A family tree is usually a record of names, dates and places. Sometimes it also holds a clue about health. This Lung Cancer Awareness Month, we are looking at how 23andMe scientists used genetic ancestry to follow a rare lung cancer risk variant back more than 200 years to the mountains of the American Southeast.

In September, we shared the results of a collaboration between the 23andMe Research Institute and Dana-Farber Cancer Institute that was published in Science. People who inherit a variant called T790M in the EGFR gene had 25 times higher odds of developing lung cancer. Among more than 10 million consented research participants in this study, 641 carried this genetic variant. While the variant is rare, we wanted to share more about where the variant came from and why that history could matter for lung cancer screening.

How Did Scientists Trace a Lung Cancer Variant to Southern Appalachia?

We combined birthplace data, shared DNA and genetic dating to show that most carriers of the EGFR T790M variant descend from settlers of Southern Appalachia who lived in the early 1800s.

The first clue was geography. Carriers disproportionately reported that they or their grandparents were born in the Southern U.S., particularly Tennessee, Alabama and Georgia.

Next, we looked at stretches of DNA that are identical by descent (IBD), meaning chunks of DNA that two people share because they inherited them from the same ancestor. We compared carriers with more than 3.4 million consented 23andMe research participants who reported where their grandparents were born. Shared DNA peaked in Southern Appalachia, with the strongest signal along the border between northern Alabama and southern Tennessee. We also saw that carriers were more likely to have connections to Genetic Groups representing colonial populations from Southern Appalachia.

Finally, we estimated when carriers’ most recent shared ancestor lived. Every time DNA passes from parent to child, it gets reshuffled, which breaks long shared segments into shorter pieces. That means the length of a DNA segment two people share says something about how many generations separate them from a common ancestor. We measured all the segments of DNA that EGFR T790M carriers share across their genomes and used a statistical model to estimate how many generations back they shared an ancestor. We estimated that carriers in the Southern Colonial Genetic Group share an ancestor who lived around 1799. Carriers with recent British and Irish ancestry were estimated to share an older ancestor, which suggests the EGFR T790M variant arose in Europe and crossed the Atlantic with settlers of British and Irish descent.

Together these results point to a founder event. A founder event happens when a small group splits off from a larger population and a once-rare variant becomes more common among the descendants of that smaller group. As settlers moved into isolated mountain communities in Appalachia around 1800, the EGFR T790M variant became more common there than anywhere else. Today, up to 1 in 2,000 people born in states in the Southeastern U.S. are carriers.

Who Carries the EGFR T790M Variant Today?

Most EGFR T790M carriers trace their ancestry to Southern Appalachia, but the variant has also spread into other communities over the past 200 years.

About 72% of carriers had recent ancestry from an American Southern Colonial group, and they shared a very large (23,700,000 base pairs long!) identical segment of DNA originating from the founder event. Others had African American ancestry, Indigenous American ancestry or Acadian and French Canadian ancestry. These other carriers were estimated to share more recent ancestors, from the early to mid-1900s, but in every case the section of DNA that contained the EGFR T790M variant traced back to European ancestry. Migration out of the Southeast after the Civil War likely carried the variant into these families. Though, even today, there are a small number of carriers still living in Europe.

This matters because ancestry is often more complex than a single label. Someone who identifies as Black or Native American could still carry a genetic variant that entered their family tree from a European ancestor generations ago.

Could Your Ancestry Help Guide Lung Cancer Screening?

Ancestry might one day help doctors identify people who may benefit from genetic testing for the EGFR T790M variant, but more research is needed before it shapes screening guidelines.

Today, U.S. lung cancer screening recommendations are based on age and smoking history. The American Cancer Society recommends a yearly low-dose CT scan for adults ages 50 to 80 who have a 20 pack-year smoking history.

That approach would miss many EGFR T790M carriers. In the study, about two-thirds of carriers reported never smoking. Further research — like that happening through the INHERIT study led by Dana-Farber or the Lung Cancer Genetics Study — could provide more insights into better lung cancer screening and prevention options for people with this or other genetic risk factors.

What You Can Do

These steps can help you understand and lower your lung cancer risk.

• Learn your family health history. Note any relatives diagnosed with lung cancer, especially those who never smoked or were diagnosed at a younger age.
• Talk with a doctor or genetic counselor if lung cancer runs in your family. They can help you decide whether genetic testing, lung cancer screening or other actions make sense for you.
• Test your home for radon, and reduce levels if they’re high. Radon is the second leading cause of lung cancer overall and the leading cause of lung cancer among people who have never smoked.
• As much as possible, avoid air pollution and workplace exposure to certain chemicals (such as asbestos) that can increase the risk for lung cancer. 
• Avoid tobacco smoke, including secondhand smoke. Smoking remains the top risk factor for lung cancer. 

If you have a history of smoking, you may be eligible for lung cancer screening that can find lung cancer early, when it’s most treatable. Talk to your healthcare professional about what screening might be right for you. 

To dig deeper into the risk findings, read our first post on the EGFR T790M variant or explore the full study in Science.

It’s Halloween night. A porch light flickers, a bowl of candy waits by the door and somewhere down the block a kid in a spider costume is about to make someone scream. Halloween is the one night a year many of us go looking for a scare on purpose. So why do some people love the thrill while others watch from behind a pillow? Part of the answer may lie in your genetics.

23andMe scientists ask consenting research participants about all kinds of traits, from whether they can curl their tongue to how they feel about spiders and horror films. This Halloween we’re revisiting some of the data to put together a few classic Halloween personalities. Which one sounds like you?

The Scaredy Cat: Is Fear of Heights and Spiders in Your DNA?

23andMe researchers identified 392 genetic markers associated with being afraid of heights. They combined those markers with age and sex to build a statistical model that estimates a person’s likelihood of having this fear. The average 23andMe research participant has a 29% chance of being afraid of heights. Across the pond, a 23andMe survey of UK research participants found that 37% of Brits have an excessive fear of something, with fear of heights topping the list.

Why heights in particular? When you stand upright, your brain uses visual cues from nearby objects to make tiny balance adjustments. At the edge of a tall building, those nearby cues disappear and everything in view is too far away to help, so most people feel a little off balance.

Spiders are another classic Halloween fright. In 2022, about 38% of 23andMe research participants said they were afraid of spiders, compared with about 22% of the general population. People who reported a fear of spiders were also more likely to report a fear of heights. Female participants were about twice as likely as male participants to say they fear spiders, 45% vs. 22%, and older participants were less likely to have a fear of spiders.

