We often hear about the &#8220;nature versus nurture&#8221; debate, framing it as a battle between our genes and our environment. But in many cases it&#8217;s not a battle at all, it&#8217;s a partnership. The way our genes impact our health and traits may change depending on our environment.



<figure class="wp-block-image size-large"><img loading="lazy" decoding="async" width="1024" height="684" src="http://35.88.189.111/wp-content/uploads/2022/09/GettyImages-981323210-1024x684.jpg" alt="" class="wp-image-30209" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/09/GettyImages-981323210-1024x684.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/09/GettyImages-981323210-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/09/GettyImages-981323210-768x513.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/09/GettyImages-981323210-880x587.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/09/GettyImages-981323210-1180x788.jpg 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



Understanding both &#8220;nature&#8221; and &#8220;nurture&#8221; is especially important when we consider complex skills critical to success in life, like reading. Thanks to the contribution of over a million 23andMe® research participants, a <a href="https://pubmed.ncbi.nlm.nih.gov/40991152/" target="_blank" rel="noreferrer noopener">new study</a>, led by scientists from the University of Edinburgh, is helping to untangle how both genes and environment work to shape literacy.



<h2 class="wp-block-heading" id="h-the-reading-puzzle-nbsp">The Reading Puzzle&nbsp;</h2>



Literacy is a powerful predictor of life outcomes, from education level to income. For decades, researchers have tried to understand the roles genetics and environment play in why some people learn to read and spell more easily than others.



<figure class="wp-block-image alignleft size-full is-resized"><img loading="lazy" decoding="async" width="425" height="282" src="http://35.88.189.111/wp-content/uploads/2008/07/twins.jpg" alt="" class="wp-image-392" style="width:309px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2008/07/twins.jpg 425w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2008/07/twins-300x199.jpg 300w" sizes="auto, (max-width: 425px) 100vw, 425px" /></figure>



Several <a href="https://pubmed.ncbi.nlm.nih.gov/23725549/" target="_blank" rel="noreferrer noopener">studies</a> of <a href="https://pubmed.ncbi.nlm.nih.gov/19076484/" target="_blank" rel="noreferrer noopener">twins</a> in the United States suggested an interaction between genes and environment. In these studies, how much influence genetics had on reading skills seemed to be higher in families with a higher socioeconomic status. In other words, genetics appeared to have a bigger impact on a child&#8217;s reading ability when they were in a more advantaged environment. This idea is called a gene-by-environment interaction.



However, the evidence of this gene-by-environment interaction was mixed in studies conducted in the <a href="https://pubmed.ncbi.nlm.nih.gov/19296213/" target="_blank" rel="noreferrer noopener">United Kingdom</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/28832969/" target="_blank" rel="noreferrer noopener">Australia</a>. This puzzle led researchers to ask: can we use modern genetic data to test this theory in large, diverse populations?



<h2 class="wp-block-heading" id="h-a-new-approach">A New Approach</h2>



Researchers utilized summary statistics from a 2022 <a href="https://blog.23andme.com/articles/study-identifies-genetic-links-to-dyslexia" target="_blank" rel="noreferrer noopener">genome-wide association study (GWAS) on dyslexia</a> to construct a polygenic score—a way of estimating someone’s genetic tendency toward a trait by adding up the small effects of thousands of DNA differences.



The team then applied this polygenic score to two large groups of children and adolescents in Australia and the United Kingdom to see if the score&#8217;s effect on reading and spelling skills was moderated by their family&#8217;s socioeconomic status. Socioeconomic status was used as a broad measure of environmental advantage, capturing factors like parental education level and household income.&nbsp;



<h2 class="wp-block-heading" id="h-what-was-discovered-two-parallel-paths">What Was Discovered: Two Parallel Paths</h2>



Both the dyslexia polygenic score (nature) and socioeconomic status (nurture) were significant predictors of reading and spelling performance. Together, demographic, genetic, and socioeconomic factors explained between 8% and 11.6% of the variation in reading skills.



However, the study found no interaction effect. Nature and nurture were both important, but they worked in parallel.



This means the influence of a person&#8217;s genetic predisposition was the same, regardless of their family&#8217;s socioeconomic background. In these groups, a higher genetic predisposition for reading provided a similar boost to children from all socioeconomic backgrounds.&nbsp;



<h2 class="wp-block-heading" id="h-the-bigger-picture">The Bigger Picture</h2>



This finding is an important reminder to scientists to consider different environments when looking for gene-by-environment interactions. While some earlier US-based studies suggested an interaction, the different environments in these large UK and Australian groups showed a different outcome. Suggesting that both our genes and our environment make their own distinct contributions to the development of this fundamental skill.



Of course, every study has its limitations. The 23andMe research participants who contributed to the original GWAS are a self-selecting group and may not be perfectly representative of the general population. Additionally, only about 5% of 23andMe research participants said they had dyslexia, which is on the lower end of the <a href="https://pubmed.ncbi.nlm.nih.gov/18652545/" target="_blank" rel="noreferrer noopener">commonly cited 5–10% range</a>.



Even so, this large-scale study provides a crucial piece of the puzzle, emphasizing how vital it is to test scientific findings in diverse environments to get the full story.

Nature and Nurture: A New Look at the Genetics of Reading Ability

This week the American Society of Human Genetics (ASHG) is having its <a href="https://meetings.ashg.org/event/ASHG25/home/" target="_blank" rel="noreferrer noopener">annual meeting</a> in Boston. Attending the ASHG annual meeting is about more than just presenting our work, it&#8217;s one way we are working to ensure that the 23andMe® Research Institute contributes to a healthier future for everyone.



