Five thousand. That is how many geographic regions, ethnolinguistic groups and cultural communities 23andMe can now connect you to. We reached that milestone today with the release of 163 new Genetic Groups across North Africa, Egypt and the Arabian Peninsula. When we last marked a milestone in early 2025, that number stood at 4,000.

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

What Are Genetic Groups?

Genetic Groups are clusters of people who share more recent DNA with one another than with the broader population, usually because their families lived in the same region or community for many generations. They are part of 23andMe’s Ancestry Composition report.

By analyzing shared DNA patterns among consented 23andMe members and looking at the information about their families that they choose to share, our scientists can identify genetic signatures more specific than a single label like “North African” can capture. 23andMe Premium members can also explore any Distant Genetic Group connections they may have to these regions.

Which Communities Are Part of This Update?

This update includes Genetic Groups for communities across Egypt, Saudi Arabia, Yemen, the Gulf states, Morocco, Algeria, Tunisia and Libya. Each group reflects a community’s history, and a few show how migration, faith and geography have shaped DNA in this region.

Coptic Communities Along the Nile

Coptic communities trace one of the longest continuous histories in Egypt. The Coptic Christian church traces its roots to the first century CE and still uses Coptic as its liturgical language. Coptic was the final stage of the ancient Egyptian language that gradually gave way to Arabic in everyday life after the Arab conquest of Egypt.

New Genetic Groups now distinguish Coptic communities up and down the Nile, from Upper Egypt to the Faiyum Oasis. Alongside them are other communities from the Nile Delta, plus a group for Egyptian Nubian peoples who have long lived along the Nile in southern Egypt and northern Sudan.

From the Gulf Coast to the Yemeni Highlands

On the Arabian Peninsula, the new Genetic Groups trace communities from the Persian Gulf to the Red Sea. Members can now see connections to communities from Bahrain or the Najd, the vast plateau of central Saudi Arabia, or from the Hijaz, home to Mecca and Medina, which have drawn pilgrims and settlers for centuries.

Farther south, Genetic Groups in the Yemeni Highlands trace to terraced mountain slopes where coffee was first cultivated commercially before merchants shipped it to the world through the port of Mocha.

Amazigh Peoples of the Maghreb

Many of the new North African Genetic Groups connect to Amazigh peoples, one of the indigenous peoples of North Africa. Members can now see connections to people from Kabylia, a mountainous region of northern Algeria, the Rif mountains along Morocco’s Mediterranean coast and the Nafusa Mountains of northwestern Libya.

How Did 23andMe Reach 5,000 Ancestry Regions?

23andMe reached 5,000 ancestry regions by steadily adding Genetic Groups as more members chose to participate and tell us about their family story. Since passing 4,000, recent updates have added new Genetic Groups across Oceania, the Philippines and Southeast Asia and Madagascar. This update brings that same level of detail to North Africa, Egypt and the Arabian Peninsula.

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

Already a 23andMe member? Sign in to see if you have connections to these new Genetic Groups in your Ancestry Composition report. New to 23andMe? Explore how 23andMe can help you discover your roots.

With this update there are now:

• 33 Genetic Groups in Algeria
• 24 Genetic Groups in Egypt
• 5 Genetic Groups in Libya
• 40 Genetic Groups in Morocco
• 15 Genetic Groups in Saudi Arabia
• 13 Genetic Groups in Tunisia
• 6 Genetic Groups in Yemen
• 17 Genetic Groups for Jewish communities in the region
• 10 additional Genetic Groups throughout the region

About one million people in the U.S. have Crohn’s disease, one of the two main types of inflammatory bowel disease (IBD). But Crohn’s disease can be hard to recognize at first, because early symptoms overlap with more common conditions and often come and go over time. 

Our new Crohn’s Disease Polygenic Risk Score report*, now available for 23andMe Premium Ancestry + Health members, can help you understand how your DNA impacts your likelihood of developing Crohn’s. It also provides information about common symptoms and non-genetic risk factors.

What is Crohn’s disease?

Crohn’s disease is a type of IBD, a group of conditions in which the immune system mistakenly attacks harmless bacteria in the gut, leading to chronic inflammation (see sidebar). Most people with Crohn’s are diagnosed between the ages of 15 and 35, but symptoms can develop at any age.

Common symptoms of Crohn’s disease include abdominal pain, diarrhea, fatigue, reduced appetite and unintended weight loss, which sometimes come and go over time. Most people can manage their symptoms with ongoing medical treatment, which may include medication to reduce inflammation and calm an overactive immune response, and they lead full, active lives. But over time, chronic inflammation can lead to serious complications, including scarring and blockages in the intestine, abnormal tunnels called fistulas and an increased risk for colorectal cancer.

Crohn’s disease can also take an emotional toll. Flares can be unpredictable, which can make it hard to plan ahead for work, school, travel or social events. And needing frequent bathroom access can make everyday activities feel stressful. The Crohn’s & Colitis Foundation offers support to people experiencing the challenges of Crohn’s disease.

What causes Crohn’s disease?

The exact cause of Crohn’s disease isn’t fully understood. But scientists believe it involves an overactive immune response, where the immune system mistakenly attacks some of the trillions of harmless bacteria that normally live in our guts. This leads to ongoing inflammation that can cause damage over time.

Research suggests a strong genetic component to Crohn’s disease: an estimated 78% of the difference in risk between different people may be explained by DNA. Scientists have discovered hundreds of genetic variants associated with Crohn’s, including variants in genes like NOD2 (which helps sense bacteria inside our bodies), ATG16L1 (which helps cells engulf and destroy harmful microbes) and IL23 (which helps immune cells communicate with each other).

Besides genetics, many other factors can influence a person’s chances of developing Crohn’s disease. For example, people with a close family member with Crohn’s or another type of IBD are more likely to develop Crohn’s, as are people with Ashkenazi Jewish ancestry or who live in industrialized and urban environments. Smoking cigarettes can also increase risk. Some studies suggest that a healthy diet and regular exercise is associated with lower risk for Crohn’s.

Ways to Take Action

There’s no sure way to prevent Crohn’s disease. But for those experiencing symptoms, learning about your genetics may help reduce the time it takes to get a diagnosis.

For those who do develop Crohn’s, most need medication, and some may also need surgery or nutritional support. But certain lifestyle habits can also help manage symptoms and reduce the frequency of symptom flares. For example:

• Certain foods and drinks may trigger symptoms, such as spicy foods, dairy, caffeine and carbonated drinks. Keeping a food diary can help you identify potential triggers to avoid. It may also be helpful to keep an eye on medications like NSAIDs that can irritate the gut.
• Eating smaller, more frequent meals can be easier on the digestive system, and drinking lots of water throughout the day can help counter fluid loss from diarrhea. 
• Stress can sometimes worsen Crohn’s symptoms, so staying active, getting plenty of sleep and practicing relaxation techniques may help.
• Smoking cigarettes is linked to more frequent and severe flares. If you need help quitting, smokefree.gov offers support and resources.

People with Crohn’s disease also have a higher risk of developing colorectal cancer, so experts recommend getting earlier and more frequent screening colonoscopies to catch potential cancers and pre-cancers.

Learn About Your Genetics

The Crohn’s Disease PRS report was made possible thanks to millions of 23andMe customers who have consented to participate in research. Their contributions help our scientists make genetic discoveries that benefit the entire research community and allow us to develop new reports and features for our members.

If you’re a 23andMe Premium Ancestry + Health member, you can now access the new Crohn’s Disease PRS report (along with your other Health Predisposition reports) to see how your genetics may influence your chances of developing Crohn’s disease.

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

* The 23andMe Crohn’s Disease PRS report is based on a genetic model that includes data and insights from 23andMe consented research participants and incorporates more than 2,000 genetic variants to provide information on the likelihood of being diagnosed with Crohn’s disease. The report does not describe a person’s overall likelihood, does not account for lifestyle or family history and has not been reviewed by the US Food and Drug Administration. The Crohn’s Disease PRS report is not intended to tell you anything about your current state of health, or to be used to make medical decisions or determine any treatment.

Cover image courtesy of Science

Anyone with lungs can get lung cancer. And while many people think exposure to tobacco smoke is the only risk factor, tens of thousands of Americans without this risk factor are diagnosed with lung cancer every year, showing that smoking is by no means the whole story of lung cancer risk. For many people with lung cancer the question of why has had no good answer. For some, a new study is starting to change that.

A collaboration between the 23andMe Research Institute and Dana-Farber Cancer Institute, one of the world’s leading centers of cancer research and treatment, has shown that a specific, rare genetic variant in the EGFR gene, the T790M variant, is the largest known single genetic risk factor for lung cancer. This research, published today in Science, is a crucial step for clinical genetics, potentially transforming lung cancer screening efforts. It is also a fascinating detective story, tracing the variant’s origins back to the colonial history of the American Southeast.

Unmasking of a Powerful Lung Cancer Risk Variant

Not all EGFR T790M changes are the same. This variant is well-known as a mutation that occurs within a tumor and helps lung cancers resist treatments. This study looked at something different: people who inherit this genetic variant and have it in each of their cells since birth. 

This inherited version of the EGFR T790M variant has been reported before in small studies of families with multiple cases of lung cancer. However, the inherited form of this genetic variant is so rare that researchers have struggled to establish precise estimates for how it impacts lung cancer risk or even understand how common this variant really is. The scale of research participation at the 23andMe Research Institute changed this entirely.