The Candy Fiend: Is Your Sweet Tooth Genetic?

Your preference for sweet or salty snacks is partly genetic. 23andMe researchers identified 43 genetic markers associated with this taste preference. A few are in or near genes involved in brain development or function, and others are in genes associated with metabolism or body mass.

Taste starts on your tongue and finishes in your brain. With each bite, your taste buds send signals to a brain area called the primary gustatory cortex, which identifies the taste. Another area, the orbitofrontal cortex, helps judge whether you like it. And you can forget the tongue map from school: receptors for sweet, salty and bitter tastes are spread all over your tongue and mouth.

Taste preferences also shift over time. In 23andMe survey data, older participants were more likely to prefer sweet candy over sour candy. That may reflect natural changes in taste perception as we age. So if your grandparents always hand out chocolate while your teenager hoards the sour gummies, there may be some science behind it.

The Creature of the Night: Are Night Owls Born That Way?

Whether you’re an early bird or a night owl is also influenced in part by your genes. 23andMe researchers identified 450 genetic markers associated with being a morning person or a night person. Your internal clock does more than nudge you toward bed. Some of the genes that run the body’s internal clock also help regulate body temperature and hormone levels. For night owls, Halloween may be one of the few holidays that runs on their schedule.

Whether you spend October 31 peeking through your fingers, sorting your candy or staying up long after the last trick-or-treater, your DNA may play a small part in how you celebrate. Your environment, experiences and other factors matter too, which is why no two Halloween personalities are quite the same. Happy Halloween from all of us at 23andMe.

Why does one person light up a crowded room while another would rather spend a quiet evening in? A study published in Nature offers a detailed look at personality genetics, drawing on data from more than 1 million people. Among them are 23andMe members who consented to participate in research and answered questions about their personalities. Their contributions helped make this one of the largest studies of its kind.

Is Personality Genetic?

Yes, in part. Your genes play a real but modest role in personality. This study looked to find genetic variants linked to the Big Five.

Researchers combined data from 46 study groups, totaling between 611,037 and 1.14 million people per Big Five personality trait. They ran genome-wide association studies (GWAS), which scan millions of points across the genome to find genetic variants that are more common in people who score higher or lower on a trait. They identified 1,260 genetic variants linked to the Big Five.

Of the 1,260 variants, 824 had never been linked to personality before. For example, before this study the number of genetic variants associated with conscientiousness was 3, this study identified 131 variants. For neuroticism, the number of genetic variants rose from 224 to 706.

Personality is polygenic, meaning thousands of variants — each with a tiny effect on its own — work together to influence it. All together, the common genetic variants identified in this study explained about 5 to 9 percent of the differences in personality between people.

That leaves plenty of room for everything else to influence your personality. As the study authors put it, “all methods find that personality is substantially influenced by a person’s environment.” Your experiences, relationships and choices shape your personality too.

Why These Genetic Findings Hold Up

The genetics associated with personality were consistent across countries, age groups and even who was describing the person.

The researchers found similar genetic associations in the United States, continental Europe, the Nordic countries, the UK and Australia. The patterns also held across age groups and different personality questionnaires. In one group from Estonia, people rated their own personalities and close friends or family members rated them too. The genetic results lined up well between the two, which suggests these genetic variants are associated with real personality differences and not just how people see themselves.

Most participants in this research were of European descent. Genetic predictions built mainly from people of European descent usually work less well for other groups. However, this study included about 43,000 to 48,000 people of African descent per trait. This allowed the researchers to show for the first time that genetic scores could predict extraversion, neuroticism and openness in people of African descent, though the predictions were less strong compared to people of European descent.

How Personality Genetics Connects to Health and Other Traits

The researchers measured how much the genetic influences of personality overlapped with everyday health habits and even the kinds of neighborhoods people choose.

The researchers found evidence that higher conscientiousness may lower body mass index (BMI), reduce the likelihood of starting to smoke and reduce hospital stays. The same analyses suggested that extraversion may increase the likelihood of COVID-19 infection, and that higher neuroticism may relate to less healthy aging.

Personality genetics even showed up on the map. Among 419,261 UK Biobank participants, the researchers looked at where people lived at age 50 and older, accounting for where they were born. People with a higher genetic likelihood of openness to experience were more likely to have moved into cosmopolitan, professional neighborhoods and away from the suburbs. People with a higher genetic likelihood of conscientiousness were more likely to have moved into suburban communities.

It’s important to remember that the genetics discovered in this study only represent a small contribution to personality and describe patterns across large groups. They cannot predict an individual’s behavior. Your genes may nudge you toward certain tendencies, but your experiences, relationships and choices all play a role in who you become.

Studies like this depend on people who share their data for research. Find out how you can make a difference here.

So we organized this guide around what each person wants to work on, not by price or product type: 20 recommended picks across five categories, from a free app that scores your groceries to a high-end smart ring. Whatever they’re focused on, you’ll find a gift that fits.

About this list: This guide is published by 23andMe and includes our own products. Our editorial team selected the other 19 gifts, and 23andMe doesn’t receive payment or commission from any of those brands. Product details come from each brand’s own information, and prices and availability may change.

Key Takeaways: Best Health and Wellness Gifts
Best Health and Wellness Gifts at a Glance
Compare All 20 Health and Wellness Gifts
Health and Wellness Gifts That Tell Them Something New About Their Body
Health and Wellness Gifts for Better Sleep
Health and Wellness Gifts for Fitness and Recovery
Everyday Health and Wellness Gifts, Including One That Is Free
Health and Wellness Gifts With Nothing to Charge or Set Up
Best Health and Wellness Gifts Under $50
How We Chose These 20 Health and Wellness Gifts
Pick the Health and Wellness Gift That Fits
FAQ: Best Health and Wellness Gifts

Key Takeaways: Best Health and Wellness Gifts

Start with what they want to work on, not the product category.

• Match the gift to their goals or something they’ve mentioned, not to what’s trending right now.
• Price doesn’t predict how much they’ll use it. A simple sound machine can get more nightly use than a high-end smart ring.
• At-home test kits are gifts that last past the holidays. They open the kit, send in their sample and get their results in the weeks that follow.
• The best wellness gifts fit a routine they already have. A gift that adds a step to their day is more likely to get used than one that asks them to start a new habit.

