Did you know 23andMe has published over 40 research papers on mental health? This Mental Health Awareness Month, we’re taking the opportunity to share some of what we have found.

We’ve spent years studying the DNA of millions of consented research participants, and with this powerful dataset we’ve been able to identify genetic variants linked to conditions like depression, bipolar disorder and obsessive-compulsive disorder. 

A rugged genetic landscape

The genetic underpinnings of mental health are complex, to say the least. There are potentially hundreds or thousands of genetic variants linked to any given condition, and it takes a huge community of research participants to uncover just a fraction of them. 

Over the years, as our research community has grown, it has enabled us and our academic collaborators to identify more and more genetic associations with psychiatric conditions. Those findings not only shed light on the biology of these conditions, but also pave the way for research seeking better treatments.

We’ve been working to ensure these studies include people of diverse ancestries, too, something that’s not only important to enable the development of treatments that work for everyone but has also been shown to power more and better genetic discoveries.

Breaking down silos

Our research has also gone beyond looking at single conditions to understand how the genetics of different mental health conditions may be related. Researchers have found that many psychiatric conditions have substantial genetic overlap with each other, and even with other kinds of health conditions. For example, studies of 23andMe consented research participants found that genetic variants linked to psychiatric conditions were also linked to chronic pain, alcohol use disorder and even endometriosis. 

The reasons for that are an ongoing topic of investigation, but one reason is that a single gene often has many roles in the body.

Filling in the broader picture

While genetics plays an important role in mental health, it’s by no means the only factor. Elements like one’s environment and stressful life experiences are important too. Of course, we’ve tackled this topic as well. 23andMe research participants respond to surveys on life experiences, health history and more, enabling studies like one that looked for ways individuals can lower their risk of depression and others seeking to understand who will experience treatment-resistant depression.

We’ve also been looking at how genetics can impact the body’s response to certain medications and lead to more side effects for some people. Researchers hope that this kind of information could help people find the best treatment for them, faster.

Research insights for real life

We also are working to return these genetic insights to our members. 23andMe+ Premium™ members receive genetic reports that provide insight into the likelihood of being diagnosed with depression, anxiety, bipolar disorder and more, based on the complex genetic associations uncovered in our research. Members can also learn whether they have genetic variants that can impact how their body processes certain medications, including certain antidepressants.

For many people, learning about all the factors that impact our and our families’ mental health — the combination of past and current stressors on a background of our unique genetics — can help illuminate a path forward to better well-being. In our research, we’ve found that learning of a genetic predisposition to depression doesn’t exacerbate symptoms of anxiety or depression, and our experience of communicating this information has shown us that many individuals find it both validating and empowering.

Today, it can take far too long to find an effective strategy for managing mental health symptoms, and the treatments that are available remain imperfect at best. It’s central to 23andMe Research Institute’s mission not only to enable research that moves the mental health field forward, but also to make insights from that research directly accessible to individuals. 

World Goth Day, celebrated every May 22nd, is typically a chance for fans of darkwave music, dramatic eyeliner and Victorian-inspired fashion to celebrate a subculture that has been going strong since the 1980s. This year, we’re marking the occasion with a slightly different kind of Goth story — one that predates the black lipstick by about 1,800 years.

This May, 23andMe is adding 35 individuals from a 2026 study to our Historical Matches^SM feature. These are not your weekend-festival Goths. These are the Goths, the actual Germanic people whose migrations and conflicts helped shape the final centuries of the Roman Empire.

Not the Same Goths (But Just as Interesting)

The modern goth subculture takes its name from the ancient Goths, though the connection is mostly aesthetic. The real Goths were a Germanic people who likely originated in Scandinavia and, over several centuries, migrated south through the Baltic region, eventually establishing themselves across a vast stretch of central and eastern Europe. By the 2nd century CE, Gothic communities occupied a dynamic frontier zone at the edge of the Roman Empire, trading with merchants to the south, maintaining ties with Baltic peoples to the north and absorbing influences from across an enormous geographic range.

Far from the brooding loners of pop culture imagination, the ancient Goths appear to have been remarkably cosmopolitan.

A Community at the Edge of the Roman World

The individuals we added to Historical Matches this month were buried at a cluster of cemeteries in the Hrubieszów Basin of eastern Poland, belonging to what archaeologists call the Masłomęcz group, a well-documented Gothic community of the Late Iron Age. The site was an ideal candidate for ancient DNA analysis in part because an unusually high proportion of its burials were inhumations (intact body burials rather than cremations), providing enough preserved skeletal material for genome-wide sequencing.

The study, published in Genome Biology earlier this year, analyzed 43 individuals buried across several of these cemeteries, dating from approximately the late 2nd to the mid-4th century CE. Of these individuals, 35 had high-quality DNA sequences, and they have now been added to the Historical Matches feature.

The DNA: Cosmopolitan from the Start

The genetic results confirmed that the community’s ancestry was primarily derived from a Scandinavian-like source population, consistent with the Goths’ proposed northern origins. But that’s where any expectation of uniformity ends.

A striking proportion of individuals carried genetic signatures characteristic of populations from the eastern Baltic, the Balkans and the eastern Mediterranean, and there were more than 30 distinct mitochondrial haplogroups represented among this small group of individuals. This shows that the community was actively absorbing outsiders from across a wide geographic range.

One individual stood out above all. Rather than the Scandinavian ancestry typical of his community, roughly half of his DNA traced to populations associated with the Iberian Peninsula, about a third to populations from Imperial Roman Italy and the remainder to the Carpathian Basin of present-day Hungary and Slovakia, with no detectable Scandinavian ancestry at all. That an individual with such distinctly southern European roots appears among the very earliest burials at the site is a remarkable testament to just how cosmopolitan this Gothic community was from its very beginnings.

Social Bonds Over Family Ties

Perhaps the most unexpected finding concerned how individuals were buried. Despite sharing graves, co-buried individuals showed no evidence of close kinship with one another. This finding suggests that in this community, burial groupings may have reflected social bonds rather than family relationships. It’s a rare glimpse into how Gothic social life may have been organized beyond the household.

Learn More

23andMe+ Premium™ members can explore whether they share a genetic link to these ancient Goths, and hundreds of other historical individuals, through the Historical Matches feature.

The 23andMe Health Summary is now available to customers participating in the Beta Testing Program*. 23andMe’s Health Summary uses AI to connect your genetics, blood labs, and lifestyle data to give you a clear, real-time picture of your health. Powered by 23andMe’s scientifically-backed AI model, it actively connects your genetic findings with your real-time lab results, surfacing the signals most worth paying attention to and discussing with your doctor. The result is a set of personalized, evidence-based recommendations giving you what you need to move from reactive to truly personalized preventative healthcare.

Why “Average” AI Falls Short

The potential of AI in healthcare is staggering, offering a future where disease is predicted rather than just treated. But to get there, we must answer this fundamental question: How can an AI truly “know” your health, if it doesn’t know your biology? Most health recommendations today still rely on “average” standards and protocols. But “average” increasingly doesn’t cut it in healthcare. 

At 23andMe, we believe the next era of medicine isn’t just about tracking your steps or one-off blood tests — it’s about closing the loop between your labs, lifestyle, and your genetics. Health data without genetic context is just numbers. 

The 23andMe perspective on Health AI

Today’s AI health tools are trained on everyone. They know what’s true for most people. But your genetics determine how much of that actually applies to you, and that gap is where 23andMe lives. Our approach is different. 23andMe benchmarks your health against your genetic peers — not just people with shared age and gender, but also ancestry and genetic risks. 