More Common and More Impactful Than Expected

Out of over 10 million consented research participants, 641 carried the EGFR T790M variant. While still rare, this is approximately ten times higher than that reported in public databases like gnomAD. 

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

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

A Genetic Ancestry Detective Story

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

People who have the EGFR T790M variant (or “carriers”) disproportionately traced their ancestry to the Southern U.S., particularly Tennessee, Alabama, and Georgia. Using sophisticated genetic dating methods, 23andMe researchers estimated that carriers of the EGFR T790M variant in the Southern Appalachian region shared an ancestor who lived in the early 19th century. Around this time was when early European settlers expanded into the Southern Appalachian region forming smaller tight-knit communities prior to the Civil War.

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

The Power of the 23andMe Research Institute

This research stands out precisely because it would have been extremely difficult using traditional methods. The study highlights the strength of the 23andMe Research Institute, which combines two crucial elements:

1. Large-Scale Data: The sheer size of the research community (over 11 million consented research participants) provided the necessary power to detect the 641 EGFR T790M carriers and characterize the risk from this rare genetic variant. For comparison, the UK Biobank and All of Us databases, while large, contained only 2 and 19 carriers, respectively, making a robust risk assessment impossible with those databases.
2. Wide Variety of Genetics Expertise: This collaboration of researchers, spanning epidemiology, oncology, statistical genetics, and population genetics, was able to go beyond a simple association. They used self-reported data, deep ancestry analysis, and complex genetic dating to not only better understand the magnitude of the lung cancer association but also to contextualize the variant in history.

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

Data analyzed in this study includes participants in the Lung Cancer Genetics Study, an initiative funded by the Susan Wojcicki Foundation and powered by 23andMe in collaboration with 22 lung cancer advocacy organizations. By uniting the stakeholders that support the patients and families living with this critically underfunded disease, the Lung Cancer Genetics Study hopes to help contribute to more discoveries like this in the future.

Additional data came from participants in the INHERIT (Investigating Hereditary Risk in Thoracic Cancers) Study, led by the Dana-Farber Cancer Institute in partnership with GO2 for Lung Cancer (GO2) and the Addario Lung Cancer Medical Institute (ALCMI), which aims to to further understand the genetic risk and predispositions for developing lung cancer.

Learn more about the Lung Cancer Genetics Study and INHERIT.

Did you know that many of the historical and ancient individuals we feature in Historical Matches were discovered by accident during construction work? For instance, in 1903, workmen digging a drainage trench in England’s Gough’s Cave stumbled on the skeleton of Cheddar Man, one of the oldest near-complete human skeletons ever found in Britain. In 1954, construction crews building a fire station in Hungary uncovered a hilltop site that turned out to be the long-lost monastery and burial ground of an 11th-century Hungarian king, Sámuel Aba, and his descendants. And in 2012, workers in Blihun Hanben, Taiwan, uncovered burials dating to the Iron Age while they were constructing a highway. 

This September 14–18th is National Construction Appreciation Week, so we thought it was the perfect opportunity to highlight the unexpected role that construction work (and construction workers) often play in the historical and ancient stories you love learning about. This month, we’re adding one of the most interesting burials construction workers have ever uncovered to Historical Matches: the Shaman of Bad Dürrenberg.

Found During a Water Pipe Job

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

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

Her fame has only grown since. A reconstruction by artist Karol Schauer has been on permanent display at the State Museum of Prehistory in Halle, Germany, for years, and in March 2026 the museum opened a dedicated exhibition on her life and burial, with loans from collections across Europe and the Near East. And ongoing studies of the artifacts she was buried with keep yielding new details. For instance, researchers recently identified microscopic traces of feathers, including goose feathers, suggesting her headdress may have been more elaborate than anyone initially realized.

An Old Genome Gets an Upgrade

The Shaman of Bad Dürrenberg’s DNA has been studied several times. Mitochondrial DNA extracted from her remains in 2009, and a full genome sequenced in 2020, already placed her ancestry firmly among Europe’s Mesolithic hunter-gatherers. This was enough information for researchers who were interested in studying her physical appearance to predict that she likely had dark skin and light eyes, a combination common among hunter-gatherers across Europe at the time.

In 2022, researchers sequenced her genome again, this time to a much higher quality, as part of a study of Neolithic farmers who settled the same general region around 2,000 years after she lived. Her high-quality genome gave them a detailed benchmark for local hunter-gatherer ancestry, which they used to measure exactly how much of it was present in the incoming farming population. The answer: very little. These farmers did carry hunter-gatherer ancestry, but this ancestry was likely acquired earlier, as farming populations expanded through southeastern Europe.

Neighbors, Two Thousand Years Later

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

Learn More

Curious whether your DNA connects you to the Shaman of Bad Dürrenberg, one of the Neolithic farmers who came after her or any of the hundreds of other historical figures in our database? 23andMe Premium members can explore the Historical Matches feature to find out.

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

Key Factors Shaping Prostate Cancer Risk

Age is one of the strongest prostate cancer risk factors. Prostate cancer is rare in men younger than 40, but the chance of developing it climbs quickly after age 50, and roughly 6 in 10 cases are found in men older than 65.

Ancestry matters too. African American men are more likely to develop prostate cancer, tend to be diagnosed at younger ages and are more likely to develop aggressive forms of the disease. In the U.S., more than 1 in 6 African American men develops prostate cancer by age 80, compared with about 1 in 8 men of European descent. Researchers are still working out how much of that difference reflects genetics, environment or unequal access to screening and care.

Family history is a third factor. Having a close relative with prostate cancer, or with certain other cancers, raises your own likelihood.

The Genetic Spectrum: From Rare to Common Variants

Your genetics can influence prostate cancer risk in two ways.

The first involves rare genetic variants that cause a large impact. An example is a variant called G84E in the HOXB13 gene. Men who have this variant have a 33 to 53 percent chance of developing prostate cancer by age 80, and they tend to develop prostate cancer earlier than those without the variant. Another example are variants in the BRCA genes, particularly BRCA2. While these variants are mostly known for increasing the risk of breast and ovarian cancer, they can also increase the risk of prostate cancer. Genetic variants like these are uncommon, and they account for only a small share of all prostate cancer cases, but for the people who have them the effect is meaningful.

The second route involves thousands of common genetic variants, each shifting the likelihood of prostate cancer by a tiny amount. Any one of these variants doesn’t make much of an impact on their own, but together they can move a person’s likelihood noticeably. Scientists capture this combined effect in a polygenic risk score, a single number that sums up the influence of many small genetic contributions at once.

That second approach comes with an important limitation. Many of the variants linked to prostate cancer, and the risk models built from them, were identified mostly in men of European descent and may be less informative for men of other ancestries. This same research gap may contribute to worse outcomes in the communities that already carry more of the burden. Closing it depends on genetic studies that include far more people from underrepresented backgrounds.

What Your 23andMe Results Can (and Can’t) Tell You

23andMe offers three reports that approach prostate cancer from these two different angles.

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

The Prostate Cancer Polygenic Risk Score report* uses more than a thousand common variants to estimate your likelihood of developing prostate cancer. It is available to 23andMe Premium Ancestry + Health members who reported their birth sex as male.

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

What You Can Do

Both reports can inform a more specific conversation with your healthcare provider. If you have a prostate, a few things are worth acting on regardless of your results:

• Talk with a healthcare professional about the benefits and risks of prostate cancer screening. Guidelines vary, but screening may be recommended starting at 50, or as early as 40 or 45 if you are African American, have an increased genetic likelihood or have a family history.
• Maintain a healthy weight. Some studies have found that men who are overweight are more likely to develop aggressive forms of prostate cancer.
• If you smoke, you can find resources and support for quitting. Smoking is associated with an increased risk of dying from prostate cancer.
• Learn and write down your family health history, including cancers on both sides of your family. It is one of the most useful things you can bring to a screening conversation.

Take a few minutes this month to check your genetic results and, if anything stands out, bring it to your next appointment. If you have learned you carry a HOXB13 variant and want help figuring out what comes next, start here.

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

Warnings & Limitations:

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

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

September is National Cholesterol Education Month, and September 24 is Familial Hypercholesterolemia (FH) Awareness Day. Together they make this a good time to ask a question that standard cholesterol testing does not answer: why is your number the way it is?

Same Number, Two Very Different Stories

A standard lipid panel measures how much cholesterol is circulating in your blood right now. It is a snapshot, and a useful one. About 55% of people in the U.S. will develop high cholesterol by their 70s, and high LDL (sometimes called “bad cholesterol”) raises the risk for heart disease, stroke and peripheral artery disease. Because high LDL usually causes no symptoms at first, regular screening matters.

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

For a smaller group, the cause is monogenic, meaning a single genetic variant is responsible for most of their LDL level. That is a fundamentally different situation, and it calls for a different response.

When One Gene Does the Heavy Lifting

FH is very high cholesterol that runs in families. Variants in genes including LDLR, APOB and PCSK9 reduce the liver’s ability to clear LDL from the bloodstream. In people with a variant in one of these genes, LDL levels can be elevated from birth rather than creeping up as you age.