Best Health and Wellness Gifts at a Glance

• For staying active on a budget: Amazfit Bip 6 (under $100)
• For learning what their DNA says about their health: 23andMe Premium Ancestry + Health
• For light sleepers on the go (under $25): Yogasleep Rohm portable white noise machine
• For smarter grocery runs (free): the Yuka app
• For blocking out light at night: Manta Sleep Mask PRO (under $100)
• For post-workout recovery: Hyperice Hypervolt Go 3 ($100–$200)
• For the serious runner (a splurge): PUMA Fast-R NITRO Elite 3 ($200–$300)
• For a last-minute gift: a year of Calm (under $100)
• For someone navigating menopause: Embr Wave 2 ($200–$300)
• For a gift exchange or a coworker: Loop earplugs ($25–$60)

Compare All 20 Health and Wellness Gifts

Prices are approximate ranges and may change. In the HSA/FSA column, Yes means the item is generally treated as an eligible expense. With doctor’s note means it can qualify if a licensed clinician writes what plans call a Letter of Medical Necessity, naming a diagnosed condition and dated before you buy. Eligibility always depends on your plan, so check with your plan administrator before you buy.

Health and Wellness Gifts That Tell Them Something New About Their Body

Most wellness gifts help the recipient do something: sleep better, train harder, unwind. These five help them understand their body, from what their DNA can reveal about their health to how well they’re sleeping. They’re a good fit for the curious, data-minded person on your list, and their results can be worth sharing at their next checkup.

Amazfit Bip 6: For Staying Active on a Budget

Under $100

The Amazfit Bip 6 covers the basics of a fitness tracker without the premium price. It runs up to 14 days on a single charge, has a bright AMOLED display that stays readable in direct sunlight and includes built-in GPS and Bluetooth calling from the wrist. With 140+ workout modes, from running and swimming to strength training, it tracks whatever they’re into, along with sleep, heart rate and blood oxygen. It’s a good fit for a first-time tracker, or for anyone curious about health tracking who doesn’t want to spend three figures to find out.

23andMe Premium Ancestry + Health: For Helping Them Learn What Their DNA Says About Their Health

$80–$200, see the 23andMe Gifts page

A sleep tracker shows how they slept last night. 23andMe Premium Ancestry + Health adds something no wearable can measure: what their DNA can reveal about their health. It comes with 100+ health and wellness reports and features, including Health Tracks, which shows how everyday choices can affect their health over time. It also includes everything in Premium Ancestry, from Family Tree to Historical Matches, and new health reports and features are added throughout the year.

It’s a natural next step for the person who already tracks their steps and sleep and wants to understand what their genes have to do with their health. A portion of your purchase may be eligible for FSA/HSA reimbursement.

Tiny Health Adult Gut Health Test: For the Person Curious About Their Gut

$200–$300

Tiny Health’s Adult Gut Health Test looks at their gut microbiome, the community of bacteria and other microbes that live in the digestive tract. They collect a small sample at home and mail it back, and it’s analyzed by a CLIA-certified, CAP-accredited lab partner.

Tiny Health’s sequencing screens for more than 120,000 microbes, with strain-level detail for key species, giving them a detailed look at what’s living in their gut. It also pairs nicely with a DNA kit: one looks at the DNA they were born with, the other at the microbes they live with today.

Oura Ring 5: The Sleep Tracker They’ll Forget They Are Wearing

$400–$500

For the person who would never wear a watch to bed, a ring is about as low-key as a wearable gets. The Oura Ring 5, announced in May 2026 and shipping since June, is about 40% smaller than its predecessor, so it looks and feels much like an everyday ring. Overnight, it tracks sleep stages, temperature trends and more, and each morning the Oura app turns that data into a readiness score and personalized insights for the day ahead.

One thing to know before gifting: most of the ring’s features require an Oura Membership, sold separately, so it’s worth factoring into your budget.

WHOOP: For the One Already Training for Something

$200–$400 per year

WHOOP skips the screen entirely. With no notifications to check, the lightweight band tracks strain, recovery and sleep around the clock and sends that data to the WHOOP app, which shows how recovered they are each day and how hard to push.

Instead of buying the device, they get it through an annual membership, and higher tiers add more advanced health features. For the person training for a race or working toward a fitness goal, it shows how their training, sleep and recovery fit together.

Health and Wellness Gifts for Better Sleep

Some of the most useful sleep gifts are also the simplest: something to block out light, something to soften noise. Most picks in this section are under $100, with two splurges at the end for the person who wants to go all in.

Yogasleep Rohm Portable White Noise Machine: For Light Sleepers on the Go

Under $25

The Rohm weighs 3.4 ounces, fits in a jacket pocket and keeps things simple. It offers three sounds (white noise, bright white noise and deep blue noise), adjustable volume and nothing else to configure, which is exactly what you want from something you use half asleep.

It’s rechargeable, runs through the night on a single charge, and a built-in lanyard lets it hang from a headboard, a doorknob or a carry-on, so it works just as well in a hotel room or a dorm as it does at home.

Loop Earplugs: For the Noise-Sensitive Person on Your List

$25–$60

Loop makes earplugs for specific situations, so the right gift depends on where they need some quiet. Loop Quiet 2 is designed for focus, travel and sleep, and Loop Dream is made for side sleepers who want comfort against the pillow. Loop Engage 2 softens background noise while keeping conversations clear, and Loop Experience 2 is built for concerts and live events. If you’re not sure which fits, Loop Switch 2 lets them switch between three levels of noise reduction in one pair.

Small and easy to wrap, they’re a simple pick for a gift exchange or a coworker.

Manta Sleep Mask PRO: For the Shift Worker or Constant Traveler

Under $100

For someone who sleeps while the sun is up, a mask has to block light without pressing on their eyes. The Manta Sleep Mask PRO uses C-shaped eye cups that wrap around the eyes instead of resting on the lids and lashes, and the cups can be placed anywhere along the strap to fit each face.

Manta designs its masks for 100% blackout and positions the PRO for side-sleep comfort and breathability, which makes it a good fit for a daytime sleep after a night shift, a long flight or a too-bright hotel room.

Hatch Restore 3: For the Person Who Uses Their Phone as an Alarm

$150–$200

A Hatch Restore gives someone a reason to leave the phone in another room. It runs a wind-down routine at night, a sunrise simulation in the morning and a large sound library in between. The alarm, sunrise and sound functions all work straight out of the box, with an optional Hatch+ subscription if the recipient wants the full content library later.

With its warm, minimal look, it’s also a good choice for the friend or loved one with a keen eye for design.

Embr Wave 2: For Someone Navigating Menopause

$200–$300

Embr Wave 2 is a wristband that delivers cooling or warming sensations at the press of a button, designed with hot flashes and night sweats in mind. The free Embr Wave 2 app unlocks six temperature modes and more than 30 personalizable sessions.