Dumping your data into a chatbot might tell you that walking 10,000 steps today is great. But if it is lacking your genetic data and the research insights for how to combine genetics and other kinds of data, those 10,000 steps might not be enough to move the needle on your specific risk. 

23andMe’s AI takes into account both your current biomarker signals and unique genetic tendencies to tell you where you are on your journey relative to the instructions your body was born with. 

Cut through the “data overload”

The Health Summary doesn’t just show your data, it tells you what levers to pull now to improve your health, given all of your data points combined. We focus on systems that greatly impact longevity and healthspan including heart health, metabolic health, and brain health.

Science-backed innovation

We know that accuracy and credibility are paramount in healthcare. That’s why our Health Summary is grounded in a proprietary framework developed by our scientific and clinical experts. This framework guides our AI in considering relevant sets of genetic results, lab values, and lifestyle data and interpreting them together appropriately. Based on this holistic picture, our AI will help you understand what areas warrant attention and how to stay on top of them. We’ve also developed specific safeguards to monitor that our AI stays true to the framework and is basing your Health Summary on established evidence.

Join our Beta Program

This is just the beginning. We will continue layering more health insights, and real-world context into your Health Summary, and will get more targeted with our insights (imagine a world where we define the exact lab value ranges you should target based on your genetics rather than relying on generic lab “normals”). Looking ahead, we see our Health Summary visualizing your health potential, showing you how much power you have to decrease your risk. We don’t just want to tell you you’re at risk, we tell you how much power you have to change that risk. 

The future of health isn’t just a chatbot where you dump information in and hope for new ideas. It’s a sophisticated synthesis of your unique biological code and real-world data, guided by experts. Your genes gave you the map, we’re here to help you lead the way. 

Join the 23andMe Beta program today to test the Health Summary. By sharing your feedback, you are helping us co-create a future where your health data becomes more understood, personalized, and actionable.

*Unfortunately this feature is not yet available on Android devices — we are working on it!

May is Asian American, Native Hawaiian and Pacific Islander Heritage Month, a time to celebrate the histories, cultures and contributions of communities whose roots span the Pacific. To mark the occasion, 23andMe is adding 31 new Vietnamese Genetic Groups to its Ancestry Composition feature, offering members with Vietnamese heritage their most detailed view yet of where in Vietnam their ancestors likely came from.

A Closer Look at Vietnamese Ancestry

Vietnam’s geography has long shaped its people. The country stretches more than 1,000 miles along the eastern edge of Southeast Asia, threading through highlands, river valleys and two great deltas. For centuries, those landscapes have channeled migration, trade and family ties, and they may show up in your DNA, too.

Genetic Groups are clusters of people who share more recent DNA with one another than with the broader population, often because their families lived in the same region for many generations. By analyzing patterns of shared DNA across thousands of 23andMe members of Vietnamese descent, our clustering algorithm identifies regional signatures finer than a single “Vietnamese” label can capture. If you have Vietnamese roots, you may now see groups anywhere from the Mekong Delta in the south to the Red River Delta in the north. These groups reflect the long shared history of families and communities, not modern political boundaries.

Most members with Vietnamese ancestry will receive at least one of these Genetic Groups, and 23andMe+ Premium™ members also get the ability to see groups they may have more distant matches to, opening a wider view of regional connections.

A Growing Picture of Asia

Vietnam joins a growing set of Asian representation in 23andMe’s Ancestry Composition. In recent years, 23andMe has added Genetic Groups in the Philippines, China, Korea and Mongolia, Japan and South Asia. 

More groups across Southeast Asia and the Pacific are on the way. 

There are also connections throughout Asia in the Historical Matches^SM feature, which compares your DNA to people who lived hundreds or even thousands of years ago. Recent additions include ancient individuals from southwest China and ancient China, a 6th-century cross-border couple and the mysterious skeletons of Roopkund Lake in the Himalayas. 

Connecting to Your Health Journey

Your ancestry is one part of the picture. 23andMe also offers reports on many health conditions relevant to people of Asian heritage, such as coronary artery disease, diabetes and high blood pressure. In addition, several 23andMe health reports examine specific genetic variants that are more common in certain Asian populations.

• The Nonsyndromic Hearing Loss and Deafness, DFNB1 (GJB2-Related) Carrier Status report* looks at variants in the GJB2 gene that can cause one of the most common inherited forms of hearing loss. Up to 1 in 4 people of East or Southeast Asian descent are carriers for this condition, and this report includes variants that are more common for them as well as those of South Asian descent.
• The CYP2C19 Drug Metabolism report** can tell you about genetic variants that can affect how your body processes certain medications for heart disease, depression, acid reflux, and other conditions. Some of these variants are more common in people of East Asian descent than in other populations. 
• The Alcohol Flush Reaction report examines a variant in the ALDH2 gene that’s common across East Asia and affects how the body breaks down a toxic byproduct of alcohol.

Expanding the Map of Asian Heritage and Health

The future of genetics depends on the diversity of stories powering it. This Asian American, Native Hawaiian and Pacific Islander Heritage Month, explore your Genetic Groups (new and old), Historical Matches and personalized reports, and see what your heritage reveals. 23andMe members who choose to participate help build a product that reflects the full breadth of the human experience. Already a 23andMe member? Sign in to discover your new regional connections, and celebrate your unique story.

* The 23andMe PGS test uses qualitative genotyping to detect select clinically relevant variants in the genomic DNA of adults for the purpose of reporting carrier status and reporting and interpreting genetic health risks. The relevance of each report may vary based on ethnicity. Our carrier status reports can be used to determine carrier status, but cannot determine if you have two copies of any genetic variant. These carrier reports are not intended to tell you anything about your risk for developing a disease in the future or anything about the health of your fetus, or your newborn child’s risk of developing a particular disease later in life. For certain conditions, we provide a single report that includes information on both carrier status and genetic health risk. The Nonsyndromic Hearing Loss and Deafness, DFNB1 (GJB2-Related) carrier status report is indicated for the detection of eight variants in the GJB2 gene. The report can tell you if you have two copies of some tested variants, and if you are at risk of having hearing loss related to DFNB1, but does not describe your overall risk of having DFNB1-related hearing loss. This test is relevant for people of many, but not all, ethnicities.

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

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’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.

Now, a new study published in Current Biology 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’s City, the researchers analyzed the genomes of 49 individuals buried in St. Mary’s City’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’s second governor.

A short lived colonial capital

Established in 1634, St. Mary’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’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 Ark and the Dove in late 1633, and arrived at Maryland’s southern shore the following year.

Though its role as a capital city was short-lived (the seat of government moved to present-day Annapolis in 1695), St. Mary’s City left a lasting mark on American history. The Chapel Field cemetery, located at the site of the colony’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.

Ancient DNA meets the world’s largest genetics database

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.

More than 1.3 million consented research participants share DNA with one or more of the St. Mary’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.

Tracking a documented migration in DNA

One of the study’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’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. 

When the research team mapped which 23andMe participants shared the closest genetic connections to the St. Mary’s individuals, they found enrichment around Louisville, Kentucky, highlighting the power of this approach.

Expanding the Calvert family tree

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

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.

A new approach to identifying the nameless dead

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.

The study team invited consented 23andMe research participants who shared the strongest genetic connections to the St. Mary’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.