<ul class="wp-block-list">
<li>Amplifying impact: Sharing our discoveries with a global audience helps our work reach those who can build upon it, accelerating the path from discovery to clinic.</li>



<li>Fostering collaboration: It&#8217;s where we connect with the brightest minds in the field. These conversations spark new ideas and forge partnerships that are essential for tackling complex diseases.</li>



<li>Staying on the cutting edge: Exposure to the latest technologies and unpublished data keeps our research relevant and innovative.</li>
</ul>



<h2 class="wp-block-heading" id="h-23andme-research-institute-at-ashg">23andMe Research Institute at ASHG</h2>



For those attending, stop by our posters in the following sessions:



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WEDNESDAY, OCTOBER 15TH 2:30 &#8211; 4:30 PM (Posters; Board #2004W) Sustaining Research Ethics in Times of Change: A Framework from the 23andMe Research Program



presented by Emily DelloRusso, Principal Regulatory Science Manager
</div>



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THURSDAY, OCTOBER 16TH 2:30 &#8211; 4:30 PM (Posters; Board #2035T) Explore23: a privacy-forward, secure, extensible, and easy-to-use web application for exploration of a large genomic research cohort



presented by Julie Granka, Director, Statistical Genetics
</div>



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FRIDAY, OCTOBER 17TH 2:30 &#8211; 4:30 PM (Posters; Board #3014F) Learning about a genetic predisposition to depression is psychologically well tolerated among those with high polygenic risk scores



presented by Rebecca Berns, Sr. Product Scientist I, Genomic Health and Sciences
</div>



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Interested in reading more? 23andMe has contributed to <a href="https://research.23andme.com/publications/" target="_blank" rel="noreferrer noopener">more than 300 research publications</a>.

23andMe Research Institute Attending ASHG 2025

Cannabis is already one of the most widely used drugs globally, and its use will likely grow even more as it becomes more socially accepted and legally available. For many the recreational use of cannabis poses few problems, but for as many as a third of users, it becomes problematic developing into an addiction or what scientists call cannabis use disorder. Research suggests that genetics may explain why.



<h2 class="wp-block-heading" id="h-searching-the-genome-for-clues">Searching the Genome for Clues</h2>



In collaboration with 23andMe Research Institute, researchers at the University of California, San Diego <a href="https://www.nature.com/articles/s41380-025-03219-2" target="_blank" rel="noreferrer noopener">published a study</a> today that found genetic links to cannabis use as well as links to psychiatric, cognitive, and physical health. The researchers used data from more than 130,000 people who consented to participate in 23andMe research. Participants answered survey questions on whether they had ever used cannabis (“lifetime use”) and, for those who had, how often they used it during their heaviest 30-day period (“frequency of use”). The team then conducted genome-wide association studies searching for genetic variants linked to ever trying cannabis and how often people used the drug.



<h2 class="wp-block-heading" id="h-what-the-data-revealed">What the Data Revealed</h2>



Researchers found that having ever used cannabis was associated with two genetic regions: CADM2—a gene <a href="https://blog.23andme.com/articles/scientists-identify-genes-associated-with-cannabis-use" target="_blank" rel="noreferrer noopener">previously linked</a> to cannabis and other substance use, impulsivity, and risk-taking—and GRM3. While GRM3 has been tied to alcohol use, schizophrenia, and certain personality traits, this is the first time it’s been linked to cannabis use. How often someone used cannabis was associated with a different variant also near CADM2, strengthening this gene’s role in cannabis behaviors. Both having ever used cannabis and how frequently someone used cannabis were genetically linked to other substance use, pain, and psychiatric conditions like depression. Researchers also created polygenic scores—which tally the effects of many different genetic variants—to estimate both the likelihood of ever having used cannabis and the frequency of cannabis use. These polygenic scores were able to replicate associations between cannabis use and substance use and mood disorders in two other independent research datasets (All of Us and BioVU). The researchers also uncovered novel associations with anxiety, celiac disease, HIV, and viral hepatitis.



<h2 class="wp-block-heading" id="h-why-this-research-matters">Why This Research Matters</h2>



Most genetic research on cannabis has focused on two points in the spectrum: first use and cannabis use disorder. But the stages in between—like how often someone uses cannabis—are just as important. Studying these “pre-addiction” traits may help determine who is more likely to progress from a casual user to someone with cannabis use disorder. This study was one of the first genome wide association studies to look at traits that may lead to cannabis use disorder.&nbsp;



Traits like frequency of cannabis use can reveal genetic factors that shape vulnerability before addiction develops. Understanding these factors could eventually help predict risk for cannabis use disorder and related health conditions.



<h2 class="wp-block-heading" id="h-more-than-just-dna">More Than Just DNA</h2>



Like all research there are some important considerations to keep in mind for this study:



<ul class="wp-block-list">
<li>While this research focused on genetics, many non-genetic factors may also play a significant role in a person&#8217;s likelihood of using cannabis or developing cannabis use disorder.</li>



<li>The study was conducted in people of European descent (based on an analysis of their local genetic ancestry), so the findings may not fully apply to people of other ancestries.</li>



<li>The measure of frequency (use days in a 30-day window) of using cannabis doesn’t capture full patterns such as the duration of regular use or quantity consumed.</li>



<li>While GRM3 is a promising lead, more work is needed to understand how the genetic variant in this region affects cannabis use biology.</li>
</ul>



<h2 class="wp-block-heading" id="h-the-road-ahead">The Road Ahead</h2>



Future research will need to expand to larger and more diverse cohorts and include other cannabis-related traits such as craving, withdrawal, and response to cannabis. Combining genetic insights from multiple stages of cannabis use could:



<ul class="wp-block-list">
<li>Improve the discovery of new genetic variants</li>



<li>Help build predictive models for problematic use</li>



<li>Clarify how cannabis genetics intersect with physical and mental health</li>
</ul>



Takeaway: Studying genetic influences on early cannabis use behaviors could eventually help predict risk for cannabis use disorder and related health conditions, and may help shed light on who is most at risk for cannabis use disorder.&nbsp; These findings mark an important step toward understanding the genetics of cannabis use and its health consequences.

New Genetic Insights Into Cannabis Use

<h6 class="wp-block-heading" id="h-a-new-study-may-help-identify-and-more-quickly-help-the-60-of-people-with-major-depression-who-do-not-get-relief-from-their-initial-treatments">A new study may help identify and more quickly help the 60% of people with major depression who do not get relief from their initial treatments. </h6>



It is estimated that 60% of patients with major depressive disorder don&#8217;t find relief from their first medication, and as many as one-third develop <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC10503923/" target="_blank" rel="noreferrer noopener">treatment-resistant depression</a>, which is often defined as still experiencing symptoms after trying at least two antidepressants.