It’s a thoughtful pick for someone whose sleep is interrupted by hot flashes or night sweats, and it’s discreet enough to wear through the day.

Health and Wellness Gifts for Fitness and Recovery

People who train tend to be particular about gear and usually buy what they need. In this category, the best gift is the one they’d love but haven’t bought for themselves.

PUMA Fast-R NITRO Elite 3: The Splurge for the Serious Runner

$200–$300

PUMA points to a small lab study it funded, which hasn’t yet been peer-reviewed: researchers led by Wouter Hoogkamer at the University of Massachusetts Amherst found the Fast-R NITRO Elite 3 improved running economy by 3.15% over its predecessor, which they estimate could theoretically save a three-hour marathoner more than four and a half minutes. In short treadmill trials, all 15 runners used less energy in it.

PUMA says it cut 95 grams from the previous model, bringing it to about 170 grams in a men’s UK size 8, while extending its carbon plate (PUMA calls it PWRPLATE) and using its NITROFOAM Elite cushioning. It’s built for racing, but any serious runner who enjoys a fast training day will appreciate it.

Hyperice Hypervolt Go 3: The Recovery Gift That Travels

$100–$200

The Hypervolt Go 3 is built for recovery on the go. It weighs 1.6 pounds, runs up to four hours on a single charge and uses Hyperice’s QuietGlide technology for quiet operation.

It’s TSA-friendly for carry-on, so it can travel to the race, the tournament and the work trip. It comes with two head attachments, a flat head and a wedge. It is also FSA/HSA eligible.

Theragun Relief: The Gentle One for a Parent or Grandparent

$100–$200

While most percussive devices are built for athletes, Theragun Relief is built for everyone else. It’s the gentlest massage gun Therabody makes, with one button, three speeds and a triangular grip that lets you reach your own lower back without a second person.

That gentler action makes it a good fit for general stiffness, including for older adults. However, as with any percussive therapy, anyone who is pregnant, has a circulatory condition or is working around a recent injury should check with their doctor first.

Owala FreeSip: The Under-$40 Gift They’ll Use Every Day

Under $40

Yes, it’s a water bottle, and it’s one they’ll reach for every day. The FreeSip has two drinking modes in one lid, a built-in straw for sipping and a wide spout for bigger gulps, and it locks shut so it can go in a bag without leaking.

Like all of Owala’s bottles and tumblers, the FreeSip is made with lead-free solder. Owala says the FreeSip isn’t meant for hot, carbonated or perishable drinks, so for someone who wants a hot beverage, one of Owala’s tumblers would be a better choice.

Everyday Health and Wellness Gifts, Including One That Is Free

Not every wellness gift has to be a device. These three fit into routines they already have, starting with one that’s free.

Yuka: The Health Gift That Costs Nothing

Free

With the Yuka app, they can point their phone at the barcode on any packaged food or cosmetic and get a score out of 100, breaking down the healthy ingredients as well as the ones to look out for. The food score weights nutritional quality at 60%, additives at 30% and organic status at 10%. When something scores badly, it suggests healthier alternatives in the same category.

But what makes it worth recommending is the funding model. Yuka carries no advertising and no brand can pay to raise a score. It’s funded by an optional Premium subscription, about $15 a year, which adds search, offline mode and personal alerts for things like gluten or palm oil. More than 85 million people use it worldwide, and for a gift that costs nothing, it can change how they shop for groceries.

LEUCHTTURM1917 Hardcover Notebook: For the Person Who Thinks Better on Paper

Under $35

The LEUCHTTURM1917 Hardcover Notebook is an A5 hardcover holding 203 numbered pages of 120gsm FSC-certified German paper, thick enough that fountain pens and markers do not show through to the next page. It opens flat, with two ribbon bookmarks, a blank table of contents, an elastic closure, a gusseted back pocket and eight detachable sheets.

You choose from 29 cover color options and the ruling: dotted, ruled, squared or plain. One notebook handles daily notes, affirmations, a weekly schedule, questions to raise at an appointment or longer journal entries. It is also the only gift in this guide that works with the phone in another room.

A Calm or Headspace Annual Subscription: The Last-Minute Save

Under $100 per year

A year of Calm or Headspace gives someone something they can use every day rather than once. It arrives by email the same day you buy it, so it works whether you planned ahead or not.

Both are built for everyday stress, winding down and getting to sleep, with sleep stories, breathing exercises and short guided sessions, some as brief as five minutes.

Health and Wellness Gifts With Nothing to Charge or Set Up

Three of the best things you can give someone this year come with no batteries and no instructions.

A Weighted Blanket: For the One Who Cannot Switch Off

$100–$250

Weighted blankets have a growing crowd of people who swear by them for winding down at night. Many companies that offer weighted blankets suggest one that’s roughly 10% of body weight, with open-knit versions running cooler than quilted ones. Just remember, weighted blankets are not meant for young children, so they’re for the adults in your life who toss and turn at night.

A Massage, Acupuncture or Float Session: The Gift of an Hour

Varies by studio

Buy this from a studio close to where the person lives, and be sure to check the expiration terms before you give someone a session gift certificate. They’re particularly good for people who will happily spend money on everyone else but never on themselves.

A Produce Box or Meal Kit Subscription: Wellness That Shows Up Weekly

Varies by provider

A month of a local CSA box or meal kit brings fresh ingredients to their door every week. It’s a thoughtful gift for anyone short on time, especially new parents. Just be sure to confirm the delivery area and ask about allergies and dietary preferences first.

Best Health and Wellness Gifts Under $50

The best health and wellness gifts under $50 are the Yuka app (free), the Owala FreeSip water bottle (under $40), the Yogasleep Rohm portable white noise machine (under $25), Loop earplugs (most pairs under $50) and the LEUCHTTURM1917 Hardcover Notebook (under $35).

How We Chose These 20 Health and Wellness Gifts

Nineteen of the twenty products in this guide were selected by our editorial team, and none are paid promotions. We receive nothing if you buy them. The exception is 23andMe Premium Ancestry + Health, which is our own product, as noted at the top of this guide.

We checked product details against each maker’s own page and linked every product to that page rather than a marketplace listing. Prices in this category change often, especially between October and December, so we list price ranges rather than exact prices. Check the maker’s site for current pricing.

Pick the Health and Wellness Gift That Fits

When choosing a health and wellness gift that fits a person well, one question gets you most of the way there: what has this person mentioned in the last month? Talk of restless nights points to the sleep section. Soreness points to recovery. Curiosity about their own body points to the health tests.