Research built with community

Cutting-edge science wasn’t the only key to the success of this study. The early Maryland descendant community, including those who trace their lineage to the original Ark and Dove voyage, provided active support of the project.

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’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.

What this means for the future of ancient DNA research

The St. Mary’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.

As the United States approaches its 250th anniversary, this research underscores the enduring connections between the nation’s earliest European settlers and millions of living Americans.

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 Asthma and Allergy Foundation of America, 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.

A decade-plus of allergy and asthma genetic research

In 2013, 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 16 genetic variants 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.

A 2017 paper in Nature Genetics 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 2019 and 2020 pushed further, surfacing eleven additional variants in or near nine genes associated with allergies, and finding additional genetic variants associated with developing allergies, asthma and eczema at a very early age.

Digging more into age of onset, a 2019 analysis 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.

A 2023 multi-ancestry analysis 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’s a reminder that studying diverse populations matters for finding new genetic associations.

Insights don’t stop at the journal page

Discoveries from the 23andMe Research Institute don’t sit on a shelf. Many of them flow directly into the reports you can see in your 23andMe+ Premium™ account, including five that are especially relevant this month: Asthma and Eczema (Atopic Dermatitis), which can be found with other Health Predisposition reports, and Cat Allergy, Dog Allergy, and Seasonal Allergies*, which can be found with other Wellness reports.

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. 

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.

What you can do this allergy season

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.

• 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. 
• 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.
• 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.
• Talk to a clinician. If symptoms are persistent or affecting daily life, allergists and dermatologists have a growing toolkit of treatments.

The science that built today’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.

*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.

Here’s a sobering number to sit with: roughly one in five Americans will develop some form of skin cancer by age 70, making it the most common cancer 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.

The Genetic Story Behind Skin Cancer

Skin cancer isn’t one disease but several. Melanoma, though less common, is often more dangerous because it’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.

23andMe Research on Skin Cancer

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.

Key milestones from our research community include:

• A 2016 study that found 14 new genetic variants associated with BCC.
• A 2022 study that identified 19 additional BCC genetic variants and 15 SCC-associated genetic variants.
• Most recently, a study that was able to identify 36 new BCC genetic variants, 33 of which also showed associations with SCC risk.

Connecting the Dots: Polygenic Risk Scores

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. 

In 2021 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.

An Unexpected Connection

One of the more intriguing findings: genes that protect against vitiligo (the autoimmune condition that causes patches of skin to lose pigment) appear to increase skin cancer risk. This suggests that the same genetic “wiring” that tells your immune system how to interact with your skin’s pigment cells may also play a role in defending against skin cancer.

The 23andMe Skin Cancer Reports

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 Skin Cancer (Melanoma)* and Skin Cancer (Basal and Squamous Cell Carcinomas)** 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 23andMe+ Premium™ members.

These reports can’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.

The Gap in Genetic Research

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. 

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.

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 here.

What You Can Do

Genetics is one part of the story you can’t change, but almost everything else about skin cancer prevention is in your hands:

• Wear broad-spectrum sunscreen (SPF 30 or higher) daily, even when it’s cloudy, and reapply every two hours outdoors.
• Seek shade, especially between 10 a.m. and 4 p.m., when UV radiation is strongest.
• Skip tanning beds. Their UV exposure can contribute to melanoma and other skin cancers.
• Do a monthly self-check. 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.
• See a dermatologist for a full-body skin exam, especially if you have a personal or family history of skin cancer.

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

If you’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.

* 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.

** 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.

Two decades ago, a small team in California decided that the human genome shouldn’t belong only to researchers in white coats. It should belong to everyone. That bet changed the course of personal genomics, and on this DNA Day it’s worth celebrating just how far that vision has taken us.

The Beginning

When Anne Wojcicki and her co-founders launched 23andMe in 2006, the direct-to-consumer genetics industry simply didn’t exist. Most people weren’t sure why they would ever want to see their own genome, and many experts thought the public couldn’t handle this information. But the 23andMe vision was straightforward: understand the human genome and help build a different kind of healthcare system — one driven by the people and for the people. At the time, that sounded audacious. Looking back, it sounds prescient.

The most consequential idea embedded in 23andMe’s founding wasn’t just that people deserved access to their own genetic data, it was that those same people, at scale, could become active participants in scientific discovery. And the discoveries shouldn’t stop at the journal page. When research yields new findings, those insights should be translated back into reports delivered directly to 23andMe members.

The goal was always for the data to come “full circle” and help the very people who contributed their information. 23andMe created something that had never existed before: a research engine powered by millions of consented participants who wanted to understand themselves and, in doing so, help others.

What Twenty Years Built

The most visible impact of this model has been on individual health. When 23andMe received its first FDA authorization to report health information directly to consumers, it was a landmark moment. It validated the entire premise that people have the right to understand their own biology without a gatekeeper standing in the way. Over the years, additional FDA clearances followed, each one expanding what members could learn about their genetic risk for health conditions, hereditary cancers, and even pharmacogenetic responses to medications. 

Those health insights also brought together a community of research participants, who made possible research at a scale that academia and pharma simply couldn’t replicate on their own. By inviting members to opt in to participate in research, 23andMe built one of the world’s largest resources for genetic discovery; and more than 90% of the member base has chosen to opt in and join us in this research. That consent-first, community-powered flywheel has now produced over 300 published studies.

The breadth of what this research community has made possible over twenty years is difficult to compress into any single list, but a few studies stand out:

• In 2016, drawing on data from over 450,000 research participants, 23andMe co-authored what became a landmark study in Nature Genetics that identified 15 genomic regions associated with major depression. This was the first time researchers had cracked the genetics of depression in people of European descent, breaking through years of failed attempts by studies simply too small to find anything.
• That same crowdsourced model powered some of the most important Parkinson’s disease genetics work of the last decade. In collaboration with the Michael J. Fox Foundation, 23andMe has helped build one of the largest Parkinson’s research cohorts in the world, identifying dozens of novel genetic associations that continue to shape drug development today.
• When the COVID-19 pandemic struck, 23andMe mobilized its community rapidly. In less than four months more than a million 23andMe customers consented to participate in this research leading to a study that showed people with type O blood were less likely to contract the virus or test positive after exposure, demonstrating the unique speed at which population-scale genomics can respond to an emerging public health crisis.
• In 2020, our researchers leveraged genetic data from nearly 50,000 people to produce one of the most comprehensive investigations of the transatlantic slave trade ever conducted. We confirmed genetic links between regions in the Americas and areas along the Atlantic coast of Africa, and dated the arrival of specific African populations to different parts of the Western Hemisphere. Three years later, researchers published a study in Science that used ancient DNA to identify nearly 42,000 living Americans with genetic connections to 27 enslaved individuals buried at Maryland’s Catoctin Furnace — including close relatives still living in Maryland, two centuries later. These studies are a reminder that a genetic database is not just a scientific instrument. It can also be a tool for healing.

A Signal of What’s Coming

Our GLP-1 paper, published just weeks ago in Nature, captures what the next twenty years could look like. Our team conducted a large-scale genome-wide association study drawing on data from over 27,000 individuals who had used GLP-1 medications: drugs like semaglutide and tirzepatide that have transformed the management of obesity, but which produce variable results from patient to patient. Just seven months after launching the survey (a remarkably rapid pace for work of this kind), 23andMe researchers found that some of that variability has a genetic explanation. At the same time this work was published we launched a new report and interactive tool related to GLP-1 medications to 23andMe+ Total Health™ members.