Researchers at Johnson &amp; Johnson and the 23andMe Research Institute used advanced machine learning techniques to accurately identify those at most risk for treatment-resistant depression, a massive breakthrough for those suffering with this condition.



The groundbreaking research, published this week in the journal <a href="https://pubmed.ncbi.nlm.nih.gov/41028019/" target="_blank" rel="noreferrer noopener">Scientific Reports</a>, used only self-reported information from about 23,000 people who consented to participate in 23andMe research. The model included a total of 101 predictive factors, including such things as age, symptoms that persist between episodes of depression, the duration of episodes of depression, stress levels, and suicidal thoughts. 



Using this predictive model, researchers were able to accurately predict those at the highest risk for treatment-resistant depression 78% of the time, according to the study.&nbsp;



The predictive model did not use either genetics or lab results, just questions that can be easily assessed by a clinician.



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



<figure class="wp-block-image alignright size-full is-resized"><img loading="lazy" decoding="async" width="508" height="531" src="http://35.88.189.111/wp-content/uploads/2025/10/drug-bottle.png" alt="" class="wp-image-34304" style="width:161px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/drug-bottle.png 508w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/drug-bottle-287x300.png 287w" sizes="auto, (max-width: 508px) 100vw, 508px" /></figure>



Typically, antidepressants used to treat major depression take a little time to work, up to a month or a month and a half. When a treatment does not work, clinicians often prescribe an alternative medication. When someone with depression fails to respond to at least two different medications, they are deemed to have treatment-resistant depression. In many cases, it can take around a year for someone to finally be diagnosed with treatment-resistant depression.



That long delay in finding effective treatment has a cost, not just in the time it takes to identify treatment but in the prolonged suffering for those in the throes of depression, unable to get relief.&nbsp;



The promise of the kind of predictive modeling described in this new study is that it would give both people with depression and clinicians who treat them a tool to flag those who might not respond to standard therapies.



Instead of waiting to see if initial treatments are effective, it may accelerate the process of finding alternatives. Additionally, this predictive model only utilizes patient-reported information; no expensive testing is required.&nbsp;



<h2 class="wp-block-heading">More About the Predictive Model</h2>



The model identified eight primary factors that predict treatment resistance, as reported by research participants. Each offers different dimensions of their depression.



<figure class="wp-block-image alignleft size-full is-resized"><img loading="lazy" decoding="async" width="275" height="252" src="http://35.88.189.111/wp-content/uploads/2025/10/depression.png" alt="" class="wp-image-34307" style="width:184px;height:auto"/></figure>



Participants reported on the different symptoms that persisted between the episodes of depression. They reported on how long each episode of depression lasted, and how many years they&#8217;d experienced these periodic episodes. Also included in the self-reported data were levels of stress, or whether they had recurring post-traumatic stress, and two critical factors that looked at more external stressors and life events. Also factored into the modeling was a participant&#8217;s age and whether they had suicidal thoughts. Finally, the model included the self-reported timing between episodes of depression, which was significant when the time between episodes was shorter.



Using these factors and advanced machine learning the researchers were able to accurately distinguish between those who were treatment-resistant and those who responded to treatment. An accurate way to identify if someone will or will not respond to treatment could translate into meaningful clinical benefits. It could mean the difference between waiting months for effective treatment instead of years.&nbsp;



<h2 class="wp-block-heading">More Personalized Depression Care</h2>



This research represents a crucial step toward more personalized mental health treatment and a move away from a &#8220;one-size-fits-all&#8221; approach to treatment of depression.&nbsp;



For the millions of people living with depression, this work represents a path toward precision care, shortening the time to effective treatment and improving quality of life.



The future of depression treatment lies not just in developing new medications, but in better understanding who needs what treatment when. This predictive model brings us measurably closer to that goal, promising a world where effective depression treatment is not a matter of luck, but of precision.



If you or someone you know is struggling with depression, please reach out to a mental health professional. The <a href="https://988lifeline.org/" target="_blank" rel="noreferrer noopener">National Suicide Prevention Lifeline</a> (988) provides 24/7 support for those in crisis.

Predicting Treatment-Resistant Depression Using the 23andMe Survey Data

National Cancer Prevention and Early Detection Month: Highlighting Customer Stories

<figure class="wp-block-image size-large"><img loading="lazy" decoding="async" width="1024" height="768" src="http://35.88.189.111/wp-content/uploads/2024/12/All-the-siblings-1024x768.jpg" alt="Image of Jenn and her three half siblings" class="wp-image-33542" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/12/All-the-siblings-1024x768.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/12/All-the-siblings-300x225.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/12/All-the-siblings-768x576.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/12/All-the-siblings-880x660.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/12/All-the-siblings.jpg 1080w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /><figcaption class="wp-element-caption">Jenn (far left) and her half siblings (from left) Joe, Mechele &#038; Lisa</figcaption></figure>



They were strangers to Jenn, so as she prepared for her first in-person meeting with her newly found brother and two sisters, her anxiety rose.



“Of course, I was nervous,” said Jenn, a 46-year-old who works in a New York real estate office. “I went over everything that can go wrong, you know, especially because of what happened when I reached out to my birth mother.”



That was in 2019. The state of New York had just opened adoption records. Jenn found the identity of her birth mother, carefully crafted a letter to her, and included photos of herself as a child and another one of her as an adult. Jenn didn’t want anything from her birth mother; she just wanted to connect. Instead of an embrace, she got the kind of response many adoptees fear the most.



“She doesn’t want to have anything to do with me,” Jenn said.



<h2 class="wp-block-heading" id="h-you-have-daddy-s-eyes">‘You Have Daddy’s Eyes’</h2>



So, five years later, after connecting through 23andMe to three half-siblings on her birth father’s side, Jenn was all butterflies. Then she walked into the pizza parlor where she’d be meeting Joe, Lisa, and Mechele. She heard Lisa say, “Welcome baby sister,” and she then got her first group hug.



“Sometimes when you meet someone for the first time, you’re nervous and you hold something of yourself back,” Jenn said. “There was none of that. It’s crazy how easily we got along.”



At one point, one of her siblings said, “You have daddy’s eyes.”



One minute, they were four strangers meeting for the first time; the next, they were family.



