p>



<h3 class="wp-block-heading" id="h-3-refining-understanding-of-sickle-cell-trait">3. Refining Understanding of Sickle Cell Trait</h3>



<p>Our research study of <a href="https://blog.23andme.com/articles/new-genetic-research-on-sickle-cell-trait" target="_blank" rel="noreferrer noopener">sickle cell trait</a> was the largest and most diverse study of this trait, and included more than 4 million consented research participants. This important study showed that those with sickle cell trait (meaning people who carry one copy of the HbS variant in the HBB gene) do have a slightly increased likelihood of developing harmful blood clots. However, the magnitude of that risk is still below other genetic factors (such as Factor V Leiden) that are also known to increase the risk of harmful blood clots. While having sickle cell trait is typically considered being a carrier without any impact to your own health, this research shows that the estimated eight to 10 percent of African Americans who have sickle cell trait may benefit from knowing about potential risks (especially in other situations that may increase the chances of harmful blood clots, such as surgeries or hospitalizations). </p>



<p><strong>Learn more about <a href="https://www.23andme.com/sickle-cell-awareness-program/" target="_blank" rel="noreferrer noopener">the Sickle Cell Carrier Status Awareness Program</a>.</strong></p>



<p style="padding-left: 20pt">Lin, Keng-Han et al. “Ancestry-independent risk of venous thromboembolism in individuals with sickle cell trait vs factor V Leiden.” Blood advances vol. 8,21 (2024): 5710-5718. doi:10.1182/bloodadvances.2024014252</p>



<h2 class="wp-block-heading" id="h-ongoing-need-for-research">Ongoing need for research</h2>



<p>Scientific progress must benefit everyone and to do that we must continue to engage diverse participants in research. We remain committed to ongoing research and collaboration with the Black and African American community to advance understanding of conditions that particularly impact them. One ongoing example is the <a href="https://www.23andme.com/genetic-insights-into-colorectal-cancer-black-community/" target="_blank" rel="noreferrer noopener">genetic insights into colorectal cancer in the Black community</a> study. Launched in collaboration with the Colorectal Cancer Alliance, the study aims to shed light on the genetics of colorectal cancer, which Black and African Americans are <a href="https://colorectalcancer.org/basics/facts-and-statistics" target="_blank" rel="noreferrer noopener">about 15% more likely to develop and 35% more likely to die</a> from compared to non-Hispanic white Americans. This study is one of many critical steps toward closing the health disparity gap. This data ensures that the next generation of treatments and preventative care is designed with <em>all</em> populations in mind.</p>



<h2 class="wp-block-heading" id="h-the-power-of-the-research-model">The Power of the Research Model</h2>



<p>This is the heart of the 23andMe Research Institute: a cycle of participation and discovery. Members contribute their data and their time to research. That research leads to new scientific insights. And those insights are then returned, through new reports, features, knowledge, and publications to the very people who made the discoveries possible.&nbsp;</p>



<p>If members choose to contribute to research, they aren&#8217;t just a participant; they are a collaborator. Their contribution fuels a cycle that makes the world’s largest genetic database of individuals with African ancestry even more representative and more useful for everyone.</p>



The Power of Representation in Genetic Research




<p>Fear and anxiety are part of a threat-response system that is essential for survival. But for up to one in three people this system can become dysregulated, leading to anxiety disorders like generalized anxiety disorder, panic disorder, and phobias.</p>



<p>Researchers have known these conditions have a genetic component and can run in families, but the exact genetic underpinnings have been hard to identify. Now, <a href="https://www.nature.com/articles/s41588-025-02485-8" target="_blank" rel="noreferrer noopener">a new study</a>, led by researchers from the Anxiety Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ANX), has identified dozens of new genetic variants linked to anxiety disorders, and data from millions of consented 23andMe research participants was used to confirm their findings.</p>



<h2 class="wp-block-heading" id="h-the-hunt-for-anxiety-associated-genetic-variants">The Hunt for Anxiety-Associated Genetic Variants</h2>