This is what precision medicine actually looks like in practice. The vision is that before starting a GLP-1 drug, a patient could receive a personalized profile indicating their likelihood of weight loss and potential side effects, a dramatic shift from the current trial-and-error approach that leaves many patients frustrated and undertreated. The 23andMe Research Institute aims to continue to share the power of our crowdsourced research community to benefit human health.

Looking Forward

The road to get here has not always been straightforward. The company has faced real challenges, recently and throughout its history; those of us who’ve been here through them feel that honestly. But the mission has not changed, it has found a new home in our nonprofit commitment. Our Founder and CEO Anne Wojcicki has said her belief in the company and its future is unwavering, and the commitment to providing access to, and benefit from, genetics remains the north star. The science hasn’t gotten less important. If anything, it’s gotten more urgent.

Anne once said “the future is dripping with possibilities.” Twenty years in, we believe that more than ever. We have discovered enough of the genome to know how much remains a mystery. We have helped enough people to know how many more could be helped. On this DNA Day, seventy-three years after Watson and Crick and twenty years after 23andMe opened our doors, we raise a glass to what’s been achieved, and roll up our sleeves to create a future where breakthroughs belong to all of us.

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.

Understanding Parkinson’s Disease

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.

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:

• Age: Risk increases as we get older.
• Sex: Males have a higher likelihood of developing Parkinson’s than females.
• Environment: Exposure to certain chemicals, such as pesticides and chemicals used for metal degreasing or dry cleaning, can increase risk.
• Family History: Having a first-degree relative (parents, siblings, and children) with the condition can increase your own chances.
• 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’s disease later in life.

The Genetic Connection

For some people, DNA plays an important role in their chances of developing Parkinson’s. Two of the most well-studied genes associated with Parkinson’s are LRRK2 and GBA (also known as GBA1). 23andMe offers the Parkinson’s Disease Genetic Health Risk report* that specifically looks at two genetic variants: one in each of these genes associated with an increased risk of developing Parkinson’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 LRRK2 G2019S carriers^[1][2], and from about 10% to 30% for GBA1 N409S carriers (formerly known as N370S)^[3][4], depending on the study and genetic ancestry.

What Our Research Adds

While most people who have these variants will not develop Parkinson’s, recent research from the 23andMe Research Institute and collaborators has helped us better understand the nuances of the condition and why it affects every individual differently.

• The researchers found that a person’s overall genetic background can “dial” their risk up or down. Among GBA1 carriers, those with a low-risk genetic background had roughly the same chance of developing Parkinson’s as non-carriers. But GBA1 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.
  
• For carriers of both LRRK2 and GBA1 carriers, the risk was even higher. This research showed that these “dual carriers” 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.
  
• Genetics don’t just influence whether someone develops Parkinson’s; it also impacts how the disease progresses. The researchers found that in those already living with PD, carrying APOE 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 APOE E4 raised the risk of these symptoms by 11% to 35%.

Power in Numbers: 17 Years of Research

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 30 publications on Parkinson’s disease, most recently a paper exploring other biological factors that might influence Parkinson’s disease risk or progression. 

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.

How You Can Get Involved

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

• Share the facts about PD symptoms and risks with your loved ones.
• If you are a 23andMe member, you can opt-in and view your Parkinson’s Disease Genetic Health Risk report.
• If you or a loved one are living with Parkinson’s or you’re just interested in this research, consider joining our research community. 

This April, consider taking a step toward greater awareness for yourself, and for the millions of people living with Parkinson’s disease around the world.

* 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  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  people of European, Ashkenazi Jewish, and North African Berber descent.

References

[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., & Marder, K. (2006). Frequency of LRRK2 mutations in early- and late-onset Parkinson disease. Neurology, 67(10), 1786–1791. https://doi.org/10.1212/01.wnl.0000244345.49809.36 

[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., & Norcliffe-Kaufmann, L. (2024). Genetic analysis and natural history of Parkinson’s disease due to the LRRK2 G2019S variant. Brain, 147(6), 1996–2008. https://doi.org/10.1093/brain/awae073 

[3] Rana, H. Q., Balwani, M., Bier, L., & Alcalay, R. N. (2013). Age-specific Parkinson disease risk in GBA mutation carriers: Information for genetic counseling. Genetics in Medicine, 15(2), 146–149. https://doi.org/10.1038/gim.2012.107 

[4] Anheim, M., Elbaz, A., Lesage, S., Durr, A., Condroyer, C., Viallet, F., Pollak, P., Bonaïti, B., Bonaïti-Pellié, C., & Brice, A. (2012). Penetrance of Parkinson disease in glucocerebrosidase gene mutation carriers. Neurology, 78(6), 417–420. https://doi.org/10.1212/WNL.0b013e318245f476

While most ancient DNA studies focus on the human DNA of the individuals whose remains were sampled, it is also possible to learn about the diseases these individuals carried by searching for pathogen DNA in their remains.

These kinds of studies have enabled researchers to investigate the origins and spread of ancient diseases that were otherwise nearly impossible to study. This is because many ancient diseases, including malaria, don’t leave clear physical evidence on skeletal remains. Furthermore, historical records of ancient epidemics often lack the specificity needed to identify exactly which diseases were present or where they originated.

In 2024, a team of researchers looked at ancient DNA to search for cases of malaria among more than 10,000 individuals. In this month’s update to the Historical Matches^SM feature, we are highlighting the stories of individuals buried at three ancient sites where malaria was detected. Each of their stories provides important new insights into the history of this ancient disease.

Spreading Malaria Along European Military Lines

In Europe, the cemetery of St. Rombout’s in Mechelen, Belgium, offers a window into the health of a continent at war. Sitting next to one of the world’s first permanent military hospitals, this site served as a burial ground for both local townspeople and foreign soldiers from the 12th to the 18th centuries.

While local residents, who were buried at this site before the hospital was established, showed fewer signs of infection, later individuals—thought to be soldiers who had traveled from the Mediterranean—were often found carrying multiple strains of malaria simultaneously. These findings highlight how the movement of armies turned European cities into crossroads for infectious disease.

Carrying Malaria to the Himalayan Peaks

The high-altitude site of Chokhopani sits 2,800 meters above sea level in the Nepalese Himalayas. This environment is far too cold and dry for the Anopheles mosquitoes that transmit malaria to survive. Yet, genomic analysis of an individual buried within one of the site’s cliffside tombs nearly 3,000 years ago revealed the presence of Plasmodium falciparum, the most virulent form of the malaria parasite.

Finding a tropical disease in a mountain environment provides clear evidence of human mobility. It tells us that this ancient individual had likely traveled to warmer, lower-altitude regions—possibly for trade—and carried the infection back to this highland site.

Tracking the Arrival of Malaria in the Americas

A central debate among disease researchers is whether malaria existed in the Americas prior to European contact or if it was brought there by European colonizers. The study of individuals from the site of Laguna de los Cóndores in Peru provides a pretty clear answer.

Researchers at the site discovered an individual with exclusively Indigenous American ancestry who lived during the period of initial European contact and was infected with Plasmodium vivax (a more widespread form of the malaria parasite). Crucially, the DNA of the parasite was most similar to historical European strains rather than those found elsewhere. This finding suggests that European colonizers acted as the primary vector for introducing these specific malaria strains to the Indigenous populations of the Andes.

Learn More

Want to see if you share a genetic connection with any of the ancient malaria-infected individuals highlighted in this study—or with hundreds of other historical individuals? The Historical Matches feature is available to 23andMe+ Premium™ members.