That lifetime exposure is what makes FH serious. About 1 in 250 people worldwide have FH, and according to the Family Heart Foundation as many as 70% of them have not been diagnosed. Left untreated, men with FH have roughly a 50% risk of a heart attack by age 50, and women roughly a 30% risk by age 60. Sometimes a heart attack is the first sign of elevated LDL.

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

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

What Your Genetics Can Add

23andMe offers a few different windows into cholesterol-related genetics.

• The Familial Hypercholesterolemia Genetic Health Risk report* looks for 24 variants, one in the APOB gene and 23 in the LDLR gene. It does not cover all of the more than 1,000 known FH variants, so a negative result does not rule FH out.
• If you do not have an FH variant, the LDL Cholesterol PRS report* uses a polygenic score built from more than 2,000 genetic markers to estimate your likelihood of developing high LDL cholesterol. This covers more typical, common genetic changes that, combined with diet and lifestyle, can lead to high LDL cholesterol.
• The SLCO1B1 Drug Transport report** covers a variant that affects a protein responsible for transporting statins out of the bloodstream and into the liver. Statins are a commonly prescribed medication used to lower cholesterol. Certain genetic changes in the SLCO1B1 gene are associated with higher chances of experiencing side effects.

None of these diagnose a condition or tell you your cholesterol level today. They can give you and your clinician more context for a conversation.

What You Can Do This Month

• Get a baseline lipid panel if you have not had one recently. Most guidelines recommend adults start in their twenties and repeat every few years.
• Ask your relatives about early heart disease, heart attacks before age 55 in men or 65 in women, or cholesterol that has been high for as long as anyone can remember. These are red flags worth mentioning to your doctor.
• If your numbers stay high despite doing everything right, ask why. A genetic counselor can help you figure out whether genetic testing makes sense.
• Ask about Lp(a) testing. Lipoprotein(a) is a cholesterol-carrying particle that can significantly raise your risk for heart disease. It’s often skipped in routine lab tests. Your Lp(a) levels are largely set by your genetics and stay fairly stable for life, so a single test may be all you need.

Curious what your DNA says about your cholesterol? Review your Familial Hypercholesterolemia Genetic Health Risk report and your LDL Cholesterol PRS report. And if you want to go deeper on how monogenic and complex conditions differ, our Genetics Learning Hub is free and open to everyone.

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

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

Imagine hearing a list of 15 unrelated words, spending the next 20 minutes on something else, then recalling nine or more of them. That is a strong performance for someone in their late 50s. Now imagine doing it in your 80s. A small group of older adults can, and researchers call them SuperAgers. Are these people simply genetically lucky? A study published in July 2026 suggests the answer is more complicated than that.

How Does the APOE Gene Affect Alzheimer’s Risk?

The APOE gene is the strongest common genetic influence on late-onset Alzheimer’s disease, and it typically comes in three versions that push risk in different directions. 

The e3 version is the most common and is considered neutral. The e4 version increases the likelihood of developing Alzheimer’s and is linked to an earlier age of onset. About 25% of people carry one copy of e4 and 2–3% carry two copies. People with two copies have been estimated to have up to a 60% chance of developing Alzheimer’s by age 85 compared to a risk of about 10% in the general population.

The e2 version is the least common, but it has been associated with a lower likelihood of developing Alzheimer’s. It also shows up more often in people who live exceptionally long lives. In an analysis of 28,297 participants across seven studies of aging, carrying a single copy of e2 was associated with greater odds of reaching extreme old age.

One important caveat runs through all of this. Most genetic studies and risk estimates for Alzheimer’s disease come from studies of people of European descent. How well those numbers transfer to people of other ancestries remains an open question, even as Alzheimer’s disproportionately affects Black and Hispanic Americans.

How Might APOE e2 Protect Neurons?

New laboratory research suggests e2 may help neurons protect their own DNA. Researchers grew human neurons from stem cells that were genetically identical except at the APOE gene, then compared them. Neurons carrying the e2 variant showed lower levels of DNA damage and were more resistant to becoming senescent, a state in which cells stop functioning normally but do not die, after being exposed to stress compared to neurons carrying the e4 variant. The team saw similar patterns in the brains of aged mice carrying human e2 and e4 variants of the APOE gene.

Notably, adding purified e2 APOE protein to neurons that had the e4 genetic variant reduced DNA damage signaling, which hints that some of the protection may come from the APOE protein itself. It’s important to remember this was observed in cells and mice. It is not a treatment, and the researchers are clear that the precise molecular steps still need to be worked out.

Do SuperAgers Have More Protective Genetics?

Here is where the story turns. If e2 lowers the chances of Alzheimer’s and e4 raises it, you might expect more SuperAgers to have the e2 variant and few would have e4. That’s not what researchers found.

They compared the DNA of 142 SuperAgers and 89 cognitively healthy adults of similar age. 12.7% of SuperAgers and 13.1% of controls had at least one copy of the e2 variant. The proportion carrying at least one e4 variant was 15.7% and 19.0%. Neither difference was statistically significant. 

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

In other words, genetic variants that impact your chances of getting Alzheimer’s, including e2, e4 and other common genetic risk factors, don’t change your chance of having the memory of a 60-year-old at age 85. 

What This Study Cannot Tell Us Yet

Does this mean that APOE doesn’t actually matter? No. The APOE e4 variant remains the strongest common genetic influence on late-onset Alzheimer’s that researchers have found, and nothing in this study challenges that. What the study asked was a narrower question: whether APOE and other common variants explain why some people keep exceptional memory into their 80s. 

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

So the question remains open: what influences your chances of healthy aging? Other genetic factors, lifestyle, environment and probably some combination of all three. Answering this question will require more research and participation from larger and more diverse groups of individuals.

Curious about your own APOE variants? 23andMe’s Late-Onset Alzheimer’s Disease Genetic Health Risk report* can tell you if you carry the e4 variant, and Premium Ancestry + Total Health members can see if they carry other APOE variants through exome sequencing. 

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

August is National Eye Exam Month, a yearly nudge to finally book the appointment you may have been meaning to schedule since spring. It’s tempting to treat that visit as a quick read of the eye chart and potentially a refreshed glasses prescription, but a comprehensive eye exam looks much deeper into the eye, and what a doctor finds there can say something about your broader health, and sometimes about your genes.

What Your Eye Doctor Is Really Looking For

An estimated 11 million Americans over age 12 need some form of vision correction. During a comprehensive exam, an eye doctor isn’t only checking how well you see, they’re also looking for early signs of conditions like cataracts, diabetic retinopathy, age-related macular degeneration and glaucoma, ideally before those conditions cause any noticeable vision loss.

The Genetics Behind Eye Conditions

Age-related macular degeneration, or AMD, damages the macula, the part of the retina responsible for sharp central vision. It’s estimated that more than 10 million people in the U.S. have some form of AMD. AMD risk is associated with variants in many genes, most notably CFH and ARMS2. Other factors like age, smoking and family history can also influence risk. 23andMe has an Age-Related Macular Degeneration Genetic Health Risk report* that can tell you whether you may have an increased risk of developing AMD based on your genetics.

Glaucoma develops when the optic nerve, which carries visual signals from the eye to the brain, becomes damaged, often due to high pressure inside the eye. Vision loss from glaucoma can be so gradual that many people don’t notice it until it’s advanced, which is part of why regular screening matters. Many different genetic variants impact the likelihood of developing glaucoma, 23andMe’s Glaucoma PRS Report** uses more than 8,000 genetic markers to estimate a person’s likelihood. Other factors like age, family history and other health conditions can also influence your chances.

Diabetic retinopathy, damage to the blood vessels in the retina caused by prolonged high blood sugar, is a leading cause of blindness in American adults and develops as a complication of diabetes. Type 2 diabetes is the most common form of diabetes, and many people with diabetes or prediabetes don’t know they have it. Because diabetic retinopathy follows from diabetes, an eye exam can sometimes be the first place these changes are caught. Thousands of genetic variants can contribute to your likelihood of type 2 diabetes along with other factors like diet, weight and lifestyle. For those curious about their genetics say, 23andMe offers a Type 2 Diabetes report**.

Nearsightedness, or myopia, is probably what you think of when you think of an eye exam. It affects an estimated 45 percent of U.S. adults and typically develops in childhood, when the eye grows just slightly too long for light to focus correctly on the retina. 23andMe’s Nearsightedness PRS Report** considers more than 2,700 genetic markers when estimating a person’s likelihood of being nearsighted, but other environmental factors like limited time spent outdoors during childhood can also contribute to your chances.

Migraines might seem like an outlier on this list, but they belong here too. Some people experience aura symptoms, which can include temporary visual disturbances, including flashes of light and blind spots, when they experience a migraine. A comprehensive eye exam is a useful way to rule out an underlying eye problem that could be contributing to head pain. The cause of migraines is still a mystery, but genetics, along with a family history of the condition, can increase likelihood of developing it. You can learn more about your genetics connected to migraines, with the 23andMe Migraine PRS report**.