<figure class="wp-block-image size-full"><img loading="lazy" decoding="async" width="360" height="480" src="http://35.88.189.111/wp-content/uploads/2024/12/Jenn-and-sister-.jpg" alt="Jenn and half-sister Mechele" class="wp-image-33543" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/12/Jenn-and-sister-.jpg 360w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/12/Jenn-and-sister--225x300.jpg 225w" sizes="auto, (max-width: 360px) 100vw, 360px" /><figcaption class="wp-element-caption">Jenn and Mechele</figcaption></figure>



<h2 class="wp-block-heading" id="h-creating-family-memories">Creating Family Memories</h2>



That was on January 26th, 2024, the 30th anniversary of their father’s death. Their bonds with each other have only grown since then, including a bigger family reunion in August and plans to gather again for the holidays this year.



“I am looking forward to creating memories with my family and learning more and more about our father,” said Jenn. “23andMe was a blessing, and we are so very grateful for the opportunity to make our family complete.”



Getting to the point where she could sit at this much, much bigger family table this holiday season wasn’t easy. It was 46 years in the making.



Jenn, and her brother, were adopted from different families, but they always felt lucky to have a mom that loved them unconditionally.



“When I say, ‘my mom,’ I mean the woman who raised me,” Jenn said. “She is my mother.”



That’s never going to change.



<h2 class="wp-block-heading" id="h-losing-mom">Losing Mom</h2>



When, as young kids, she and her brother learned that they’d been adopted, they didn’t tell their mom.



“I couldn&#8217;t even think about looking for (my birth parents) while she was here because it would have broken her,” Jenn said. “I would not do that.”



For Jenn, being adopted felt special. She believed that unlike other kids who just get the parents they’re born to, she and her brother had been chosen by their parents, and they won the parent lottery with their mom.



“She was my world,” Jenn said, her voice filled with emotion.



When their mom died in 1997, Jenn was devastated. She was 19.



It would be a long time before she’d start searching for where she came from and who her birth parents might have been. It wasn’t so much to make a connection but more about trying to understand herself and her story.



“I wanted to know where I came from and who I was,” she said.



She loved her mom and loves her brother, but she also felt different.



“Growing up, my mom was very quiet, very calm, cool, and collected,” Jenn said. “My brother is also like that, and here I come along and I’m loud, I&#8217;m fresh. I’m the person at the party saying &#8216;let&#8217;s dance.’ I wanted to know why I was that way.”



<h2 class="wp-block-heading" id="h-taking-a-chance-at-finding-family">Taking a Chance at Finding Family</h2>



Her first quest in 2019 started with getting ahold of her adoption records in New York and ended in rejection. She thought that was the end to her search for family.



“I closed the book on all that,” she said.



In 2017 she used 23andMe, but it wasn’t to find her family. She wanted to learn more about her ethnicity. She learned she was mostly British and Irish and had some German ancestry. She had some very distant cousins that popped up, but she didn’t really think about family connections. Then she got an email in December of 2023 notifying her that a relative had messaged her on 23andMe.



It was a message from Joe.



She scrolled down, saw his photo and that he was predicted to be a half-brother.



“I dropped my phone,” she said.



<figure class="wp-block-image size-full"><img loading="lazy" decoding="async" width="240" height="320" src="http://35.88.189.111/wp-content/uploads/2024/12/Jenn-and-Joe.jpg" alt="Jenn and half-sibling Joe" class="wp-image-33544" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/12/Jenn-and-Joe.jpg 240w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/12/Jenn-and-Joe-225x300.jpg 225w" sizes="auto, (max-width: 240px) 100vw, 240px" /><figcaption class="wp-element-caption">Jenn and Joe</figcaption></figure>



<h2 class="wp-block-heading" id="h-meeting-for-the-first-time">Meeting for the First Time</h2>



They feverishly began exchanging messages. Joe was as eager as she was to learn more. He eventually asked if he could loop in his sisters. Jenn thought, “Wait, I have sisters.” Then using Facebook, she was able to put more faces to names.



Along with Joe, there was Mechele and Lisa. They all had questions for her as well. Their dad had divorced from their mom in the early 1970s, and afterward he dated for a while. That’s when Jenn had been conceived, but the three siblings believe their father didn’t know anything about Jenn.



“He had no idea about me,” Jenn said. “Everyone swears that if he knew, he one hundred percent would have looked for me, would have found me, and would have been a part of my life.”



But he never got that chance, and then he died of a heart attack in 1994.



<h2 class="wp-block-heading" id="h-nature-versus-nurture">Nature Versus Nurture</h2>



Now Jenn is learning about her birth father from her siblings. She’s learning that they all share the same kind of boisterous personality as she does, and odd little things.



“Okay. So here&#8217;s one thing that happened when,” Jenn said offering one example. “We took a picture, all four of us for the first time and we&#8217;re all joking and just kind of sitting there living in the moment. And my sister Mechele goes, ‘Put a leg up!’”



She kicked her leg up and her sister grabbed it for the photo.



“I stopped for a second and she said, ‘Wait, what happened?’” Jenn said. “They all stopped and looked at me.”



That’s something she’s always doing for photos.



“I looked over at my boyfriend and we&#8217;ve been together for 20 years, and he just shook his head, (because) I do that all the time. I say, ‘Put a leg up!’ and you throw a leg up in the picture.”



It’s such an odd thing to imagine that could be something genetically shared, but it was also so distinctive like something she has always done.



“I was baffled, it’s so weird, but cool, in a cool way,” Jenn said.



<h2 class="wp-block-heading" id="h-your-people">Your People</h2>



&nbsp;As she gets closer to visiting again with her newfound family for the holidays, Jenn also marvels at how fortunate she has been.



“It’s beautiful, this is my family, and I finally get like, I get it all. I get sisters. I get an extra brother. I don’t know how it was so perfect or how I’m so lucky. But I am. I’m the luckiest person in the world.”



There is no question that they are going to stay in each other’s lives. The family is just bigger now.



Her brother, who she was raised with, saw it too.



“He’s my brother. We’re not blood related, but we were raised together. And he said to me when he saw the photos of that first meeting, he said, ‘Jennifer, those are your people.’”