<p>To find the genetic variants involved in complex traits like anxiety disorders, scientists need a lot of study participants. To get this large group, the researchers combined data from 36 different studies of people from Europe, the United States, and Australia. In total they had 122,225 people diagnosed with an anxiety disorder and 729,960 unaffected controls.&nbsp;</p>



<p>Then the researchers performed a genome-wide association meta-analysis, which scans the entire genome looking for genetic variants that are more common in people with anxiety disorders. By comparing the genomes of those with anxiety disorders to those without, the team identified 58 significant genetic variants associated with anxiety disorders.</p>



<h2 class="wp-block-heading" id="h-confirmation-the-critical-role-of-replication">Confirmation: The Critical Role of Replication</h2>



<p>Finding genetic variants associated with anxiety disorders is just the first step. To be confident it&#8217;s a <em>real</em> association and not a statistical fluke, results must be replicated in a completely independent group of people.</p>



<p>This is where the <a href="https://www.23andmeresearchinstitute.org/" target="_blank" rel="noreferrer noopener">23andMe Research Institute</a> came in. The researchers tested their 58 variants in a massive cohort of consented 23andMe research participants, which included 1,175,012 participants who self-reported having anxiety and 1,956,379 participants who reported they did not.</p>



<p>Of the 55 variants they could test, all showed the same direction effect as in the discovery study, and 51 were significantly replicated. This gives researchers high confidence that these genetic variants are genuinely associated with anxiety in this population.</p>



<h2 class="wp-block-heading" id="h-a-critical-reminder-about-ancestry-groups-and-diversity">A Critical Reminder About Ancestry Groups and Diversity</h2>



<p>The study&#8217;s next step is an important lesson for the future of genetic research. The team attempted to replicate their findings using data from over 30,000 African American participants in the Million Veteran Program.</p>



<p>The result? Of the 53 variants tested in this cohort, only 27 (about 51%) showed the same effect, a rate no better than random chance.</p>



<p>This is not a flaw in the study; it is a crucial finding. It demonstrates that genetic discoveries made in one group (in this case, people of European descent) do not always reliably apply to other groups. This underscores the urgent need for diverse populations to participate in future genetic studies to ensure that the scientific and medical benefits of this research can be shared by everyone.</p>



<h2 class="wp-block-heading" id="h-what-do-these-genes-do">What Do These Genes Do?</h2>



<p>Identifying the 58 genetic variants and replicating the finding was just the first step. Researchers also wanted to know what these variants do. Functional analysis provided a major clue.</p>



<p>The variants were found to be active in all major brain regions. More specifically, the results highlighted GABAergic signaling as a potential biological mechanism underlying anxiety disorders. GABA is the brain&#8217;s primary inhibitory neurotransmitter, meaning it is a chemical messenger that calms down brain activity.</p>



<p>This is particularly exciting because many current anti-anxiety medications (like benzodiazepines) work by targeting this exact system. And there are also other genes in the GABAergic signaling pathway that could be good targets for future drugs to treat anxiety disorders.</p>



<figure class="wp-block-image size-full is-resized"><img loading="lazy" decoding="async" width="481" height="208" src="/wp-content/uploads/2026/02/anxiety-Img.png" alt="" class="wp-image-34814" style="width:230px;height:auto" srcset="https://blogcms.23andme.com/wp-content/uploads/2026/02/anxiety-Img.png 481w, https://blogcms.23andme.com/wp-content/uploads/2026/02/anxiety-Img-300x130.png 300w" sizes="auto, (max-width: 481px) 100vw, 481px" /></figure>



<p>This study represents a major leap in our understanding of the genetic basis of anxiety. These 58 variants provide a foundational genetic basis that can guide scientists in future investigations into the biological pathways that lead to anxiety, with the ultimate hope of developing new and better treatments.</p>



<p><em>Learn more about 23andMe Research <a href="https://www.23andme.com/research/" target="_blank" rel="noreferrer noopener">here</a>. Research participants provided informed consent and volunteered to participate in the research online, under a protocol approved by the external, independent review board AAHRPP-accredited <a href="https://www.versiticlinicaltrials.org/salusirb" target="_blank" rel="noreferrer noopener">Salus IRB</a>.</em></p>



Research