What You Can Do This Eye Exam Month

• Book a comprehensive exam. Even if your vision feels fine, a dilated eye exam can catch changes to the retina and optic nerve well before you’d notice symptoms.
• Know your family history. Glaucoma, AMD, migraine and diabetes all run in families, and sharing that history with your doctor helps them recommend the right screening schedule.
• Ask about blood sugar and blood pressure. Since diabetic retinopathy and some AMD risk factors connect back to broader metabolic health, managing these numbers can support your eyes as well as the rest of your body.
• Don’t ignore new visual symptoms. Experts agree sudden blind spots, flashes of light or eye pain warrant a prompt visit rather than a wait and see approach.
• And if you have kids, encourage outdoor time for them. More time spent outdoors during childhood is linked to a lower likelihood of developing nearsightedness.

Curious what your own DNA suggests about your likelihood of developing AMD, glaucoma, nearsightedness or migraine? A 23andMe Premium Ancestry + Health membership unlocks these reports and many more, giving you one more part of the picture to bring to your next eye appointment.

* 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 Age-Related Macular Degeneration (AMD) genetic health risk report is indicated for reporting of the Y402H variant in the CFH gene, and the A69S in the ARMS2 gene and  describes if a person has variants associated with an increased risk of developing AMD. The variants included in this report are common in many ethnicities, but are best studied in people of European descent.

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

Some ancient peoples get to be famous. The Vikings have blockbuster shows. The Romans have, well, an empire’s worth of pop culture. The Sarmatians don’t get nearly as much attention, despite once dominating a vast stretch of Central Europe for centuries. In fact, many historians describe the Sarmatians as a “forgotten people,” a once-formidable presence on the edge of the Roman world not claimed as ancestors by any modern nation. This month, we’re helping to restore their legacy by adding 44 of them to Historical Matches.

Who Were the Sarmatians?

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

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

156 New Genomes, and Some Genuine Surprises

Last year, researchers published a study in Cell sequencing 156 new ancient genomes from Sarmatian- and later Hun-period sites across the Carpathian Basin and the Romanian plains in order to learn about the genetics of the Sarmatians. 

Most of the individuals they sequenced carried a distinct steppe ancestry that linked them to their distant Sarmatian relatives who never left the Ural and Kazakh regions. This signal was strongest in the earliest generations and gradually diluted as later Sarmatians mixed with the region’s existing population.

But a handful of individuals didn’t fit this pattern at all. Two men buried at the same cemetery in southern Hungary had ancestry that traced entirely to Scandinavia, thousands of kilometers to the north, suggesting a previously undetected wave of migration into this Sarmatian community. Others carried substantial East Asian-related ancestry, thousands of kilometers to the east.

Genetic Foreshadowing of a Migration to Come 

Perhaps the most surprising discovery didn’t come from a Sarmatian burial at all. Two individuals from an even earlier Iron Age population in the Carpathian foothills, who lived centuries before the Sarmatians’ documented arrival in the region, turned out to have ancestry that closely resembled the later Sarmatian populations that migrated into the region. It’s a hint that Sarmatians may have trickled into the region in small numbers long before their main migration, a genetic foreshadowing of a migration to come.

A Much More Well Known Genetic Group Also Gets an Update

This month’s Historical Matches update isn’t only about a people history nearly forgot, though. We’ve also added five new individuals to our existing Hungarian Royalty group, including King Béla II, a medieval Hungarian ruler identified for the first time after going unnamed among royal remains for centuries. We also added Béla, Duke of Macsó, a prince murdered by rival noblemen in 1272 whose identity was only recently confirmed through DNA. Their genomes were recently sequenced as part of a large scale study of over 400 individuals who were buried in the Royal Basilica of Székesfehérvár, the traditional coronation and burial site of Hungarian monarchs. 

Learn More

Want to see if your DNA connects you to the Sarmatians, Hungarian Royalty, or to hundreds of other historical individuals? 23andMe Premium members can explore these new additions through the Historical Matches feature.

Have you ever looked at your ancestry results and wondered, “Where did this Scottish ancestry come from, my mom’s side or my dad’s?” If you’re one of the millions of 23andMe members who haven’t connected with a parent who has tested with us, that question has been sitting unanswered.

That changes today.

We’re launching Premium Parental Inheritance, a feature that shows you which side of your family each ancestry region in your results came from regardless of whether or not a parent has ever taken a 23andMe test. Powering this expansion is a DNA analysis we call Family Phasing, a method that uses your existing DNA relatives to determine which side of your family your ancestry comes from. The feature is now available to all 23andMe Premium members.

Your Ancestry Has Two Sides. Now You Can See Them.

Parental Inheritance has long let customers see their Ancestry Composition split by parent: how much of your Andalusian, Asturian & Castilian ancestry came from one side, how much of your Nigerian ancestry came from the other. For people who had it, the reaction was often an “aha” moment. Suddenly your results became a story about blending two distinct family histories.

But accessing it required connecting with a biological parent in the 23andMe database. If your parents had passed away, were unknown to you, or simply weren’t interested in testing, Parental Inheritance wasn’t available to you. That left many without a way to access a feature that helps answer so many questions.

Family Phasing changes that for many people who have enough relatives in the dataset. Using these relatives, we can often confidently determine parental inheritance for large sections of your DNA.

If you’re a 23andMe Premium member, you’ll now see your Ancestry Composition results split into Parent 1 and Parent 2 — showing how much of each ancestry region you inherited from each side.

Some people won’t immediately know which labels map to their maternal or paternal sides. You can use your ancestry percentages as clues. If Parent 1 shows a high percentage of Irish ancestry and you know that Irish ancestry runs on your dad’s side, you can rename Parent 1 to “Paternal Side.” But if one of your parents has tested with 23andMe and is participating in DNA Relatives, you’ll see them connected to their corresponding side.

The Science: How Family Phasing Works

To understand what’s new, it helps to understand how Parental Inheritance worked before.

Your 23 chromosomes come in pairs: one chromosome in each pair comes from your mother, the other from your father. Figuring out which genetic information came from which parent is called phasing. Previously, 23andMe could perform a high-quality phasing by directly comparing your DNA to a connected biological parent’s.

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

Family Phasing solves this for portions of your genome by looking at the DNA relatives, even distant ones, you already have in the 23andMe database. The key insight: if you and a relative share a segment of DNA, and that relative is on your mother’s side, that shared segment probably came from your mother. Family Phasing uses these shared DNA segments across many of your relatives to build a confident picture of which portions of your ancestry came from each parent, no connected parent required. 

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

Your Upgraded Path to Parental Inheritance

Thanks to our new Family Phasing technology, Parental Inheritance is getting a major upgrade and moving to 23andMe Premium. If your parents have never tested with 23andMe, this is what you’ve been waiting for. Premium members without parents connected can now explore their parental inheritance for the first time.

If you’re a 23andMe Premium member and you previously had Parental Inheritance through a connected parent, your experience is evolving. The underlying science is now powered by Family Phasing. 

If you’re not already a 23andMe Premium member, your previous Parental Inheritance is no longer available. However, if you upgrade to a 23andMe Premium membership, your results will begin computing automatically, and you’ll receive a notification when your report is ready.

What’s Coming Next

Parental Inheritance is more than a single feature — it’s a lens that can be applied across your entire genetic story. We’re exploring how to bring the same Parent 1 / Parent 2 view to other parts of your 23andMe experience, so you can understand not just what your DNA says, but which side of your family it came from.

Your ancestry has always had two sides to it. Ready to see both? If you’re not currently a 23andMe Premium member, but interested in this feature, check out the 23andMe Premium membership to unlock Premium Parental Inheritance and find out which side of your family shaped the ancestry you carry.

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

Today, 23andMe added 137 new Genetic Groups across Cambodia, Indonesia, Laos, Malaysia, Myanmar, Madagascar and Thailand, rounding out the most detailed ancestry breakdown available for this region yet. 

Southeast Asia isn’t one history so much as many histories layered on top of each other, and it’s one of the most genetically intricate regions on Earth. Cambodia’s Khmer Empire once stretched from the Mekong Delta into what is now Thailand and Vietnam. Myanmar’s government officially recognizes 135 distinct ethnic groups within its borders. Further west, Madagascar’s people speak a language whose closest relatives sit nearly 4,000 miles away, across the Indian Ocean in Borneo. Now, 23andMe’s Ancestry Composition report better reflects these diverse stories from a region that has historically been underrepresented in genetic research.  

What Are Genetic Groups?

Genetic Groups are part of 23andMe’s Ancestry Composition report. They’re clusters of people who share more recent DNA with one another than with the broader population, usually because their families lived in the same region, city or community for generations. By analyzing shared DNA patterns across thousands of 23andMe members with ancestry from this region, our scientists can identify genetic signatures more specific than a single label like “Thai” or “Indonesian” can capture. Most 23andMe members with ancestry from this region will see at least one new Genetic Group reflected in their results, and 23andMe Premium members can also explore any distant Genetic Group connections they may have to these regions.

Communities Written Into the Update

Some of the 137 new groups trace back to communities whose histories rarely make it onto a genetic map. In Myanmar’s Chin Hills, near the border with India, members can now see if they have connections to specific Chin subgroups, including the Falam, many of whom still speak a dialect known as Falam Chin.

In Cambodia, these new Genetic Groups now distinguish communities across the Khmer heartland, from the Tonlé Sap Basin to the Khmer Krom, a community in Vietnam’s Mekong Delta. A separate new group traces to the Cham, descendants of the once-powerful kingdom of Champa, which ruled along the coast of central Vietnam for centuries.