For many women, the decision to start estrogen-containing hormone replacement therapy (HRT) or oral contraceptives (OCPs) is a pivotal health moment.

These medications can be life-changing. They regulate cycles, prevent pregnancy, relieve perimenopausal and menopausal symptoms, and protect bone health. For millions of women, estrogen improves quality of life.

But estrogen is not risk-free.

One of the most important considerations is the risk of developing blood clots, including deep vein thrombosis (DVT), pulmonary embolism (PE), or stroke. While the overall risk is low for most healthy women, it is not the same for everyone.

The difference often lies in your genetics.

Hereditary Thrombophilia: The Hidden Variable

Some individuals carry inherited genetic variants that increase their tendency to form blood clots, a condition known as hereditary thrombophilia.

The two most common variants are Factor V Leiden (F5 gene) and Prothrombin G20210A (F2 gene). These variants are common. Approximately 1 in 20 people of European ancestry carries one of them.

To put this in perspective, the baseline annual risk of a serious blood clot is roughly 1 in 1,000. Carrying one of these variants can double that risk. When estrogen is added, particularly oral estrogen, the risk can increase substantially, in some cases several-fold higher than baseline.

Without genetic information, we are estimating risk.
With genetic information, we are personalizing it.

What About MTHFR?

Another gene that has been proposed to be a hereditary clotting risk factor is the MTHFR gene. Some studies have suggested an increased risk of blood clots in individuals who carry two copies of the C677T variant, while others have found no clear association. 

Because the evidence is mixed, genetic results should be interpreted with caution. However, knowing your status can still be informative: if you carry these variants, a simple blood test to measure homocysteine levels may help clarify your overall risk profile and guide further discussion with your clinician.

Read more about MTHFR here

Genetics Is Only Part of the Picture

While your tendency to develop blood clots is primarily determined by genes, life events and circumstances are also important. The most widely recognized DVT and PE risks are injuries, surgeries, and long airplane flights (more than four hours long). Cigarette smoking and hypertension are risks for developing stroke. 

Estrogen is a mild pro-thrombotic factor (a factor that increases the likelihood of forming a blood clot), whether during pregnancy or through hormone therapy.

The key question is not “Is estrogen safe?”
The key question is “Is estrogen safe for you?”

Risk Mitigation Is Possible

If a woman carries a clotting-risk variant, that does not automatically mean she cannot take estrogen.

Instead, it opens the door to informed strategies such as choosing transdermal estrogen, which carries lower clot risk than oral formulations, using low-dose aspirin while taking estrogen, short-term anticoagulation during high-risk periods (e.g., surgery or long travel), or close clinical monitoring.

Knowledge allows preparation. Preparation reduces fear.

The Role of 23andMe in Understanding Your Genetic Risk

This is where resources like 23andMe become invaluable. They provide easily understandable and reliable access to important genetic information related to blood clotting, empowering both patients and physicians.

The 23andMe Hereditary Thrombophilia report* specifically includes analysis for the two most common variants linked to hereditary thrombophilia: factor V Leiden and prothrombin G20210A. 23andMe also offers a report that includes MTHFR variants.

Why I Recommend 23andMe for My Patients

As a hematologist specializing in women’s health hematology, I frequently discuss genetic clotting risk with patients who are planning pregnancy or considering estrogen therapy. 

In recent years, many insurance carriers have stopped covering inherited thrombophilia testing. Instead, direct-to-consumer genetic testing platforms like 23andMe have made validated variant testing more accessible and affordable. For appropriate patients, it can provide clinically useful information that guides safer, more confident decision-making.

Personalized Medicine Is Not the Future-It’s the Present

Understanding your genetic profile allows your physician to contextualize your clotting risk, weigh the benefits and risks of estrogen therapy, and develop individualized risk-mitigation strategies.

This is personalized medicine in action!

Before starting estrogen therapy, have a conversation with your physician about your family history, personal risk factors, and whether genetic testing may be appropriate for you. In some cases, it may also be helpful to consult a hematologist who has expertise in women’s health.

Because when it comes to your health, guessing is no longer necessary.

This post reflects the personal insights and opinions of Dr. Fein. It does not necessarily represent the views of 23andMe. We appreciate the unique perspective shared here.

* The 23andMe PGS test uses qualitative genotyping to detect clinically relevant variants in the genomic DNA of adults, from saliva collected using an FDA-cleared collection device (Oragene·DX model OGD-500.001) for the purpose of reporting and interpreting genetic health risks.  The relevance of each report may vary based on ethnicity.  Our genetic health risk reports describe if a person has variants associated with a higher risk of developing a disease, but do not describe a person’s overall risk of developing the disease. The reports are not intended to diagnose any disease, 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 or how much of a medication you should take. The Hereditary Thrombophilia genetic health risk report (i) is indicated for reporting of the Factor V Leiden variant in the F5 gene, and the Prothrombin G20210A variant in the F2 gene, (ii) describes if a person has variants associated with a higher risk of developing harmful blood clots, and (iii) is most relevant for people of European descent.

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.^[1] 

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%.^[2][3] 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.^[4] 

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. Scientists at the 23andMe Research Institute published a study in Nature that has identified genetic variants associated with weight loss and side effects among those who have taken GLP-1 medications.

The Mystery of Medication Response

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?”.

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 “spelling differences” (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’ bodies responded to GLP-1 medications. 

Discovering the Genetic Links

23andMe Research Institute scientists uncovered fascinating genetic associations for response to GLP-1 medications, including a person’s potential for weight loss and their risk of experiencing nausea or vomiting.

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 GLP1R gene, which codes for the receptor protein that is the target of GLP-1 medications.

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 GIPR gene, which explains why it impacts tirzepatide response but not semaglutide.

Describing the impact of the study, Dr. Adam Auton, Vice President of Human Genetics at the 23andMe Research Institute said, “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 ‘precision medicine’ isn’t just an aspiration.”

Translating Emerging Science into Personalized Insights

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.

That is why a new report and interactive tool related to GLP-1 medications is now available exclusively through the 23andMe+ Total Health™ 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.

What You Need to Know About the New Report

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.

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: “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.”

A Sincere Thank You to Our Participants

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.

Participate in the next discovery

References

1. Montero, A., Sparks, G., Presiado, M. & Hamel, L. KFF Health Tracking Poll May 2024: The Public’s Use and Views of GLP-1 Drugs | KFF.

2. Wilding, J. P. H. et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. New Engl J Med 384, 989–1002 (2021). https://pubmed.ncbi.nlm.nih.gov/33567185/

3. Ryan, D. H. et al. Long-term weight loss effects of semaglutide in obesity without diabetes in the SELECT trial. Nat Med 30, 2049–2057 (2024). https://pubmed.ncbi.nlm.nih.gov/38740993/

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. Endocrine 91(1), 23 (2026). https://pubmed.ncbi.nlm.nih.gov/41489846/

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.

The Challenge: Teaching Complexity

The paper explores a fundamental shift in genetics education: moving from a “one-gene, one-trait” Mendelian model to an understanding of complex traits that are influenced by hundreds or thousands of genetic variants working in tandem with environmental factors.

Teaching this complexity isn’t easy. This case study followed a “co-design process” involving a middle school science teacher and educators from the University of North Carolina at Greensboro and the Exploratorium Museum in San Francisco working together to create professional activities for other science teachers to update how they teach more complex genetics.