Image of Jenn and her three half siblings

New Family Gathering This Holiday Season

Bella doesn’t know how it started, but genetics has fascinated her since she was little.



<figure class="wp-block-image alignright size-medium"><img loading="lazy" decoding="async" width="228" height="300" src="http://35.88.189.111/wp-content/uploads/2024/08/Bella-Photo-228x300.jpg" alt="A photo of Bella." class="wp-image-33300" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/Bella-Photo-228x300.jpg 228w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/Bella-Photo-768x1009.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/Bella-Photo-779x1024.jpg 779w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/Bella-Photo-670x880.jpg 670w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/Bella-Photo-898x1180.jpg 898w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/Bella-Photo.jpg 1080w" sizes="auto, (max-width: 228px) 100vw, 228px" /></figure>



“I don’t know what triggered it; it just appealed to me,” said Bella, a 22-year-old college student with a passion for biology.



For Bella, genetics is like a giant puzzle, with scientists still trying to piece it together to reveal something about us as humans or why some people get sick, and others don’t. 



During the pandemic, she devoured details of how scientists used a small piece of messenger RNA, mRNA, to create a vaccine that would produce an immune response and antibodies against COVID-19. She also contemplates what might be possible in the future; as most people know, certain genetic variants can dramatically increase one’s risk for a disease. But Bella likes to imagine discovering genetic variants that might do the opposite and protect one against disease.



“There’s still so much more to discover,” she said.



<h2 class="wp-block-heading" id="h-a-gift-of-knowledge">A Gift of Knowledge</h2>



She soon learned that the same was true about her own genetics. Her mom gifted her a 23andMe Health + Ancestry kit for Christmas one year. Bella thought it was a perfect choice.



“It’s really easy to use and super detailed,” she said.



She was interested in her ancestry because she never knew much about her family tree. It turns out that she’s Turkish, Iranian and Italian. She was also interested in her health reports. She opted in to view the reports, went through a short tutorial, and opened up her reports, including her Cystic Fibrosis Carrier Status Report.*



“I found out I was a carrier of cystic fibrosis,” Bella said.



<h2 class="wp-block-heading" id="h-what-it-means-to-be-a-carrier">What it Means to Be a Carrier</h2>



Being a carrier does not typically impact your health, and it’s not unusual; depending on ethnicity, between one in 25 and one in 100 people in the United States are carriers for cystic fibrosis. But there is a chance that if you are a carrier and your partner is a carrier, you could have a<a href="https://www.23andme.com/topics/carrier/cystic-fibrosis/"> child with cystic fibrosis</a>. P



eople with cystic fibrosis inherit variants in the CFTR gene from both parents. It is relatively rare; about 35,000 people in the United States have<a href="https://www.cdc.gov/cystic-fibrosis/about/"> cystic fibrosis, according to the CDC</a>. It’s a very serious condition affecting breathing and digestion. There is no cure, but new treatments have helped people with the disease live longer.  



Learning that she was a carrier initially was a big surprise and a little scary. But it triggered some essential family conversations. 



<h2 class="wp-block-heading" id="h-planning-ahead">Planning Ahead</h2>



Bella talked to her mom and then contacted her dad to find out if there was any family history of cystic fibrosis. Then she spoke to her older brother and then a cousin. She thought this would be important information for them to know since they might be considering having children.



Her mom told her she was glad she used 23andMe.



“’Now you know,’” Bella’s mom told her.



Knowing meant she could plan ahead if she decided to have children. It would be essential to know if her partner was also a carrier.



&#8220;Knowledge is power!&#8221; Bella said more than once.&nbsp;



&nbsp;She continues to stress the importance of genetic testing and planning for the future.



Learn More



<a href="https://www.23andme.com/dna-health-ancestry/">23andMe Health &amp; Ancestry</a>, <a href="https://www.23andme.com/membership/">23andMe+ Premium</a>, and <a href="https://www.23andme.com/total-health/">23andMe+ Total Health </a>customers can all <a href="https://you.23andme.com/health/carrier_status/">learn about their carrier status here</a>. 



Not yet a customer? Find out more about <a href="https://www.23andme.com/compare-dna-tests/">all that 23andMe offers here</a>.



<hr class="wp-block-separator has-alpha-channel-opacity"/>



<h2 class="wp-block-heading" id="h-note">Note:</h2>



*The 23andMe PGS test uses qualitative genotyping to detect select clinically relevant variants in the genomic DNA of adults to report carrier status and reporting and interpreting genetic health risks. The relevance of each report may vary based on ethnicity. 



Our carrier status reports can be used to determine carrier status but cannot determine if you have two copies of any genetic variant. These carrier reports are not intended to tell you anything about your risk for developing a disease in the future, the health of your fetus, or your newborn child’s risk of developing a particular disease later in life. We provide a single report for certain conditions that includes information on carrier status and genetic health risk. 



The Cystic Fibrosis Carrier Status report is indicated for detecting 29 variants in the CFTR gene and is most relevant for people of Ashkenazi Jewish, European, and Hispanic/Latino descent.

Bella Learns About Her Carrier Status

Lillian Newman decided to use 23andMe in part because she wanted to learn about her grandfather, who was from Cuba and had some Sephardic ancestry, but she thought testing could reveal so much more than that.



&#8220;The reason I chose 23andMe is that (it has) a focus not only on the ancestry side but on how your DNA relates to your health,&#8221; Lillian said.



<h2 class="wp-block-heading" id="h-what-i-know-now">What I Know Now</h2>



<figure class="wp-block-image alignright size-medium"><img loading="lazy" decoding="async" width="225" height="300" src="http://35.88.189.111/wp-content/uploads/2024/08/IMG_3775-225x300.jpg" alt="A photo of Lillian Neuman" class="wp-image-33205" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/IMG_3775-225x300.jpg 225w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/IMG_3775-768x1024.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/IMG_3775-660x880.jpg 660w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/IMG_3775-885x1180.jpg 885w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/08/IMG_3775-scaled.jpg 1920w" sizes="auto, (max-width: 225px) 100vw, 225px" /></figure>



Little did she know that her 23andMe health reports would help her profoundly. She shared her story because she thought it might help others. Lillian believes that she&#8217;s not the only one who didn&#8217;t know that genetics affects how one&#8217;s body processes many commonly prescribed medications.* Despite this, clinical guidelines rarely call for testing people before prescribing those medications.