And if the answer is that they have wondered for years where their family came from, or what their genetics might mean for their health, a 23andMe kit could be a meaningful gift. Have a look at the 23andMe gift options, or read what other people found out at 23andMe stories.

FAQ: Best Health and Wellness Gifts

Prices verified 22 October 2026. Every product in this guide was selected by us and checked against the maker’s own published information.

What do a 5,000-year-old iceman, a famous composer and a Mayan sacrifice victim have in common? They are all part of a growing collection of more than 1,000 people from the past whose DNA you can compare with your own through 23andMe’s Historical Matches feature.

When we launched Historical Matches in March 2024, it included 335 historical individuals from around the world. Earlier this month we added the 1,000th. To mark the milestone, we’re explaining the science behind each match, looking back at how the feature has grown and sharing what we’ve learned from the first 1,000+ historical individuals.

How Does Historical Matches Work?

Historical Matches compares your DNA to genomes sequenced from ancient and historical remains and looks for identical stretches of DNA you share with each person. Scientists recover this DNA from bones and teeth found at archaeological sites and, in rare cases, from other sources. Beethoven’s genome, for example, came from authenticated locks of his hair. Researchers publish these genomes in peer-reviewed studies, and 23andMe uses that publicly available data to build the feature.

To find a match, 23andMe scientists search for segments of DNA that are identical by descent, or IBD. An IBD segment is a piece of DNA that two people both inherited from the same ancestor. It’s the same approach that powers our DNA Relatives feature. In order to ensure that matches are real, and not false positives, a shared segment has to meet a minimum length. This minimum segment length we use depends on the quality of the genome we have for each historical individual, but it typically ranges from 3-10 cM.

Getting a Historical Match typically doesn’t mean you descend directly from that person. It means you and the historical individual likely share a common ancestor, someone who may have lived long before either of you. Most matches reflect very distant connections, though some may be closer.

Not every historical figure can be included. Ancient DNA breaks down into short fragments over time, and only some remains yield enough high-quality, genome-wide data to work with. That’s why the feature can include Beethoven but not Mozart or Bach. Even Richard III, whose remains were identified in 2012, isn’t included because researchers sequenced only his mitochondrial DNA and parts of his Y chromosome, not his full genome.

How Has Historical Matches Grown Since 2024?

Historical Matches launched with just over 300 individuals from only 10 groups such as the Viking Age, Iron Age Taiwan, the First Peoples of the Caribbean and the ancient city of Beirut. 

Since then we’ve updated the feature regularly, adding people from new places and time periods. Additions have included Ancient Romans and Medieval Avars, Neolithic Ireland, Colonial Mexico, young boys who were ritually sacrificed during the Maya civilization, the Sarmatians of the Eurasian steppe and the Shaman of Bad Dürrenberg, a woman buried in what is now central Germany about 9,000 years ago.

1,000 Historical Matches: What We’ve Learned So Far

With more than 1,000 historical individuals now in the feature, we thought you might be curious about how common Historical Matches actually are. Here’s what we found in an analysis comparing the first 1,000 historical individuals added to Historical Matches with the DNA of more than 9.3 million consented 23andMe research participants who were genotyped on our v5 genotyping chip.

Among these participants, 97.6% share DNA with at least one historical individual, and most have more than just one or two Historical Matches. The average participant matches about 23 historical individuals, and more than 60% match 20 or more.

Which historical individuals do participants match most often? So far, the single most widely matched historical individual in the feature is King Béla II of Hungary, a 12th-century member of the Árpád Dynasty known as Béla “the Blind.” He shares DNA with nearly one in four participants (23.3%). For comparison, the typical historical individual in the feature shares DNA with about 1.4% of participants, or roughly 125,000 people. Viking Age individuals also rank among the most widely matched, making up most of the top ten.

Most Historical Matches reflect very distant connections, pointing to a common ancestor who may have lived hundreds or even thousands of years ago. But for some historical individuals in the feature, we can also identify matches who share enough DNA to suggest a common ancestor in the more recent past. In our relationship predictions we label these matches as “significantly related” as opposed to the “very distantly related” prediction that most people see. These matches are genuinely rare: among the more than 9.3 million participants, we’ve identified only about 9,100 significant matches, or roughly 1 significant match for every 1,000 participants. If you’re one of the lucky few with a significant match, we’d love to hear your story at https://www.23andme.org/shop/stories/.

At the other end of the spectrum, nine historical individuals included in the feature don’t yet match anyone in our database. They include Late Stone Age South African bab001, Iron Age Taiwanese Individual I3611 and Pre-Contact Period Remote Oceanian I4451, from what is now the Pacific island nation of Vanuatu.

So why does a medieval king match millions of people, while others match no one at all? A historical individual’s match rate is shaped by several factors:

• The quality of their genome. Ancient DNA breaks down over time, and the amount and quality of DNA recovered varies widely from one individual to the next. With a higher-quality genome, we can confidently detect shorter shared segments of DNA. Because shorter segments reflect more distant relationships, a higher-quality genome lets us identify connections reaching further back in time, and those more distant connections are shared by many more people.
• Their own ancestry. Some historical individuals belonged to populations that contributed broadly to the ancestry of people living today. Others belonged to communities whose descendants are fewer in number, or whose ancestry has since mixed with other populations.
• The ancestry of our members. Most 23andMe members have European ancestry, so historical individuals from Europe tend to have more matches than those from other parts of the world. Low match rates for some regions reflect who has taken part in 23andMe research so far, not the importance of these historical individuals or the legacies they left behind.

What Research Has 23andMe Contributed to Historical DNA?

Our team has also helped lead research in this field, connecting the genomes of historical individuals to people living today. In 2023, we worked with researchers at Harvard and the Smithsonian to analyze DNA from 27 enslaved and free African Americans who labored at Maryland’s Catoctin Furnace soon after the founding of the United States. By comparing their genomes with those of consented 23andMe research participants, we identified more than 42,000 of their living relatives.

In 2026, the team studied 49 colonists buried in St. Mary’s City, Maryland’s first capital, founded in 1634. More than 1.3 million consented 23andMe research participants share DNA with one or more of these individuals, enabling us to identify Maryland’s second governor, Thomas Greene, among those buried at the site. Individuals from both studies are part of the Historical Matches feature, so you can see whether you share DNA with them too.

Why Does Every New Genome Matter?