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

• A lack of real-world examples tailored to hook students’ interest.
• Nuanced word choices that can be confusing when describing the relationship between genes and a trait.
• How and when to introduce core ideas and activities to help students build their understanding step-by-step.

A Collaborative Solution

In order to find interesting examples to capture students’ 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 classroom activity, using height as a relevant example, to demonstrate the impact of multiple genetic variants on a trait.

“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,” said Hilleary Osheroff, of the Teacher Institute at the Exploratorium, one of the authors of this study. 

Co-author Sara Porter, from the Teacher Education and Higher Education Department at University of North Carolina at Greensboro added, “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.”

Why It Matters

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.

“At the 23andMe Research Institute, we believe that genetic literacy is a fundamental tool,” says Anne Greb, Director of Genomics Education at 23andMe. “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.”

The responsive nature of the co-design process described in the paper shows that when scientists and teachers work together, they create a “resource-rich” 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.

Interested in helping a young person in your life learn more about genetics? Check out more educational activities from the Exploratorium and the 23andMe Genetics Learning Hub.

March is Sleep Awareness Month, a time to focus on one of the most vital pillars of our health: sleep. While we often prioritize diet and exercise, the quality of our rest plays a massive role in how we feel, think, and function every single day — and research is showing sleep is  increasingly important for living a longer, healthier life.

The Power of a Good Night’s Rest

Getting enough, and getting high-quality sleep is about more than just avoiding grogginess. According to the CDC, consistent, healthy sleep can help you:

• Boost your immune system, helping you get sick less often.
• Maintain a healthy weight and improve your metabolism.
• Lower your risk for serious chronic conditions like type 2 diabetes, heart disease, high blood pressure, and stroke.
• Support mental health by reducing stress and improving your overall mood.
• Sharpen your mind, improving your attention and memory for daily tasks.
• Keep you safe, reducing the risk of motor vehicle crashes and injuries.

Introducing the New Sleep Paralysis PRS Report

23andMe members can already explore genetic insights into certain sleep-related topics (such as insomnia and obstructive sleep apnea), and we are excited to expand these insights for 23andMe+ Premium™ members with our new Sleep Paralysis Polygenic Risk Score (PRS)* report.

Sleep paralysis is the temporary inability to move or speak while falling asleep or waking up. While these episodes can be brief and sometimes distressing, they are not dangerous. Our new report uses a polygenic score (a model that looks at thousands of small genetic variants) to help you understand your genetic likelihood of experiencing sleep paralysis.

Tips for Better Sleep Hygiene

Regardless of your genetic predispositions, good sleep hygiene can make a world of difference. If you experience sleep paralysis or struggle with general sleep quality, consider these tips:

• Adjust your sleeping position: Sleep paralysis is more common when sleeping on your back; try switching to your side.
• Do your best to stay consistent: Go to bed and wake up at the same time every day, even on weekends, to regulate your internal clock.
• Try to create a sanctuary: Keep your bedroom dark, quiet, and comfortable.
• Unwind early: Try meditation or a warm bath before bed to lower stress.
• Watch your intake: Limit alcohol and caffeine in the evening, as both can interfere with deep, restorative sleep.

More Genetics of Sleep

What about other ways genetics impacts sleep? Have you ever wondered why you’re a night owl while your partner is an early bird? Or why some people can fall asleep the second their head hits the pillow while others toss and turn? Your DNA may hold some answers.

At 23andMe, we have a number of sleep-related reports, including:

• Wake-up Time: Explore how your genetics nudge you toward being a natural morning person or a night owl.
• Insomnia: Discover how your DNA may influence your likelihood of having trouble falling or staying asleep.
• Obstructive Sleep Apnea: Identify if your genetics give you an increased likelihood of developing this common sleep-related breathing disorder.
• Restless Legs Syndrome: Understand the genetic components of this uncomfortable nighttime sensation.

Ready to see what your DNA says about your sleep? 23andMe+ Premium members can find the new Sleep Paralysis report and other sleep-related reports in the Wellness section of their account today.

The Philippines is a land of incredible diversity, with over 7,000 islands and a rich tapestry of cultural and regional communities. We are now able to identify if members share DNA segments with those who have a known family history from a specific location or community. More than 75% of our members of Filipino descent, who are on our latest genotyping chip, will now see matches to one or more of these new Genetic Groups. And 23andMe+ Premium™ members will also be able to see any distant Genetic Group connections they may have to these regions. 

A Shared Heritage

In addition to 141 Genetic Groups across the Philippines this update includes 1 new group in Taiwan and 2 groups in Borneo, reflecting the shared Austronesian ancestry in this region. 

Who are Austronesians? Around 4,000 to 5,000 years ago, seafaring groups originating from what is now Taiwan began migrating southward into the Philippine archipelago, likely entering through the Batanes Islands and Northern Luzon. These migrants brought with them new technologies, such as the outrigger canoe, along with agricultural practices, including the cultivation of rice and the domestication of animals. Over millennia, these populations fanned out across the 7,000+ islands of the Philippines, developing distinct linguistic and cultural identities while maintaining a shared genetic and naval heritage. 

This movement didn’t stop in the Philippines; the archipelago served as a vital jumping-off point for further expansion into Indonesia, Malaysia, and eventually as far west as Madagascar and as far east as the remote islands of Polynesia, forever linking the Filipino people to a vast Austronesian cultural network.

Check out your results

With this update, discovering more about your Filipino heritage with 23andMe has never been more specific. This is part of our ongoing commitment to improving our science and representation for all our customers. We can’t wait for you to see it. Log in to explore your updated results in your Ancestry Composition report today.

Is age 45 actually the right time for your first colonoscopy? While standard guidelines offer a baseline for colorectal cancer screening, your genetics offer a potential path for further precision. As we see a significant shift in colorectal cancer trends among younger adults, understanding your inherited risk factors is a critical tool for early detection and personalized care.

As we observe Colorectal Cancer Awareness Month, we’re looking at how your genetic data can help you move beyond the one-size-fits-all model and take better control of your health.

The Changing Face of Colorectal Cancer

The traditional milestone for your first colonoscopy used to be age 50. Recently, experts lowered it to 45. Why? Because the landscape of this disease is shifting.

According to the American Cancer Society, an estimated 158,850 people in the U.S. will be diagnosed with colon or rectal cancer in 2026, making colorectal cancer the fourth most common cancer. Perhaps most startling is that 45% of new cases are now occurring in adults under 65, a massive jump from just 27% in 1995. While the overall number of cases in young people is still relatively low, the rates of colorectal cancer in people between the ages of 20 and 40 is increasing at about 3% per year. This trend of younger adults being diagnosed means that for some, waiting until a standard screening age might already be too late.

The Genetic Spectrum: More Than One Way to Measure Risk

Standard screening guidelines already note that some people who are at higher risk (for example, due to a family history or having certain health conditions) should have their first colonoscopy before age 45. But many people don’t know they have higher risk, and genetics can unlock some of that knowledge. 23andMe offers a tiered look at your genetic risk to help you and your doctor move from a one-size-fits-all approach to more precise prevention.

• The MUTYH Report: Our MUTYH-Associated Polyposis Genetic Health Risk* report looks at specific variants in the MUTYH gene linked to a particular form of hereditary colorectal cancer. While having two variants significantly increases risk, even carriers of a single variant might benefit from sharing that information with their healthcare provider.
• High-Impact Variants: Particularly impactful genetic variants can also be found through sequencing, such as the clinician-ordered exome sequencing available through our Total Health™ service. This looks at over 100 high-impact genes, including some associated with significantly increased risk of developing colorectal cancer (specifically related to Lynch syndrome, MUTYH-associated polyposis, and APC-associated polyposis).
• Polygenic Risk Scores (PRS): Most cancer risk isn’t caused by a single variant or gene, but by the combined effect of thousands of small genetic variations. Our Colorectal Cancer PRS** report uses these markers to calculate whether you have an increased genetic likelihood for the most common forms of the disease.