&#8220;I wish I had known then what I know now,&#8221; Lillian said. &#8220;Using 23andMe+ Premium and finding out about the SLCO1B1 gene was huge. Huge.&#8221;



Her reference to the SLCO1B1 gene refers to how different genetic variants in SLCO1B1 can affect how you process certain medications.&nbsp; Like millions of Americans, Lillian Newman has high cholesterol, which, left untreated, can lead to a whole host of issues, including heart disease, heart attacks, and strokes. She learned about her high cholesterol after a routine blood test in 2018. To address the problem, Lillian&#8217;s doctor prescribed a statin.



<h2 class="wp-block-heading" id="h-statins-save-lives">Statins Save Lives</h2>



Statins are among the most prescribed medications in the United States. According to the CDC, an estimated one in four adults in the U.S. takes a cholesterol-lowering medication, and the vast majority of those are statins.



Statins work by inhibiting an enzyme in the liver so the liver makes less cholesterol but pulls in more cholesterol from the bloodstream. That lowers the amount of bad cholesterol in the blood, stabilizing any plaques along the artery&#8217;s walls, and preventing even more plaque from building up. That, in turn, reduces the chances of a stroke or heart attack. Statins have proven<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5126440/"> mostly safe and effective</a> in lowering cholesterol and thus have helped to prevent heart attacks and strokes.



<h2 class="wp-block-heading" id="h-side-effects">Side Effects</h2>



But there are some side effects from taking statins — headache, brain fog, fatigue, and sometimes intense muscle cramping and pain. Sometimes, these side effects are related to a person&#8217;s genetics, which can affect how they process medications. In turn, the side effects sometimes lead people to either change how they take their medication or stop taking it altogether, which in turn can lead to poor health outcomes.



For Lillian, the side effects — severe muscle pain — began after her doctor increased the dose of the statin she was taking. Within a few weeks, the muscles in her legs started cramping. At one point, she had such crushing chest pain that she thought she was having a heart attack and was rushed to the ER. After a cardiologist determined it wasn&#8217;t her heart, her doctor told her that sometimes people experience cramping as a side effect of taking statins but that the benefits of taking the statin outweigh the pain.



&#8220;I remember I went home feeling despondent,&#8221; Lillian said.



Lillian said no one ever mentioned genetics or how using a different statin dose might help. She thought she just had to grit her teeth and bear it. Periodically, the pain was so bad that she&#8217;d go off her medication, something that can be very risky.



<h2 class="wp-block-heading" id="h-a-simple-change">A Simple Change</h2>



A person&#8217;s genetics — specifically a genetic variant that affects the function of the <a href="https://blog.23andme.com/articles/new-23andme-report-on-simvastatin">SLCO1B1 transporter protein</a>, which in turn affects how a person&#8217;s body processes the statin known as simvastatin — plays a role in side effects like muscle pain in some people. Other non-genetic factors also play a role, but very few people are tested to see if they have a genetic marker that might impact how they process a drug. Lillian didn&#8217;t know anything about what&#8217;s known as <a href="https://blog.23andme.com/articles/23andme-granted-the-first-and-only-fda-authorization-for-direct-to-consumer-pharmacogenetics-reports">pharmacogenetics</a> or how DNA variants influence the body&#8217;s ability to process medication.



&#8220;In the five years of dealing with cholesterol issues, no one tested me for SLC01B1,&#8221; Lillian said.



Although she had been a customer of 23andMe for years, last year, she decided to upgrade to 23andMe+ Premium, which includes pharmacogenetic reports. When she opened the report on SLCO1B1 Drug Transport, specifically looking at the medication insights for simvastatin, it felt personal to her experience.



&#8220;It provided me with critical information to discuss with my doctor,&#8221; Lillian said.



Her doctor lowered her statin dosage, and that small change made a huge difference in her life, allowing her to continue to manage her cholesterol but without the debilitating pain.&nbsp;



&#8220;Now, I wanted to tell you that doing the 23andMe+ membership is the best (money) I spent this year,&#8221; Lillian said. &#8220;I am deeply grateful to 23andMe. You truly made a difference for me by having that test available. I think everyone should know about this.&#8221;&nbsp;



<hr class="wp-block-separator has-alpha-channel-opacity"/>



<h2 class="wp-block-heading" id="h-note">Note:</h2>



*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 to report and interpret information about the processing of certain therapeutics to inform discussions with a healthcare professional. It does not describe if a person will or will not respond to a particular therapeutic and does not describe the association between detected variants and any specific therapeutic. 



Our CYP2C19 Pharmacogenetics report provides certain information about variants associated with metabolism of some therapeutics and provides interpretive drug information regarding the potential effect of citalopram and clopidogrel therapy. Results for SLCO1B1 and 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 Pharmacogenetics reports, visit <a href="http://23andme.com/test-info/pharmacogenetics/">23andme.com/test-info/pharmacogenetics/</a>

Customer Learns Her Genetics Impacts How She Processes Statins

<h5 class="wp-block-heading" id="h-data-initiative-accelerates-access-to-vital-genetic-and-clinical-insights">Data initiative accelerates access to vital genetic and clinical insights</h5>



<figure class="wp-block-image size-large"><img loading="lazy" decoding="async" width="1200" height="675" src="http://35.88.189.111/wp-content/uploads/2025/09/lung-double-edited-2.png" alt="Illustration of lungs on a background with a larger illustration of lungs" class="wp-image-34192" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2.png 1200w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2-300x169.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2-1024x576.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2-768x432.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2-880x495.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/lung-double-edited-2-1180x664.png 1180w" sizes="auto, (max-width: 1200px) 100vw, 1200px" /></figure>



At the 2025 World Conference on Lung Cancer in Barcelona, the 23andMe Research Institute, in collaboration with Troper Wojcicki Philanthropies and the health data software company Lifebit, introduced an open-source platform that could help fast-track research discoveries through a powerful new cancer data repository.