Madagascar tells one of the more unusual stories in this update. The Malagasy people trace to Austronesian seafarers who reached Madagascar roughly 1,500 years ago, likely sailing from what is now Borneo. Their descendants later mixed with East African populations. That voyage connects Madagascar to the same Austronesian expansion that carried seafaring peoples across the Philippines, Indonesia and the far islands of Polynesia.

Réunionnais and Seychellois communities in this update trace to a much more recent chapter in history. Both Réunion and Seychelles were uninhabited until European colonization began in the 17th and 18th centuries, when French settlers brought enslaved people from East Africa and Madagascar to work sugar and spice plantations. It’s a reminder that many stories can be hidden within a broad Ancestry Composition population.

Rounding Out the Map of Southeast Asia

Southeast Asian and Malagasy communities have historically been underrepresented in genetic research, which has often meant broader labels and fewer specific insights for 23andMe members with roots in the region. This update builds on Genetic Groups 23andMe has already added across Oceania, the Philippines and Vietnam, and makes 23andMe’s Ancestry Composition report the most detailed breakdown available for this part of the world.

None of this would be possible without the 23andMe members who chose to share their family stories and participate in research. There are more stories to be told, and we’re committed to finding ways to tell them with DNA.

Already a 23andMe member? Sign in to see if you have connections to these new Genetic Groups in your Ancestry Composition report.

With this update there are now:

• 34 Genetic Groups in Indonesia
• 24 Genetic Groups in Cambodia
• 23 Genetic Groups in Thailand
• 15 Genetic Groups in Myanmar
• 12 Genetic Groups in Laos
• 9 Genetic Groups in Malaysia
• 5 Genetic Groups in Madagascar and nearby islands
• 15 additional Genetic Groups throughout the region

Finding the right antidepressant is often a long, frustrating process. Fewer than half of people respond to the first SSRI (selective serotonin reuptake inhibitors, a common type of antidepressant including escitalopram (Lexapro®), citalopram (Celexa®), and sertraline (Zoloft®)*) they try. Within a year of starting treatment, roughly 80% of patients switch medications or stop taking them altogether. And side effects are the most common reason why people switch or stop.

The CYP2C19 gene affects how your body processes many medications, including many commonly prescribed SSRIs, and that in turn can affect whether you experience side effects. A new 23andMe study published in The Pharmacogenomics Journal is showing how certain changes in CYP2C19 impact specific side effects people experience when taking SSRIs.

Tracking the Connection Between DNA and Antidepressants

23andMe researchers analyzed survey responses from more than 114,000 consented research participants who reported having taken escitalopram, citalopram or sertraline. Each was asked whether the medication worked for them, what side effects they experienced and why they stopped taking it if they did. 

The genetic focus was the CYP2C19 gene, which is important for processing or ‘metabolizing’ SSRIs. The participants were sorted into categories of metabolizer types, ranging from poor (slowest) to ultrarapid (fastest) based on which genetic variants they had.

How Your Genes Impact Side Effects

This study painted a clear picture of the frustrating “trial-and-error” process of mental health treatment: roughly 63% of participants had taken at least two antidepressants in the hopes of finding one that worked. It also gave researchers a rare, clear picture of how common different side effects are in a large, diverse group of people. Participants reported a range of effects, including anxiety, sleep problems, emotional numbness, sexual problems, gastrointestinal issues, tremors and weight gain, and researchers were able to see how common these side effects were broken down by which drug people were taking as well as their sex and ancestry.

DNA also plays a massive role in how participants tolerate these drugs. If you have a version of the CYP2C19 enzyme that works more slowly, the drug lingers in your system at higher concentrations, which raises your likelihood of side effects.

Slower metabolizers reported side effects more often than faster metabolizers. But this study was large enough to look at specific side effects as well. Among participants taking escitalopram, slower metabolizers were significantly more likely to suffer from sleep and sexual problems compared to faster metabolizers. Similarly, among those taking sertraline, more slower metabolizers reported experiencing tremors than did faster metabolizers.

These side effects contributed to slow processors quitting their medication altogether due to side effects (depending on which drug they took, between roughly 25–30% of poor metabolizers stopped compared with about 20% of ultrarapid metabolizers).

Finally, this study highlights why diversity in genetic research matters. Genetic ancestry can shape how common these variants are in different populations. Roughly 17.8% of East Asian-ancestry participants were poor metabolizers, compared with about 2.3% of European-ancestry participants. 

Unlocking Patterns That Smaller Studies Couldn’t

Earlier studies on how genes impact how well antidepressants work for individuals were too small to spot patterns, especially when it came to specific side effects. But because 23andMe has such a massive community of people choosing to participate in research, 23andMe researchers could pair genetic data with real, personal experiences on these medications. Other large genetic databases are only just starting to collect this kind of medication history, which has slowed down progress in the past. This study shows exactly what can happen when millions of people come together to further advance medical science.

Translating Findings into Better Care

For those who are considering an SSRI, or who have struggled with side effects on one in the past, genetics may offer important insights. 23andMe+ Premium™ members can view their CYP2C19 Drug Metabolism report** and see how it may affect response to certain medications including citalopram. Reviewing your result with your healthcare provider can give you one more data point as you work together to help find a treatment that fits.

* Lexapro® is a registered trademark of H. Lundbeck A/S; Celexa® is a registered trademark of Forest Laboratories, Inc; Zoloft® is a registered trademark of Viatris Specialty LLC.

** 23andMe PGS Pharmacogenetic 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 Pharmacogenetic 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. Certain CYP2C19 results should be confirmed by an independent genetic test prescribed by your own healthcare provider before taking any medical action. 

Warning:

Test information should not be used to start, stop, or change any course of treatment and does not test for all possible variants that may affect metabolism or protein function. The PGS test is not a substitute for visits to a healthcare professional. Making changes to your current regimen can lead to harmful side effects or reduced intended benefits of your medication, therefore consult with your healthcare professional before taking any medical action. For important information and limitations regarding Pharmacogenetic reports, visit www.23andme.org/test-info.

What if your DNA says you should have a disease but you don’t? In most cases a genetic predisposition only increases the chances of developing a condition, it doesn’t guarantee it. However, certain genetic variants, especially those linked to a severe, early-onset disease such as sickle cell disease or cystic fibrosis, have been treated as fate: inherit the genetic variants, and the disease follows. But a small, growing body of research is complicating that picture. Scientists are finding people who carry genetic variants that should cause severe conditions and yet these people are healthy.

These rare, resilient individuals have “escaped” their fate. Figuring out why is starting to reshape how we think about genetics and how new treatments can be discovered.

The Search for Genetic “Escapers”

Very often scientists study sick people to find the DNA changes behind their disease. Studying healthy people to find genetic changes that protect against disease can be much harder, since finding a handful of resilient people can mean sorting through hundreds of thousands of genomes. 

The first large effort to do this, called the Resilience Project, screened data from 589,306 people (the majority of whom were consented 23andMe research participants) and found 13 adults carrying genetic variants for 8 severe childhood conditions who never developed symptoms.

Since then, similar searches have turned up similar results. A 2026 study of more than 9,600 healthy adults in Singapore found nine people carrying variants associated with severe conditions such as limb-girdle muscular dystrophy and hereditary spastic paraplegia that typically appear in infancy or childhood. Several studies have found a strikingly consistent pattern: for any given disease-associated gene that’s screened, between one and three resilient individuals turn up per 10 million people. That is rare, but real.

What Might Help Someone Escape?

So what might separate an “escaper” from someone who develops the disease their DNA predicts? Researcher points to a few overlapping explanations, from additional genetic variants that may cancel out the damage, to differences in how actively a gene is expressed in the first place, to the environment a person lives in.

Protective Genetic Variants

“Escapers” may have additional genetic variants elsewhere in their DNA that counteract a disease-causing variant. A notable example is sickle cell disease. Some people carry a variant in the BCL11A gene that keeps a fetal form of hemoglobin switched on into adulthood, offsetting the effect of the sickle cell variant. This discovery helped lead to new, approved gene-editing treatment for sickle cell disease.

Another example was found looking at people who had naturally very low LDL cholesterol and a subsequent low risk for heart disease. It turns out these people had genetic variants that lower the expression of the PCSK9 gene. This discovery led to the development of a class of cholesterol-lowering drugs that’s often used to treat people with genetic variants that lead to very high cholesterol (known as familial hypercholesterolemia). In rare cases there are “escapers” who carry both familial hypercholesterolemia variants and protective PCSK9 changes and end up with cholesterol levels that are milder than expected.

Variable Activation

A second, more surprising, explanation for how “escapers” manage to stay healthy could involve how actively each copy of a gene gets used. For most genes you inherit one copy from each parent, and it was assumed both copies are equally active. However, that’s not necessarily true.

The best-known example of this is X-inactivation. For those with two X chromosomes, each cell randomly shuts off one of them early in development. Something similar, though far less understood, appears to happen with genes on the other 22 pairs of chromosomes we carry. In some cells, one parent’s copy of a gene can be turned up while the other is turned down, a phenomenon called autosomal random monoallelic expression, or aRMAE.

If you inherit one healthy copy of a gene and one disease-causing copy, which copy is more active in a given cell type can make the difference between staying healthy and developing disease. Depending on how it’s measured, as many as 50% of our genes may show this kind of activity bias.