Closing the Data Gap: Equity in Research

Precision medicine works best when the science behind it reflects the diversity of the people it serves. Historically, genetic research has been disproportionately centered on people of European descent. This has created a gap that we are working to close.

The stakes are especially high for the Black community. Black and African Americans are 15% more likely to develop colorectal cancer and 35% more likely to die from it than non-Hispanic white Americans.

Science shouldn’t have a blind spot like this. We have an ongoing study specifically designed to improve our Colorectal Cancer PRS report for our Black and African American members. Because of our currently limited data, the PRS driving this report failed to meet our performance standards for members of certain communities; these members are thus not able to receive a personalized genetic result. This study hopes to change that. Our goal is to work toward a future where preventive medicine is equitable and accurate for all.

Taking Control of Your Timeline

Colorectal cancer is one of the most preventable cancers, and when caught early it’s often more treatable. By understanding your genetic predisposition you’re equipping yourself with the knowledge needed to help lead the conversation with your doctor. Whether you are 25 or 55, knowing your risk allows you to advocate for the screenings you may need.

* 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, including the 23andMe PGS Genetic Health Risk Report for MUTYH-Associated Polyposis. Your ethnicity may affect the relevance of each report and how your genetic health risk results are interpreted. The test is not intended to diagnose any disease and does not describe a person’s overall risk of developing any type of cancer. It is not intended to tell you anything about your current state of health, or to be used to make medical decisions, including whether or not you should take a medication, how much of a medication you should take, or determine any treatments. Warnings & Limitations: The 23andMe PGS Genetic Health Risk Report for MUTYH-Associated Polyposis is indicated for reporting the Y179C and G396D variants in the MUTYH gene and an increased risk for colorectal cancer.  The two variants included in this report are most common in people of Northern European descent.  This report does not include variants in other genes linked to hereditary cancers and the absence of variants included in this report does not rule out the presence of other genetic variants that may impact cancer risk. The PGS test is not a substitute for visits to a healthcare professional for recommended screenings or appropriate follow-up. Results should be confirmed in a clinical setting before taking any medical action. For important information and limitations regarding genetic health risk reports, visit  https://www.23andme.com/test-info.

** The 23andMe Colorectal Cancer PRS report is based on a genetic model that includes data and insights from 23andMe consented research participants and incorporates more than 1,700 genetic variants to provide information on the likelihood of experiencing colorectal cancer. 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 Colorectal Cancer 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.

Now, thanks to a new study published in the Journal of Archaeological Science earlier this year, the stories of these individuals are coming to light. This month, 23andMe is adding four individuals from this cliff-side site to our Historical Matches^SM feature.

A Landscape in Transition

During the 14th century, the Yun-Gui Plateau was a region of immense cultural and political transformation. As the Ming Dynasty sought to consolidate power and expand its borders into the southwest, the area became a frontier of conflict. The rugged karst landscape, characterized by its towering limestone cliffs and deep river valleys, served as both a strategic stronghold for the military and a vital sanctuary for local communities caught in the crossfire of imperial expansion.

Historically known for its incredible ethnolinguistic diversity, the plateau was home to various indigenous groups who had inhabited these mountains for millennia. The transition between the Late Yuan and Early Ming periods in the 14th century brought an influx of new people and upheavals in local government, creating a complex social tapestry. For the families found in Pingtang Cave, these remote, high-altitude caverns were not just geological features—they were essential places of refuge during a time of profound uncertainty.

A Refuge, Not a Cemetery

When researchers first investigated Pingtang Cave, they quickly realized this was no ordinary burial ground. Unlike traditional sites of the era, there were no coffins, no grave goods, and no signs of formal interment. Instead, the skeletons were found in the deepest recesses of the cave, far from the light of the entrance.

While most of the group appeared to be healthy prior to entering the cave, the genetic analysis revealed that one individual was suffering from paratyphoid fever, caused by the bacterium Salmonella enterica. Her genome also revealed that her parents were likely closely related, perhaps as closely as second cousins, a finding that provides unique insight into the social and mating structures of isolated plateau communities during this era.

The lack of physical trauma or signs of violence ruled out a massacre, while the absence of a widespread plague suggested something else entirely. Researchers believe these families fled to the cave to escape external conflict, perhaps the unrest of the Ming Dynasty’s expansion into the region, only to succumb to the low oxygen of the cave’s deepest chambers.

The Families of Pingtang Cave

The genetic data reveals that those who fled to the cave were not strangers; they were a tightly-knit community of relatives. Most of these individuals shared the same maternal lineage (haplogroup M7b1a1), suggesting that the group was a multi-generational family, who were connected through a shared maternal lineage.

A Window into Heritage

All of the members of this group shared a similar ancestral profile, characterized by a mixture of ancient northern and southern East Asian ancestry. This genetic signature persists today in the present-day inhabitants of southwest China, bridging the gap between the people living during the transition into the Ming Dynasty and the modern world.

Learn More

23andMe+ Premium™ members can now explore whether they share a genetic link to these ancient Chinese individuals, and hundreds of others, through the Historical Matches feature.

When I was invited to contribute a chapter on direct-to-consumer (DTC) genetic testing to The Oxford Handbook of Genetic Counseling, it gave me the opportunity to reflect on how the genetics landscape has evolved and the important role education plays in helping both healthcare professionals and the public navigate it.

Each year on March 14, Science Education Day highlights the importance of making scientific knowledge accessible and meaningful for society. In genetics, this goal has become increasingly important as more people gain direct access to their own genetic information.

Today, millions of individuals have explored their DNA through DTC genetic testing. As a result, healthcare professionals increasingly encounter patients who arrive with genetic results in hand, and questions about what those results mean for their health.

For genetic counselors, understanding this evolving landscape is essential.

The inclusion of DTC testing in The Oxford Handbook of Genetic Counseling reflects how consumer genomics has become an established part of the broader genetics and healthcare ecosystem.

Why DTC Genetic Testing Matters for Genetic Counselors

Direct-to-consumer genetic testing has expanded access to genetic information and changed how many people first encounter genetics. For some individuals, their first exposure to genetics may come not in a clinic, but through a consumer test ordered online from companies like 23andMe.

This shift creates new opportunities, and new responsibilities, for healthcare professionals.

Genetic counselors are uniquely positioned to help individuals understand what genetic results can and cannot tell us. They help place findings in the context of personal and family health history, clarify the limitations of testing, and guide next steps when clinical follow-up is needed.

As consumer genomics becomes more integrated into healthcare conversations, it is increasingly important that genetic counselors are prepared to navigate these discussions. Education about DTC genetic testing — including how results are generated, the types of health and non-health information consumers receive, how these tests differ from clinical testing, and what motivates individuals to pursue testing — is becoming an important component of genetic counseling training.

Genetic Counselors as Educators in Healthcare

Genetic counselors play another critical role beyond direct patient care: they are educators within the healthcare system.

As genetics becomes relevant across many areas of medicine, physicians and other healthcare professionals increasingly encounter genetic information in their practice. Yet many clinicians received limited formal training in genomics during their medical education.