The announcement comes just a year after the start of the<a href="https://www.23andme.com/lung-cancer" target="_blank" rel="noreferrer noopener"> Lung Cancer Genetics Study</a>, spearheaded by 23andMe and bringing together more than 20 lung cancer advocacy and science organizations to recruit 10,000 people diagnosed with lung cancer. Their goal is to develop new ways to identify those at highest risk for lung cancer early, while also finding possible new treatments for this deadly cancer.



<h2 class="wp-block-heading">The Personal Drive Behind the Mission</h2>



The effort is personal for many of the advocates who are part of the collaboration and also for Anne Wojcicki, founder and CEO of the 23andMe Research Institute. Anne&#8217;s sister Susan Wojcicki died of lung cancer last year, just as the study began.



&#8220;My sister was passionate about understanding the science behind lung cancer so future generations could prevent the disease and treat it. The Lung Cancer Genetics Study is a step towards achieving that.” Anne said.



In the months before her death, <a href="https://blog.23andme.com/articles/a-legacy-of-hope-in-the-fight-against-lung-cancer" target="_blank" rel="noreferrer noopener">Susan had been very involved in helping to create the study with the hope that it could help others</a>. The idea was not just to leverage genetic data for insights into lung cancer but also to create a repository of data that would be available to as many qualified researchers as possible.&nbsp;



The platform — created through the collaboration between the 23andMe Research Institute, Troper Wojcicki Philanthropies, and Lifebit — offers a secure, open-source data platform for researchers to access this novel dataset. Powered by Lifebit&#8217;s Health Data Ecosystem, the platform provides qualified researchers with no-cost access to de-identified data from people diagnosed with lung cancer who have consented to participate in this research.&nbsp;



&#8220;More people die of lung cancer each year than breast, colon, and prostate cancer combined, yet it is one of the least funded for research. It’s important for this powerful new tool to be available at no cost to qualified researchers so that the best minds can work on unlocking the genetic insights that may lead to a cure,&#8221; said Anne.



<h2 class="wp-block-heading">Building a One-of-a-Kind Data Resource</h2>



Since launching the <a href="https://blog.23andme.com/articles/23andme-launches-new-genetic-study-of-lung-cancer" target="_blank" rel="noreferrer noopener">Lung Cancer Genetics Study</a>, more than 1,200 people diagnosed with lung cancer have enrolled to participate in the research. The goal is to enroll 10,000 people by 2027, but the study has already assembled one of the most diverse cohorts ever for lung cancer genetic research.&nbsp;



<figure class="wp-block-image alignright size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="464" src="http://35.88.189.111/wp-content/uploads/2025/09/teal_waldos-1024x464.jpg" alt="" class="wp-image-34183" style="width:242px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/teal_waldos-1024x464.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/teal_waldos-300x136.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/teal_waldos-768x348.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/teal_waldos-880x399.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/teal_waldos-1180x534.jpg 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



Genetics is just one of many factors involved in why some people develop lung cancer. Exposure to tobacco smoke is perhaps the best-known risk factor; however, <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC2409903/" target="_blank" rel="noreferrer noopener">80 to 90%</a> of people with a history of tobacco exposure never get lung cancer, and many people without tobacco exposure get the disease. These facts underscore the importance of investigating other, less well-known risk factors, like air pollution, radon exposure, and workplace-related exposures.



And there&#8217;s much more we don&#8217;t know about lung cancer. Many do not realize, for instance, that lung cancer is the <a href="https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2025/2025-cancer-facts-and-figures-acs.pdf" target="_blank" rel="noreferrer noopener">number one cause of cancer death in women</a> and <a href="https://www.massgeneralbrigham.org/en/about/newsroom/articles/most-common-cancers-in-women#:~:text=It%20may%20not%20surprise%20you,in%20women%20and%20people%20AFAB." target="_blank" rel="noreferrer noopener">the second most common cancer in women</a>. Although lung cancer overall is decreasing because of declines in tobacco use, lung cancer among people who have never smoked <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431055/#:~:text=As%20expected%2C%20the%20primary%20factor%20leading%20to,non%2Dsmokers%20has%20been%20noted%20to%20be%20increasing." target="_blank" rel="noreferrer noopener">is stable or increasing</a>, and <a href="https://www.webmd.com/lung-cancer/features/lung-cancer-women-who-never-smoked" target="_blank" rel="noreferrer noopener">two-thirds of people diagnosed with lung cancer with no smoking history are women</a>.&nbsp;



Understanding the genetics of lung cancer may help unravel some of the factors underlying those statistics. Additionally, learning more about the underlying genetics could provide researchers with more insight into the biological mechanisms of the disease, aiding in the development of improved therapies and new diagnostics.&nbsp;



The de-identified data that participants in the Lung Cancer Genetic Study consented to share isn’t limited to just genetics. Many participants also chose to provide self-reported clinical, lifestyle, and even tumor biomarker data. The study will also follow participants over time, gathering important longitudinal data to help researchers understand the progression of cancer as well as the response to treatments.&nbsp;



<h2 class="wp-block-heading">Empowering Researchers</h2>



By opening up access to qualified researchers, the collaborators aim to address significant gaps in current lung cancer research, break down institutional silos, and remove barriers to dataset access, thereby accelerating research progress.&nbsp;



&#8220;We&#8217;re delivering more than a data system — we&#8217;re enabling an entirely new model for research equity and access,&#8221; said Nadia Litterman, PhD, Director of Scientific Affairs and Partnerships at Troper Wojcicki Philanthropies.



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



Anyone who has been diagnosed with lung cancer can learn more and enroll in the study at<a href="http://23andme.com/lung-cancer" target="_blank" rel="noreferrer noopener"> 23andme.com/lung-cancer</a>.



Interested researchers can begin the data access request process by contacting TWP study program manager Caitlin Nichols at <a href="mailto:caitlin@twphilanthropies.org">caitlin@twphilanthropies.org</a>.&nbsp;

Illustration of lungs on a background with a larger illustration of lungs

Powerful New Tool Opens Lung Cancer Data for Research Breakthroughs

Health Huddle LIVE from New Orleans brought together top athletes, medical professionals, and community leaders for powerful conversations on health, genetics, and early detection. Hosted at Dillard University during Super Bowl Week, the event was part of 23andMe’s Community Health Huddle, featuring expert panels and free health screenings. 