Environment and Lifestyle 

Finally, environment and lifestyle can shift the odds for people carrying a disease-causing variant. Take the case of a 75-year-old individual who is cognitively healthy despite carrying a variant for a dominantly inherited form of Alzheimer’s disease that typically causes symptoms decades earlier, particularly in his family. Researchers suspect his resilience may trace back to years of heavy heat exposure earlier in life, which may have raised his levels of heat shock proteins, a class of proteins that help cells clear out misfolded proteins like the ones that build up in Alzheimer’s disease.

Most of us won’t stumble into that kind of protection by accident, and you don’t need an extreme lifestyle to benefit from this idea. Many everyday genetic predispositions, not just rare ones, respond to the basics: a healthy diet, quality sleep and regular exercise.

Why This Research Matters

Resilient individuals remind us that there are many exceptions to genetic rules. Genetics can’t always predict with 100% certainty who will get sick. Looking at healthy individuals, and individuals from diverse genetic backgrounds, can help us find new potential treatments that may benefit us all. 

At 23andMe, important advances in genetics research start with the participation of customers like you. Join our research community.

How old are you, really? Your birth certificate gives one answer. The cells in your body may be telling an entirely different story.

Researchers have debated how much of a long life comes down to your genes versus your habits. But it’s not simply one or the other, and how we measure your age can help us understand your health long before your next birthday. Your organs, and even individual cell types within them, can age faster or slower than your calendar age suggests. And for the first time, scientists are starting to measure that directly.

The Genetics of a Long Life

Genetics has always been part of the longevity story. Some estimates suggest up to about 50 percent of lifespan can be attributed to genetics, particularly once you set aside causes of death like accidents or infections. 

The clearest example is the APOE gene. The e4 variant is linked to a higher likelihood of late-onset Alzheimer’s disease, while the e2 variant is associated with longer lifespan. Other genes, including FOXO3A, show up again and again in studies of people who live exceptionally long lives.

But genetics alone isn’t the whole story.

Aging in Waves, Not a Straight Line

A new review in Nature Medicine highlights research that’s challenging an assumption many of us have carried around without questioning: that aging is a slow, linear march through the decades.

But first, how are we measuring aging? Biological age isn’t tested with one specific method, instead a family of approaches that includes DNA methylation or “epigenetic” clocks (the original approach, measuring chemical tags on your DNA), proteomic clocks (measuring thousands of proteins in a tissue sample), and clinical biomarker-based models (based on standard bloodwork markers such as cholesterol or blood sugar) can be used.

When we use these methods we see that your body’s age doesn’t always line up with your calendar age. One proteomics study found something closer to three waves of accelerated change, clustering around ages 34, 60 and 78.

And aging doesn’t move at the same speed throughout your body. A landmark study built separate aging clocks for 11 individual organs, from the heart to the kidneys, using blood plasma proteins from more than 5,600 adults. This analysis found that nearly 20% of people had faster aging in one organ, and this aging was connected to organ-specific diseases.

Across multiple studies, faster aging in a given organ tends to line up with higher risk for the diseases tied to that organ. A heart that ages quickly has a higher risk of heart failure, and accelerated aging of the brain and blood vessels tracks with faster progression of Alzheimer’s disease.

Where Genetics and Biological Clocks Meet

Being able to measure aging in specific organs, and even at the cellular level, is beginning to allow us to combine genetics and biological clocks to make better risk predictions. Carrying the APOE e4 variant raises your predisposition to Alzheimer’s, but it doesn’t tell the whole story. 

A recent study looked at the astrocytes, the cells that keep neurons nourished and healthy, of people with two copies of the e4 variant. The researchers found that people with faster aging astrocytes had 3 times the Alzheimer’s risk of those with normally aging astrocytes. And those with younger astrocytes had a lower Alzheimer’s risk even with the same genetics. In other words, knowing both how your cells are aging and your genetic predisposition for Alzheimer’s disease can tell you more about your risk than either measure alone.

What You Can Do

Biological clocks are still in the early stages of moving from research labs into everyday medical care. But research is showing associations between your lifestyle and biological age:

• Staying physically active, not smoking and limiting alcohol were each associated with slower aging and lower disease risk in a large study of more than 17,000 European adults.
• Lower stress was associated with slower aging in African American research participants.
• Better sleep quality was associated with a younger biological age in a study of more than 360,000 UK Biobank participants.
• Loneliness was linked to faster aging and more chronic health conditions in a study of over 1,300 diverse participants in the United States.

Direct measurements of your biological age can build on what you know about your genetics to tell you how you’re actually doing today. And your habits may change tomorrow’s outcomes.

Track Your Own Biological Age

23andMe’s Biological Age feature allows you to investigate your own aging clock. Using 13 blood-based biomarkers, a model estimates your biological age and flags which biomarkers may be pulling it away from your calendar age. It’s available to 23andMe Premium Ancestry + Total Health members through biannual blood testing, and it’s also available as a standalone blood test for other 23andMe members.

Curious how genetics and lifestyle fit into the bigger longevity picture? Read more in How Genetics and Lifestyle Shape Longevity.

Ever notice that some days you can power through a spreadsheet but still can’t stop your mind from wandering during a long meeting? That split experience, sharp problem solving on one hand and wandering focus on the other, might not just be a mood or a bad night’s sleep. According to a recent study these two experiences may be shaped by genetically distinct systems in the brain.

The study, published in Molecular Psychiatry, is the first large-scale look at the genetics of sustained attention (your ability to stay locked in on a task over time) and executive function (the mental toolkit you use to plan, remember and switch between tasks). The findings suggest these two forms of cognition, long assumed to overlap heavily, are influenced by largely separate genetic factors, and that each has its own distinct relationship with psychiatric conditions like ADHD and alcohol use disorder 

Two Cognitive Systems, Two Genetic Signatures

Previously, more than 23,000 participants in the AFFECT study, a research collaboration between 23andMe and the brain health company Lundbeck, completed a battery of computerized cognitive tasks over nine months. One task measured sustained attention by tracking how consistently people responded to a stream of frequent images while withholding responses to occasional oddball images. Others measured executive function skills such as processing speed, working memory and how quickly people can select the correct response among competing options.

This new study found that six cognitive measures could be grouped into two genetic factors. The first, which the researchers labeled Executive Function, was strongly tied to processing speed, working memory and response selection. The second, Sustained Attention, was most closely tied to vigilance (moment-to-moment consistency) and how often attention lapsed altogether.

For both factors, common genetic variants explain a real, though modest, share of the differences between people. That’s in line with what’s typically seen for complex cognitive traits, where hundreds of genetic variants each contribute a small effect rather than any single gene calling the shots.

Notably, the Executive Function and Sustained Attention factors were not significantly correlated, meaning that at the genetic level your capacity to stay focused over time and your capacity to juggle and manipulate information appear to be independent. 

What This Means for ADHD, Depression and Other Conditions

Because psychiatric conditions so often involve attention and cognitive control problems, the researchers also tested how each genetic factor related to 13 different psychiatric conditions. Researchers found that the genetic variants linked to stronger executive function are also linked to a lower predisposition for many conditions including ADHD, anxiety disorder, bipolar disorder and schizophrenia. The genetic variants linked to stronger sustained attention were linked to a lower predisposition for just ADHD and alcohol use disorder.

After researchers accounted for the genetic overlap between the two factors, Sustained Attention and Executive Function each still showed their own separate association to ADHD. This suggests that attention problems in ADHD may involve more than one genetic pathway. In other words, ADHD isn’t just tied to one set of attention-related genes, it’s tied to at least two separate ones.

The researchers also looked for genetic links between these cognitive factors and brain structure. In the end, no relationships reached statistical significance, a reminder that connecting genetic differences to changes in brain anatomy typically requires far larger sample sizes than are currently available.

What Comes Next

The AFFECT cohort, while one of the largest of its kind for these particular cognitive tasks, is not yet large enough to pinpoint the individual genetic variants involved. Additionally, the analysis was limited to participants with European genetic ancestry, meaning genetic insights like these may apply best to those with European ancestry, leaving other communities underrepresented. Expanding these studies to more ancestrally and demographically diverse cohorts will be an important next step toward research that benefits everyone.

None of this means your genes lock in your ability to focus. Genetics is only one factor among many, such as sleep, stress, environment and practiced habits, that shape how attention and executive function show up in daily life. What this study does offer is a clearer map of where the underlying biology diverges, which may eventually help researchers understand why some treatments for attention and mood difficulties work better for some people than others.

Findings like these exist because thousands of research participants have generously shared their genetic data and time with our researchers. Their contributions are helping build a better understanding of health for all of us. Your DNA could help us make new discoveries. Learn more about our research.

More than a million Americans are living with hereditary hemochromatosis, and many are unaware of the condition. July is National Hemochromatosis Screening and Awareness Month, a fitting moment to ask why a condition this common stays so quiet.

Hereditary hemochromatosis is a genetic condition that causes your body to absorb more iron from food than it needs. Since the body has no efficient way to get rid of the extra iron, it slowly builds up in the liver, heart, joints and other organs, where it can cause lasting damage over time. The good news: once caught, it’s highly treatable. The challenge is catching it.