Each historical individual in the feature represents years of work by archaeologists, geneticists and the communities connected to these sites. As researchers continue to sequence and publish new ancient genomes, we plan to keep growing Historical Matches. While most of the matches we report are distant, we hope they remind you that we are all connected to the past, sometimes in unexpected ways. The first 1,000 individuals are just the beginning. 23andMe Premium members can explore whether they share a genetic connection with any of the more than 1,000 historical individuals in Historical Matches. Not a member yet? Learn more about 23andMe Premium.

Every year on the third Saturday in October, International Archaeology Day invites people around the world to celebrate the discipline that lets us dig into the human past, quite literally. Archaeologists piece together the lives of people who lived hundreds or thousands of years ago from the traces they left behind: their homes, their tools, the objects they were buried with and increasingly their DNA.

This year, we have a second reason to celebrate. With this month’s update, 23andMe’s Historical Matches feature now includes more than 1,000 historical individuals. Each one represents years of careful work by archaeologists, museum curators and geneticists, and each one carries a story that can now connect to the people living today.

To mark both occasions, we’re highlighting new historical individuals whose archaeological stories we think are especially worth telling, from a pot burial in ancient Egypt to hanging coffins from the cliffs of southwest China. We’re also bringing back some old favorites, adding new individuals to groups that have proven especially popular with our community.

A Rare Glimpse of Old Kingdom Egypt

Ancient Egypt is one of the most famous civilizations in history, but ancient Egyptian DNA has been remarkably hard to come by. Egypt’s hot climate is poorly suited to preserving DNA, and until recently, genetic data from ancient Egypt was limited to partial genomes from a handful of individuals who lived thousands of years after the first pharaohs.

That changed with a 2025 study published in Nature, which reported the first whole genome from ancient Egypt. It belonged to a man who lived between 2855 and 2570 BCE, around the time the Great Pyramid of Giza was built. He wasn’t mummified. Instead, he was buried in a large pottery vessel inside a rock-cut tomb near the village of Nuwayrat, a burial style that may have helped preserve his DNA for more than 4,500 years. His skeleton showed signs of a lifetime of physical labor, and some researchers suggest that the patterns of wear are consistent with the work of a potter.

Most of his ancestry was best matched by older genomes from North Africa, but about one-fifth was most closely related to ancient people from the eastern Fertile Crescent, including Mesopotamia. This provides the first genetic evidence that contacts between early Egypt and Mesopotamia involved the movement of people, not just the exchange of goods and ideas.

Bronze and Iron Age Mesopotamia

Mesopotamia, the land between the Tigris and Euphrates rivers, was home to some of the world’s earliest cities and one of its earliest writing systems. Yet, much like Egypt, its harsh climate has made ancient DNA from the region scarce.

A 2026 study published in Genome Biology analyzed DNA from people buried at Bakr Awa, a large ancient settlement in present-day Iraqi Kurdistan that sat along routes connecting Mesopotamia and Iran. We’ve added nine of the individuals from this study to Historical Matches. The researchers found that the city’s Bronze Age residents had remarkably diverse ancestries, with genetic ties to Anatolia, the Levant and the Caucasus, mirroring the mix of cultures and languages recorded in ancient texts from the site.

The Hanging Coffins of Southwest China

For roughly 3,000 years, communities across southern China and Southeast Asia practiced a striking funerary tradition: placing the coffins of their dead high on cliff faces, in caves or in rock crevices, sometimes hundreds of meters above the ground. In southwest China, historical records attribute these hanging coffins to the Bo people, a group that largely disappeared from written history during the Ming Dynasty. Local legends describe the Bo as “Sons of the Cliffs,” and even say they could fly.

A 2025 study published in Nature Communications sequenced the genomes of people buried in hanging coffins, and we’ve added six of them to Historical Matches. Most shared ancestry with Neolithic populations from China’s southeastern coast, consistent with archaeological evidence that the tradition began there. But two women buried at the same site in Yunnan around 1,250 years ago had very different ancestries, linked to populations from northern China and Northeast Asia, suggesting that hanging coffin communities welcomed people from distant regions. Perhaps most strikingly, the researchers found that a small present-day Bo community in Yunnan inherited much of its ancestry from the people buried in these coffins, supporting long-standing oral traditions linking them to this custom.

Bringing Back Some Old Favorites

Alongside these new groups, we’re adding individuals to some of the most popular groups in the feature.

Our new Viking Age additions include two individuals buried in Sweden around the end of the Viking Age, both of whom had a rare inherited form of dwarfism. When their skeletons were first studied, archaeologists suspected they were closely related, but couldn’t tell whether they were brother and sister, mother and son or father and daughter. DNA analysis settled the question: they were siblings. Joining them is a young warrior from an elite cemetery at Bodzia, in present-day Poland, whose grave contained a belt fitting bearing the emblem of Prince Sviatopolk, a ruler of Kyiv in the early 11th century, hinting at connections stretching across medieval Europe.

The Sarmatian group is growing as well. The Sarmatians were a nomadic people who dominated the steppe grasslands north of the Black Sea before moving west and settling across the Great Hungarian Plain in the 1st century CE. For centuries, they were one of the major powers on the edge of the Roman world. Yet unlike many of the peoples they lived alongside, no modern nation claims them as ancestors, leading some researchers to call them a “forgotten people.” Ancient DNA is now helping to bring their story back into view.

We’re also adding individuals to our Iron Age Durotriges group from southern Britain, a community in which women stayed with their maternal families while men moved to live with their wives’ families.

Finally, we’re adding a medieval king to our Hungarian Royalty group. King Saint Ladislaus I ruled Hungary in the late 11th century, and his skull has been preserved as a relic for centuries. After a turbulent history that included a fire and a rescue during regional conflicts, historians had questioned whether the relic was authentic. Ancient DNA confirmed that it carries the same rare paternal lineage as other members of his dynasty.

Learn More

23andMe Premium members can explore whether they share a genetic connection with any of these newly added individuals, and with more than 1,000 others, through the Historical Matches feature.

And if you are interested in finding ways to celebrate International Archaeology Day, check out organizations like the Archaeological Institute of America, which has an exciting calendar of Archaeology-related events.

First held in 1948, ASHG has grown into the world’s largest annual gathering of human genetics and genomics professionals. Over five days, researchers, clinicians, genetic counselors and students share new findings, many not yet published, on questions ranging from rare disease diagnosis to the genetics of common conditions. For the 23andMe Research Institute, as a nonprofit medical research organization, being in Montréal is about listening as much as presenting. Our scientists will share their latest work, including new findings from 6 million consented research participants showing how many people receive a medically actionable result through direct-to-consumer genetic testing. But some of the most valuable moments happen in poster halls and hallway conversations. That’s where we learn about new methods, see emerging data and make connections with other scientists and future collaborators. Those exchanges keep our research sharp and help move discoveries closer to the clinic, where they can make a real difference in research and health.