In some cases, genetic information can provide additional context about an individual’s risk factors, helping clinicians and patients think more proactively about prevention, screening, and more personalized approaches to care.

Genetic counselors often help bridge this gap, educating clinicians on how to interpret genetic information, understand its limitations, and apply it appropriately in patient care.

Expanding Genetics Education for a Genomic Era

The growing intersection of consumer genomics, clinical care, and population-level genetic screening highlights a broader need: expanding genetics education for multiple audiences.

At the 23andMe Research Institute, we are working to support this goal through initiatives like the Genetics Learning Hub, which currently provides accessible learning resources for the general public and will expand to include resources for healthcare professionals. These structured educational modules are designed to help people better understand how genetics influences health and how genetic information can be used responsibly.

Efforts like these reflect a broader priority across the field: ensuring that both the public and healthcare professionals have the knowledge needed to interpret and apply genetic information in an increasingly genomics-informed healthcare landscape.

The Role of Education in Responsible Genomics

Science Education Day serves as a reminder that scientific discovery alone is not enough, people must also have the knowledge and tools to understand and apply that science.

In genomics, this means ensuring that healthcare professionals are prepared to interpret and communicate genetic information responsibly. As more people access their genetic information through consumer testing, expanding genetics education across the healthcare workforce — including genetic counselors — will remain essential to helping individuals understand and appropriately use genetic insights in their healthcare decisions.

At 23andMe, we believe your DNA holds the key to stories you’ve never heard and people you’ve never met. Today, we’re excited to introduce a groundbreaking new feature that uncovers ancestral stories hidden in your DNA: Reconstructed Ancestors.

This innovative experience uses the DNA you share with close and distant relatives to piece together the genetic profiles of your ancestors, revealing insights into their ancestry composition and what they passed down to you.

Unlocking Your Family’s Untold Stories

For many of us, family history has blank spaces. Maybe it’s because records were lost or destroyed or never existed in the first place. Maybe no one really talked about “that side” of the family. Reconstructed Ancestors helps bridge those gaps by using DNA to learn about how ancestry from different global populations moves through branches of your family tree.

23andMe can use your genetic relatives to rebuild parts of your ancestors’ genetic profiles. That means you can learn more about ancestors who were never genotyped and who may no longer be here to share their stories.

GRAMPA: The DNA Detective Behind the Scenes

Behind the scenes is our GRAMPA algorithm (Genotype Reconstruction and Ancestral Mixture Proportions in Ancestors). Think of it like a genetic jigsaw puzzle: each piece of DNA you share with another relative has traveled through a shared ancestor. GRAMPA uses these overlapping segments, scattered across hundreds or even thousands of relatives to piece together the genome of that shared ancestor.

The more relatives who test, and the more relatives you add to your family tree, the more pieces we have and the clearer the picture becomes.

An Ever-Growing Portrait of Your Family’s Past

Reconstructing an ancestor starts with our DNA Relatives feature. By opting in, you allow 23andMe to identify and connect you to people who share DNA with you. These connections form the foundation of your automatic, DNA-based Family Tree and it’s from this tree that we can begin to reconstruct your recent ancestors. First, we scan the database for shared DNA segments between you and your relatives. Then we begin piecing together those segments into an ancestor profile, revealing what we can for now and continuing to add more over time.

Each reconstructed ancestor profile is unique and dynamic. As you build out your Family Tree, and as the 23andMe DNA database grows, more puzzle pieces are added to the ancestor profile. You can see what percentage of your DNA you inherited from that ancestor, explore their likely ancestry and begin to imagine who they might have been. The story deepens, details emerge, and a clearer picture of your family history begins to take shape.

Importantly, your privacy remains central. You control who sees your Reconstructed Ancestors, your Family Tree and how your information is used, ensuring your journey into your family’s past is both meaningful and secure.

Why It’s Different

Reconstructed Ancestors is the first and only feature of its kind. It covers more than just inheritance; it rebuilds the genome of the person behind the inheritance. And it’s not limited to parents. At launch, the feature will include ancestors up to grandparents. Our hope is that one day you will be able to accurately piece together your entire family tree, including the gaps, with DNA as your guide. 

Real Stories, New Connections

More than 200,000 23andMe customers who self-report as an adoptee have already found close relatives in our database. For those who cannot make that connection yet, Reconstructed Ancestors offers a new kind of discovery, a way to learn about their ancestry inheritance, a way to feel closer to a relative they’ve never met.

It’s about more than just genetics. It’s about reclaiming pieces of your past that history forgot.

Available for Subscribers

Reconstructed Ancestors will be available for 23andMe+ Premium™ and Total Health™ members. There’s no need to provide another DNA sample or wait for results.

And this is just the beginning. Your family story is still unfolding. Every new relative who joins 23andMe helps add more pieces to the puzzle and brings you one step closer to understanding where you come from.

DNA shapes who we are in countless ways, from our health and family story to traits we might not expect. Yet for many people, genetics can feel complex, technical, or out of reach.

We created the 23andMe Genetics Learning Hub to change that.

The Genetics Learning Hub is a free, easy-to-explore online resource designed to help anyone understand the fundamentals of genetics, no science background required. Whether you’re curious about your own DNA, interested in your family’s health history, or simply want to better understand how genetics influences health, this is a place to start.

Why Genetic Literacy Matters

We didn’t build this hub just for fun (although it is fun!); we built it to help give you the fluency to navigate the world of DNA with confidence. From dinner table discussions about your family history to navigating healthcare, genetic literacy turns you from an observer into an expert of your own story. Here is how we’re bridging the gap:

• Combating Misinformation: Learn to distinguish between hard science and common genetic myths that circulate online.
• Empowering Doctor-Patient Conversations: Understand the “how” and “why” of your genetic risks to have more informed, productive conversations with your healthcare professional.
• Turning Data into Action: Move beyond just knowing your results to understanding how lifestyle, environment, and genetics intersect, giving you a clearer roadmap for potential proactive health decisions.
• Reducing Uncertainty: Gain the confidence to ask better questions, not just of your doctor, but of the world around you.

What You’ll Find in the Learning Hub

The Learning Hub breaks down complex genetic concepts into short, engaging modules that build understanding step by step. Topics include:

• The basics of genes and how they work
• How some health conditions are caused by changes in a single gene
• How genetics, lifestyle, and environment work together to influence health
• How to gather your family health history and spot potential risks

Each module is designed to be approachable, practical, and grounded in science. We focus not just on definitions and concepts, but on helping you understand why genetics matters in real life.

Built for Curiosity

You don’t need prior knowledge to get started. The Learning Hub was designed for everyone, from those just beginning to learn about genetics to those who want to connect genetic concepts to real-world health and family decisions.

Our goal is simple: make genetic science more accessible, more understandable, and more empowering.

Why Genetics Education Matters

Genetics plays an increasingly important role in healthcare, research, and everyday decision-making. As access to genetic information expands, so does the need for clear, trustworthy education.

The Genetics Learning Hub reflects our commitment at the 23andMe Research Institute to scientific accuracy, transparency, and inclusion. It was developed by a multidisciplinary team that includes genetic counselors, scientific experts, and other collaborators working together to translate complex science into clear, meaningful learning experiences.

Start Exploring

If you’ve ever wondered how genes influence health, why similar conditions can have different genetic causes, or how to collect your family’s health history, the Genetics Learning Hub is for you.

Start exploring today and build your genetic toolkit, one step at a time.