Symptoms Vague Enough to Miss

Not everyone with hereditary hemochromatosis develops iron overload. Among people who do, fatigue and joint pain are the most common symptoms among people with hemochromatosis, but both show up in dozens of other conditions, which is exactly why diagnosis is often delayed. Some people also notice abdominal pain, memory fog, skin darkening, a drop in sex drive or heart flutters. Aching pain in the knuckles of the pointer and middle fingers, sometimes called “the iron fist,” is more specific to the condition, though not everyone experiences it.

For years, many clinicians were taught that hemochromatosis was rare and mostly a disease of older men, an assumption that made it easy to overlook in women and anyone else who didn’t fit that picture. That’s part of why genetic testing is useful. It can flag a predisposition before symptoms appear or before a doctor has reason to look for it.

Why Men and Women Experience It Differently

Genetically, hemochromatosis doesn’t discriminate. The HFE gene most often responsible sits on chromosome 6, not a sex chromosome, so men and women have the same chances of inheriting risk from their parents. What mostly differs is timing. Men often show symptoms starting in their 40s, while women more typically develop symptoms later after their periods stop.

The reason comes down to blood loss. A safe and effective treatment for hemochromatosis (in addition to limiting iron intake from foods or supplements) is regularly removing blood from the body. This causes the body to pull stored iron out of tissues like the liver, in order to replace iron-rich red blood cells. Menstruation causes women to regularly shed and replace red blood cells, a built-in, unintentional version of the treatment doctors prescribe today.

An Ancient Variant With a Modern Nickname

Thousands of years ago, people migrating into the British Isles likely carried the small changes in the HFE gene that may have helped their bodies hold onto iron during periods of scarcity. Two of those variants, C282Y and H63D, became especially common in Ireland. What once may have been a survival advantage is now linked to a condition nicknamed the “Celtic Curse,” since hemochromatosis disproportionately affects people with Irish and British ancestry.

What You Can Do

• Learn your family history. Ask relatives whether anyone has been diagnosed with hemochromatosis or unexplained liver disease.
• Ask about an iron panel. Transferrin saturation and ferritin blood tests can catch iron overload early, often before organ damage occurs.
• Learn about your genetics. Not everyone with HFE variants develops hemochromatosis, but knowing whether you carry these variants can prompt earlier monitoring, well before symptoms might show up.
• Act early if you’re diagnosed. Dietary changes and regular phlebotomy, essentially donating blood on a schedule, are simple and highly effective at preventing long-term damage.

Curious what your DNA says about your own hemochromatosis risk? 23andMe Health + Ancestry customers can check their Hereditary Hemochromatosis (HFE-Related) Genetic Health Risk report* to see whether they carry the most common variants most associated with this condition.

NOTE: Within this blog post, we use the words “men” and “women” to refer to people whose sex assigned at birth is male and female, respectively. However, we recognize that being categorized by birth sex may be an uncomfortable experience for some people. We do not mean to delegitimize anyone’s gender identity. Learn more about how 23andMe uses your genetic sex, birth sex and gender.

* 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 Hereditary Hemochromatosis (HFE-Related) genetic health risk report is indicated for reporting of the C282Y and H63D variants in the HFE gene and describes if a person has variants associated with an increased risk of developing iron overload related to hereditary hemochromatosis. The variants included in this report are best studied in people of European descent.

The Pacific Ocean covers nearly a third of the Earth’s surface, yet scattered across its waters are island communities with some of the most distinct and tightly kept family histories anywhere in the world. Thanks to 23andMe members who chose to share their stories of Pacific heritage, we recently added 47 new Genetic Groups spanning Oceania, from the Hawaiian Islands to the Mariana Islands, Micronesia, Melanesia, Samoa, Tonga and Fiji. This is the most detailed genetic view yet of Pacific Islander and Native Hawaiian ancestry available to date.

What Are Genetic Groups?

Genetic Groups are part of 23andMe’s Ancestry Composition feature. They’re groups of people who share more recent DNA with one another than with the broader population, typically because their families lived in the same region, often on the same island or archipelago, for many generations. By analyzing shared DNA patterns across thousands of 23andMe members with Pacific heritage, our clustering algorithm can identify specific regional genetic signatures.

This update covers a vast swath of Oceania. It includes:

• Five groups across the Hawaiian Islands, from the Big Island and Maui to Kaua?i and O?ahu.
• Broader regional groups for Melanesian, Micronesian, Polynesian and South Pacific Islander ancestry.
• Specific groups within the Mariana Islands, Palau, the Federated States of Micronesia, the Marshall Islands, Samoa, Tonga and Fiji, in some cases narrowing all the way down to a single island or or even regions within a single island.

Most 23andMe members with Pacific Islander or Native Hawaiian ancestry will see at least one of these groups reflected in their results. In addition, 23andMe+ Premium™ members can dive deeper into their heritage and see if they have any distant Genetic Group connections across this region.

Three Stories Written in DNA

Among the 47 new groups, a few stand out for what they reveal about the region’s history. The Chamorro (or CHamoru) people of Guam and the Northern Mariana Islands have called the islands home for nearly 4,000 years, a heritage visible today in the latte stones, ancient pillars once used to support elevated buildings, that still dot the landscape. 23andMe members with Chamorro ancestry can now see connections not just to the Marianas broadly, but to specific islands like Guam, Rota, Saipan and Tinian.

Farther east, near Pohnpei in the Federated States of Micronesia, lies Nan Madol, a UNESCO World Heritage Site built atop nearly 100 artificial stone islets connected by tidal canals. It served as the ceremonial seat of the Saudeleur dynasty until 1628, and the new Marshallese and Eastern Micronesian Genetic Group traces to this same stretch of ocean.

And Melanesia, which includes Papua New Guinea, the Solomon Islands, Vanuatu and Fiji, is home to a staggering linguistic diversity. Papua New Guinea alone has more than 800 distinct languages, roughly one-eighth of all languages spoken on Earth. Melanesian peoples have lived in the region for tens of thousands of years, making it one of the oldest continuously inhabited parts of the Pacific. 23andMe members can now see if they have connections to specific regions within Melanesia.

A Shared Voyage

Many of these new groups connect to a much older migration story. Around 5,000 years ago, seafaring peoples speaking Austronesian languages began expanding out from what is now Taiwan, eventually reaching the Philippines, Indonesia, Madagascar and the far islands of Polynesia. If you’d like to dig deeper into that journey and how it shaped the genetic map of the Pacific, check out our blog: What Is Austronesian Ancestry?

Many people from Oceania carry DNA connected to both the “Filipino & Austronesian” and “Melanesian” ancestry populations, a reflection of the seafaring Austronesian expansion and the region’s long history of cultural and genetic exchange. This diversity shows up in how some of these new Genetic Groups are organized within the Ancestry Composition report. Genetic Groups normally appear nested under a specific ancestry population; however, some of the new Genetic Groups in this update fall within parts of Oceania where we don’t yet have a dedicated ancestry population. Members from these areas may see their Genetic Groups nested under either the “Filipino & Austronesian” or “Melanesian” ancestry population, depending on which population is most commonly assigned to people who share DNA with that group.

Building a More Complete Picture

Pacific Islander and Native Hawaiian communities have historically been underrepresented in genetic research, which has meant fewer tools and less specific insights for people tracing their roots to the region. Expanding Genetic Groups across Oceania is thanks to the 23andMe members of Pacific heritage who chose to take part in research. There’s more work ahead, and we’re committed to continuing it.

Already a 23andMe member? Sign in to see if you have connections to these new Genetic Groups in your Ancestry Composition report.

This July 4th, as America celebrates its 250th birthday, we’re adding 29 individuals from the nation’s founding era to the Historical Matches® feature. Their DNA connects them to more than 1.3 million consented 23andMe research participants members.

But here’s the remarkable part: one of them was lost to history until your DNA helped name him again.

Lost Colonists, Now Discoverable

In May, we shared the story of a groundbreaking study published in Current Biology. 23andMe researchers, working with colleagues at Harvard University, the Smithsonian Institution’s National Museum of Natural History and Historic St. Mary’s City, analyzed the DNA of 49 individuals buried at St. Mary’s City, Maryland, the first colonial capital of Maryland, founded in 1634.

We compared their DNA to millions of consented 23andMe research participants. We found that more than 1.3 million 23andMe research participants share DNA with at least one of the St. Mary’s individuals. 

The strongest genetic connections were to participants with ancestry from western England and Wales, consistent with the likely origins of many of the colony’s earliest residents. Several individuals also showed strong connections to Ireland, lending weight to historical accounts of Irish settlers among the founding colonists.

Among the burials at St. Mary’s City’s Chapel Field cemetery was a man whose identity had been lost to time. By analyzing his skeletal remains, we knew roughly his age at death, date of death, and where he was born, but his name was lost. That is, until we used genetic data to find him.

The Story Participants Helped Solve

This individual, known as Burial 56, left DNA that allowed us to search across our database for genetic relatives living today. When we compared his DNA to thousands of consented research participants, several thousand shared genetic connections with him. We then looked at the family trees of two 23andMe research participants with the strongest genetic links and found the same name appearing in both: Leonard Greene.

Leonard’s story aligned with what we knew about Burial 56. He was the son of Thomas Greene, Maryland’s second governor, and Anne Cox—who were both reidentified as burials in the Chapel Field cemetery through their genetic connection to Leonard. This marked the first time ancient DNA has been used to identify unknown historical individuals without any prior hypothesis about who they might be.