Research at 23andMe has always been a team effort. Our 11 million consented research participants make it possible, and collaborations with academic, nonprofit and industry partners have helped turn that participation into more than 300 peer-reviewed publications. Recent studies published in Science and Nature, show what research at this scale makes possible, from identifying the largest known single genetic risk factor for lung cancer to discovering genetic variants that influence how people respond to GLP-1 medications.

At ASHG, we’re introducing new capabilities designed to give researchers more flexibility, depth and clinical context by connecting genetics with de-identified real-world health data. We’ll also discuss our commitment to expanding access to genetic and phenotypic data, so more scientists can bring their own questions and expertise to our cohort. All of this rests on our longstanding commitment to participant consent, privacy and trust, and to rigorous research practices. The questions facing human genetics are too big for any one team to answer alone, and we’re eager to find new partners who share that view.

Are you a researcher looking to benefit from the scale and depth of 23andMe genetic and phenotypic data? Visit us at booth #400 to explore new research capabilities and opportunities for collaboration, or connect with us to start a conversation.

Connect with the 23andMe Research Institute at ASHG

Join us at booth #400

Presentations

FRIDAY, OCTOBER 23RD 01:30 pm – 02:30 pm
Platform Session 86: Returning ‘Omics Results to Patients to Improve Health (Room 510/Level 5)
One in ten individuals receives a medically actionable result through direct-to-consumer genetic testing: Insights from 6 million research participants

presented by Noura Abul-Husn, 23andMe Research Institute, Chief Medical Officer

THURSDAY, OCTOBER 22ND 05:00 pm – 05:30 pm (CoLab Session; CoLab Theater 2, Exhibit Hall)
Genetic Discovery at Population Scale: What Becomes Possible with 11 Million Research Participants

presented by Adam Auton, Vice President of Research

Posters

THURSDAY, OCTOBER 22ND 04:15 pm – 06:15 pm (Poster #8468T)
Validation of Self-Reported Phenotypes in a Real World Genotyped Cohort

presented by Wanwan Xu, Sr. Scientist I

THURSDAY, OCTOBER 22ND 04:15 pm – 06:15 pm (Poster #4006T)
Genome-wide burden testing of imputed rare variants recovers sequencing-based signals

presented by Keng-Han Lin, Sr. Scientist II, Statistical Genetics

Can’t make it to Montréal? Reach out to start a conversation with us.

Genetics is no longer just for specialists. Today, DNA insights help guide cancer screenings, flag inherited health risks and tailor medication choices. As more people learn about their DNA, including through at-home tests, a practical question follows: who helps you make sense of your genetic test results? 

Our new paper in Trends in Genetics shares what we learned from building and running a genetics training program for primary care doctors and nurse practitioners, and what it takes to prepare them for this role.

Why Are Primary Care Doctors Taking On Genetics?

Genetics is quickly becoming part of routine medicine. Polygenic risk scores, which combine the small effects of many genetic variants, are starting to help evaluate risk for common conditions like coronary artery disease. At the same time, more people are bringing at-home DNA test results to their annual checkups, looking to discuss what their genetic data means for their day-to-day health.

The U.S. does not have enough medical geneticists and genetic counselors to meet growing demand. Distance, cost and logistics make access especially hard in rural and underserved communities. Relying solely on specialist referrals is not sustainable. Equipping primary care professionals to handle routine genetic questions allows specialists to focus their expertise on high-complexity cases.

How Did We Prepare Primary Care Professionals to Use Genetics?

Effective genetics training for primary care should focus on the tasks healthcare professionals perform with patients, not on turning them into specialists. Our team developed a 20-hour training program for 42 healthcare professionals (10 physicians and 32 nurse practitioners) at a nationwide U.S. telehealth medical group that cares for patients with direct-to-consumer genetic test results.

Our first step in developing this program was defining what genetics care should actually look like in primary care. We identified the specific tasks primary care professionals would need to perform and incorporated these into the training. The five skills we identified included:

• Assessing family health history
• Interpreting genetic test results in a clinical context
• Communicating risk and uncertainty
• Making appropriate management decisions
• Recognizing when to consult or refer to a genetics specialist

Learning by doing was central to the program. We combined self-paced learning with small-group sessions designed to encourage discussion. Case discussions focused on clinical situations relevant to primary care. The healthcare professional participants also analyzed personal or sample genetic data and completed a practice visit with a simulated patient.

Each participant also built a guide to one genetic condition using a structured template. Each guide covers:

• Background information: The condition, how common it is and how it’s inherited
• Clinical assessment: Symptoms, family history, risk factors and lab findings
• Genetic testing: Which tests to order, what results mean and their limitations
• Clinical management: Treatment guidance, prescribing, lifestyle and referrals
• Family and resources: What results mean for relatives, plus resources for patients and healthcare professionals

Building these guides gave participants practice applying genetics to patient care and a consistent way to evaluate genetic conditions. After training ended, participants could still use similar quick-reference guides and consult genetic counselors as questions came up.

Does Training Alone Make Doctors Feel Ready?

Passing an exam is an important step, but true clinical confidence develops through repeated practice and ongoing support over time. At the end of the program, the healthcare professionals averaged 84.6% on a 25-question exam and scored well in a practice visit with a simulated patient. They rated the hands-on activities as the most valuable part of the program.

Six months later, participants reported feeling more prepared for some aspects of genomics-informed care than others. For example, 76% felt prepared to take a family health history, while 32% felt prepared to address genetic test results across a range of conditions. This variation reinforced an important lesson from the program: education can build foundational knowledge and skills, but primary care professionals also need ongoing resources and access to genetics expertise as they encounter different clinical situations.

With every study, there are limitations: the program had no comparison group, not every participant completed follow-up and follow-up lasted six months, so results may not apply to every setting.

What Helps Doctors Use Genetics in Everyday Care?

Following participants over time showed us that education is only one piece. Based on that experience, we developed a three-part framework.

• Foundational education: Practical, case-based training rooted in real primary care situations.
• Point-of-care tools: Condition-specific guides healthcare professionals can check during a visit, covering testing, management and family implications.
• Genetics expertise: Access to genetic counselors and referral pathways for complex cases.