Today, Leonard Greene is one of 29 colonists whose stories you can now explore through Historical Matches.

The Path from Maryland to Kentucky

When researchers looked at who shares DNA with the St. Mary’s colonists today, they also found that 23andMe participants with roots in Kentucky showed strong genetic connections with these early Maryland settlers.

This pattern has a historical explanation. After the Revolutionary War, many Maryland Catholic families faced economic hardship and mounting religious pressure. Between roughly 1780 and 1820, many migrated to Kentucky, where they established communities in what are now Nelson and Washington counties. Nearly four centuries after their ancestors first set foot at St. Mary’s City, the genetic echo of that migration is still visible in your DNA.

If your family has deep Kentucky roots, you might find you have connections to these new Historical Matches.

Learn More

The colonists at St. Mary’s City came from Great Britain and Ireland, seeking religious freedom and opportunity in a new world. Their names are being restored. Their stories are being recovered. And now, 23andMe+ Premium™ members can explore whether they share a genetic connection to the founding colonists of St. Mary’s City, and hundreds of other historical individuals, through the Historical Matches feature.

Around 13 million people in the U.S. have PTSD, yet stigma and lack of awareness mean many go without support. In recognition of PTSD Awareness Month this June, 23andMe has released a new Post-Traumatic Stress Disorder (PTSD) Polygenic Risk Score report* to help 23andMe+ Premium™ members understand how their genetics may influence their chances of developing PTSD, and to help all of us better understand this complicated condition.

What is PTSD?

Post-traumatic stress disorder (PTSD) is a mental health condition that can develop after experiencing or witnessing a traumatic event, such as a serious accident, a natural disaster, assault or war. While many people experience strong emotional reactions in the days and weeks after a trauma, PTSD is diagnosed when symptoms last for at least a month and significantly interfere with daily life.

Symptoms of PTSD fall into four main groups:

• Intrusive memories, like flashbacks or nightmares
• Avoiding reminders of the event, including places, people or activities
• Negative changes in mood or thinking, such as guilt, detachment and loss of interest
• Changes in arousal, including feeling on edge, being easily startled or angered and having trouble concentrating and sleeping

PTSD can affect people of all ages and backgrounds. In the U.S., about 5% of people experience PTSD each year. Symptoms usually begin within a few months of the traumatic event but can sometimes start years later.

The Role of Genetics

After experiencing a potentially traumatic event, some people will develop PTSD and others won’t. Genetics can help explain some of this difference. 

Like many other mental health conditions, genetic risk for PTSD is polygenic: rather than single genetic variants with a big impact on risk, the chances of developing PTSD are influenced by many genetic variants, each with a small impact. For example, a recent large-scale genome-wide association study (GWAS) identified nearly 100 locations in the genome associated with PTSD. Some of these variants were in or near genes that play important roles in how brain cells communicate with each other and how the brain is physically structured, providing insights into the biological basis of PTSD and why some people are more likely to develop the condition than others.

23andMe scientists independently investigated if it was possible to build a polygenic risk score (PRS) for PTSD. A PRS is a statistical model that estimates a person’s likelihood of developing a condition based on the combined impact of thousands of small genetic variants. Thanks to the contribution of more than 3 million consented 23andMe research participants, we were able to generate a PRS that analyzes more than 11,000 genetic variants to estimate the likelihood of being diagnosed with PTSD.

Beyond Genetics

Researchers believe that genetics combine with other factors to influence how likely a person is to develop PTSD after experiencing a traumatic event. These factors include:

• Previous exposure to trauma, particularly during childhood
• Ongoing life stress, such as job loss and discrimination
• A personal or family history of other mental health conditions like anxiety or depression
• Having limited social support after a traumatic event

Taking Care of Yourself After Trauma

While PTSD is impacted by some factors that can’t be changed, it’s also impacted by some things that can. Research shows that seeking support and maintaining a healthy lifestyle after a traumatic event can help with recovery and may help prevent short-term stress reactions from developing into PTSD.

• Talk to a mental healthcare professional. Although it can take time, many cases of PTSD respond well to therapy, medication or a combination of the two.
• Try to prioritize sleep and other healthy routines. Healthy sleep habits, exercise and mindfulness activities can help reduce stress.
• Avoid using alcohol and drugs to cope. Leaning on alcohol or drugs can worsen symptoms of PTSD and can interfere with treatment.
• Stay connected. Supportive friends, family and community can provide comfort and help with recovery.

Importantly, getting support from a healthcare professional is a normal and recommended part of PTSD care, and research shows that treatment can make a real difference.

If you or someone you know needs support, contact the National Alliance on Mental Illness (NAMI) helpline, or find a helpline in your area.

Fighting Stigma Around PTSD

Many misconceptions contribute to stigma around PTSD. Some people wrongly assume that PTSD only affects certain groups, like veterans. Others assume that people with PTSD are dangerous or a threat to others.

The reality is that PTSD can impact anyone and can result from a wide range of life experiences. It is treatable, and many people benefit from support from a mental healthcare professional. And while PTSD is a serious health condition, it doesn’t define you.

PTSD Awareness Month is a perfect time to help fight stigma by learning the facts and offering kindness and support to those living with PTSD.

Learn About Your Genetics

The Post-Traumatic Stress Disorder (PTSD) PRS report was made possible thanks to millions of 23andMe customers who have consented to participate in research. Their contributions enable our scientists to make genetic discoveries that help the entire research community better understand health and disease, and allow us to develop new reports and features that deliver personalized genetic information to our members.

If you’re a 23andMe+ Premium member, you can now access your Post-Traumatic Stress Disorder (PTSD) PRS report (along with your other Health Predisposition reports) to see how your genetics may influence your chances of developing PTSD.

23andMe+ Premium members also have access to several other mental health-related reports:

• Anxiety
• Bipolar Disorder
• Depression
• Panic Attacks

* The 23andMe Post-Traumatic Stress Disorder (PTSD) 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 being diagnosed with PTSD. 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 Post-Traumatic Stress Disorder (PTSD) 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.

Summer is on the way, and we’d be lying if we said heading to the beach wasn’t at the top of our minds when preparing this month’s Historical Matches^SM update. So without further ado, we’d like to tell you the story of an aptly named Roman era woman: Beachy Head Woman. 

She’s named after Beachy Head, a stretch of coastline on the south coast of England, and she lived during the Roman occupation of Britain. While her story doesn’t actually have anything to do with the beach (the site derives its name from the Old French for ‘beautiful headland’) it does involve a decade of conflicting scientific interpretations and a fascinating mystery that took until 2026 to resolve.

A Skeleton Without a Story

In 2012, researchers sorting through the archaeological collections in the south of England made an unexpected find: a skeleton in a storage box in the basement of Eastbourne’s Town Hall. The only information included with the box was a label reading “Beachy Head, 1959.”

So the team embarked on a series of archaeological and biomolecular analyses to learn about the identity of the skeleton inside. Radiocarbon dating indicated that the individual lived between 129 and 311 CE, during the Roman occupation of Britain. An analysis of the skeleton’s morphology revealed that it likely belonged to an adult woman, estimated to be between 18 and 25 years old at the time of her death.

Through an initial craniofacial analysis in 2013, researchers concluded that her skull had features consistent with sub-Saharan African ancestry. This preliminary interpretation spread fast. She was described in news outlets, books and educational materials as one of the earliest individuals of African descent identified in Roman Britain, and she entered public consciousness under the name “Beachy Head Woman”.

The Headline Ran Ahead of the Evidence

The strontium and oxygen isotope analysis carried out around the same time told a different story. Values from her tooth enamel were consistent with a childhood spent on the south coast of Britain, not overseas. Then, in 2017, a preliminary ancient DNA study generated tentative evidence of east Mediterranean ancestry, possibly Cyprus, but the dataset was too limited to settle the question. 

Despite never being formally published, these findings circulated in the media regardless. For nearly a decade, who Beachy Head Woman really was remained an unresolved mystery.

A Local Woman All Along

In early 2026, researchers at London’s Natural History Museum finally helped to resolve this question. They published genome-wide ancient DNA data from Beachy Head Woman’s remains for the first time.

They showed that her ancestry was similar to local British and Northern European populations, with no detectable evidence of sub-Saharan African ancestry. Her mitochondrial haplogroup, K1a26, is also associated with Northern European and British populations and has been identified in individuals from rural Iron Age Britain. 

They even used her DNA to try to predict what she may have looked like, concluding that she likely had blue eyes, light hair and intermediate skin pigmentation — a significant departure from the original facial reconstruction. A new reconstruction was produced in light of the DNA results.

What Her Reassessment Reveals

Beachy Head Woman’s story has implications beyond her own origins. The craniofacial analysis that initially identified her as being of sub-Saharan African ancestry used methods that have since come under substantial scrutiny. The field of bioanthropology, like all scientific fields, is always evolving and has moved away from these kinds of ancestry estimation in recent years, in part because human skeletons are incredibly diverse; people with the same ancestry can have bone structures that look completely different from one another, making hard-and-fast classifications unreliable. The case of Beachy Head Woman is a concrete illustration of what can go wrong when those methods are applied without corroborating evidence.

Learn More

Want to see if you share a genetic connection to Beachy Head Woman, or with hundreds of other historical individuals? The Historical Matches feature is available to 23andMe+ Premium™ members.