Elements like self-paced learning, digital support tools and virtual access to genetic counselors can help this approach work across many kinds of primary care settings. The objective isn’t to replace specialists, but to foster collaborative care that benefits both patients and healthcare professionals.

What Does This Mean for You?

For healthcare professionals and health systems, our experience suggests that genetics belongs in primary care, and that the right mix of training, tools and expert support can help make it work.

For individuals, if you have genetic test results you would like to explore, your primary care doctor or nurse practitioner is a great place to start the conversation. Bring your results and what you know about your family health history, and ask whether a genetic counselor could help with anything complex. And to learn more about how genetics works and what your DNA can tell you, explore the 23andMe Genetics Learning Hub.

October is Breast Cancer Awareness Month, and the statistic you’ll see most often is this one: about 1 in 8 women in the United States will develop breast cancer in her lifetime. Here’s a number you’ll see far less often. More than 80% of people who carry a BRCA1 or BRCA2 variant that raises breast, ovarian, prostate and pancreatic cancer risk have no idea they carry it.

Why So Many People Slip Through the Cracks

BRCA1 and BRCA2 are tumor suppressor genes, meaning their normal job is to repair breaks in your DNA before those breaks can lead to cancer. Everyone has both of these genes, but some people inherit a genetic variant that keeps one of these genes from doing that repair work properly. This raises the likelihood of breast, ovarian, prostate and pancreatic cancer. Those variants can be passed down from either parent.

Clinical guidelines generally recommend BRCA testing for people with a personal or family history of certain cancers. That sounds sensible until you look at who it misses. 

Family history is easier to lose than many people assume. Small families, adoption, estranged relatives, donor conception or simply a branch of the family tree nobody talks about can lead to missing family history information. Ancestry information can get lost the same way. This is important because certain genetic variants may be more common in certain populations. For example, three specific BRCA variants are much more common in people of Ashkenazi Jewish descent, roughly 1 in 40 people in that population have a BRCA variant compared to about 1 in 200 in the general population.

When 23andMe scientists studied more than 2,800 members who consented to research and had one of the three Ashkenazi BRCA variants originally included in our BRCA1/BRCA2 (Selected Variants) Genetic Health Risk report*, 44% reported no close family history of a BRCA-related cancer. This means that nearly half of people with a BRCA variant would have been unlikely to qualify for clinical testing at all. In that same study, 21% of people with an Ashkenazi BRCA variant reported no Jewish ancestry, yet 62% of them had detectable Ashkenazi Jewish genetic ancestry.

Men are also often missing from this conversation, and BRCA variants affect them too. Studies suggest around 7% of men with a BRCA2 variant and 1% with a BRCA1 variant develop male breast cancer in their lifetime, compared with about 0.1% of men overall, and BRCA variants also raise prostate and pancreatic cancer risk. 

Finally, Black women in the US are about 38% more likely to die of breast cancer than white women despite being slightly less likely to be diagnosed with it. This disparity is shaped by access to care, time to treatment and tumor biology rather than by genetics alone. Most genetic research has been conducted in people of European ancestry, so detection rates vary by ancestry and polygenic models perform unevenly across populations. 23andMe has worked to narrow this, including a 2023 update that expanded our BRCA report from three variants to 44, improving detection for people of African American, East Asian, non-Ashkenazi European and Hispanic/Latino descent.

Inherited Risk Is Bigger Than One Famous Gene

BRCA1 and BRCA2 are the most famous genes connected to breast cancer, but inherited risk comes in more than one form.

While the 23andMe BRCA1/BRCA2 (Selected Variants) Genetic Health Risk report looks at 44 specific variants in the BRCA1 and BRCA2 genes more than 4,000 BRCA variants are known to increase cancer risk. However, BRCA1 and BRCA2 aren’t the only genes where inheriting a single variant matters. Researchers have identified other genes, including PALB2, CHEK2 and ATM, where one variant meaningfully raises breast cancer risk.

The 23andMe Breast Cancer PRS report** works from a third direction. A polygenic risk score, or PRS, is a statistical model that adds up the tiny effects of thousands of common genetic variants. No single variant contributes much alone, but together they can shift the picture, and it’s these common variants combined with lifestyle and environment that account for the majority of breast cancer cases. The Breast Cancer PRS report was built by 23andMe scientists using data from thousands of consented research participants and is available to 23andMe Premium Ancestry + Health members who self-reported their birth sex as female.

What You Can Do This Month

There’s a word for someone living with an increased likelihood of cancer who has not been diagnosed with it: previvor. Acting on that knowledge while you’re healthy is the entire point, and it starts with information that’s free to gather.

• Map your family history on both sides. Breast cancer risk can be inherited from your father as well as your mother, and paternal history is what people most often overlook. Note who had cancer, what kind and at what age. If your history is incomplete, that’s ok. Focus on the information you do have. Your own personal health records or genetic testing may provide additional helpful insights.
• Keep up with recommended screening. Mammography and other screening guidelines depend on your age and risk factors, so ask what applies to you.
• If your family history raises questions, ask about a broader clinical genetics panel. A selected-variant result that finds nothing does not rule out a variant it doesn’t test for.
• Tell your relatives what you find. Because genetic risk factors can be passed down through a family, sharing your own genetic information could help alert family members about a potential health risk they might have. Learn more about how to talk to family members about genetic results.
• Lean on the advocacy community. FORCE, Susan G. Komen, Breastcancer.org and Sharsheret all offer free education and support.

23andMe has returned BRCA risk information to more than 15,000 customers, and many may have never been offered traditional genetic testing. Start with the Genetics Learning Hub to understand how inherited cancer risk actually works, read customer stories of those who have found out about their cancer risk, then open your own reports and bring what you find to your next 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 including the 23andMe PGS Genetic Health Risk Report for BRCA1/BRCA2 (Selected Variants). 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. Warnings & Limitations: 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 in people of most ethnicities. This report does not include variants in other genes linked to hereditary cancers and the absence of variants included in this report does not rule out the presence of other genetic variants that may impact cancer risk. This report is for over-the-counter use by adults over the age of 18, and provides 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 in a clinical setting before taking any medical action. For important information and limitations regarding each genetic health risk and carrier status report, visit 23andme.com/test-info/

** The 23andMe Breast Cancer 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 developing breast cancer. The report does not describe a person’s overall likelihood, does not account for lifestyle or family history and has not been reviewed by the US Food and Drug Administration. The Breast Cancer PRS report is not intended to tell you anything about your current state of health, or to be used to make medical decisions or determine any treatment.

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