Watch the Highlights: 



<figure class="wp-block-embed alignwide is-type-video is-provider-youtube wp-block-embed-youtube wp-embed-aspect-16-9 wp-has-aspect-ratio"><div class="wp-block-embed__wrapper">
<iframe loading="lazy" title="The 23andMe Health Huddle: Live from New Orleans" width="500" height="281" src="https://www.youtube.com/embed/5hOR4o5PkAU?feature=oembed" frameborder="0" allow="accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture; web-share" referrerpolicy="strict-origin-when-cross-origin" allowfullscreen></iframe>
</div></figure>



<h2 class="wp-block-heading" id="h-experts-athletes-amp-actionable-insights">Experts, Athletes &amp; Actionable Insights</h2>



Panelists included Dr. Jen Caldwell, Dr. Joel Bervell, and Dr. Mathew Knowles—a breast cancer survivor and 23andMe Global Brand Ambassador—who shared personal stories and insights on health disparities, preventive medicine, and genetic testing. They were joined by NFL Total Health Ambassadors, highlighting how genetic insights shape performance, recovery, and longevity in sports.



<h2 class="wp-block-heading" id="h-key-takeaways">Key Takeaways</h2>



<ul class="wp-block-list">
<li>Genetic Testing Saves Lives – Understanding your genetic risks enables early detection and prevention, reducing the burden of chronic diseases. </li>



<li>Your Family History is Your Health Roadmap – What runs in your family doesn’t have to define your future, but knowing your risks empowers healthier decisions. </li>



<li>Health Inequities Must Be Addressed – Underserved communities continue to lack access to vital genetic and preventive care. This must change. </li>



<li>Athletes Rely on Science to Perform &amp; Recover – The same genetic insights that help pros optimize their health can help everyone make more informed health choices.</li>
</ul>



<h2 class="wp-block-heading" id="h-beyond-the-event-driving-change">Beyond the Event: Driving Change</h2>



Health Huddle LIVE reinforced a core truth: genetic insights aren’t just about ancestry—they’re a tool for taking control of your health and advocating for better healthcare access. By bringing together medicine, sports, and community leadership, 23andMe continues to lead the movement for health equity and empowerment.



 #HealthHuddleLIVE #GeneticHealth #CommunityWellness

Inside Health Huddle LIVE: Athletes, Experts & Doctors on Longevity, Genetics & Wellness

September is Sickle Cell Awareness Month, which offers us another chance to highlight some of the work 23andMe and its collaborators have done over the years.



Earlier this month, researchers from 23andMe,<a target="_blank" href="https://www.nih.gov/" rel="noreferrer noopener"> the the National Institutes of Health</a>, and <a target="_blank" href="https://www.hopkinsmedicine.org/som/" rel="noreferrer noopener">Johns Hopkins University School of Medicine</a> published new data on the association between sickle cell trait and blood clots. The new findings highlight the importance of this ongoing research and our overall efforts to illuminate this condition.



At 23andMe, knowledge is power, and understanding risks offers people opportunities to mitigate them.&nbsp;



<h2 class="wp-block-heading" id="h-awareness-and-research">Awareness and Research</h2>



But more than that, 23andMe also offers a unique research model that allows individuals to learn about their genetic likelihood of developing a condition and participate in innovative genetic research that could potentially find new treatments.



As part of our <a href="http://www.23andme.com/sickle-cell" target="_blank" rel="noreferrer noopener">Sickle Cell Carrier Status Awareness Program</a>, 23andMe has collaborated with academics and advocacy organizations to increase <a href="https://blog.23andme.com/articles/sickle-cell-awareness-2">understanding of sickle cell</a>. In addition, we’re providing resources for those with sickle cell trait and sickle cell disease. With the help of the<a href="https://www.sicklecellga.org/" target="_blank" rel="noreferrer noopener"> Sickle Cell Foundation of Georgia, Inc. (SCFG)</a>,<a href="https://www.btsscycle.org/" target="_blank" rel="noreferrer noopener"> Breaking the SSickle Cell Cycle</a>,<a href="https://www.sc101.org/" target="_blank" rel="noreferrer noopener"> Sickle Cell 101</a>, and the<a href="https://www.msm.edu/" target="_blank" rel="noreferrer noopener"> Morehouse School of Medicine</a>, we’re working with Black communities to promote awareness. 



We are not alone in this effort. Recently, the NBA, the WNBA, and Wilson Sporting Goods began the #IBall4SickleCell social media campaign to raise awareness. The groups participating in the effort are Breaking the SSickle Cell Cycle, the American Red Cross of Tennessee, and New York Presbyterian’s Dalio Center for Health Justice. Learn more about sickle cell, the campaign, and how to help<a href="https://www.sicklecellball.com/" target="_blank" rel="noreferrer noopener"> here</a>. 



From all this work and research, we have learned much about sickle cell and the people it impacts most. However, much work is still needed to improve people’s understanding of sickle cell.



<h2 class="wp-block-heading" id="h-more-on-sickle-cell-anemia-sickle-cell-trait">More on Sickle Cell Anemia, Sickle Cell Trait</h2>



Although many people have heard of sickle cell, often they do not know the difference between sickle cell trait and sickle cell anemia.



To have sickle cell anemia, one must inherit two copies of the HbS variant in the HBB gene—one copy from each biological parent. Typical signs and symptoms include anemia, pain episodes, and frequent infection.



People with just one copy of the HbS variant are called carriers. They’re also said to have <a target="_blank" href="https://www.cdc.gov/ncbddd/sicklecell/traits.html" rel="noreferrer noopener">sickle cell trait</a>. People with sickle cell trait are not expected to have sickle cell anemia. They typically do not experience any health complications. However, in rare cases, people with the sickle cell trait may experience some health impacts. Current research, including our study, is underway to understand better and spread awareness about the complications someone with SCT may experience.



Importantly, carriers can pass their variant on to their future children. If their partner has the HbS variant or another variant in the HBB gene, there’s a 25 percent chance that each child may have sickle cell anemia or a related blood disorder.&nbsp;&nbsp;



<h2 class="wp-block-heading" id="h-23andme-s-sickle-cell-anemia-carrier-status-report">23andMe’s Sickle Cell Anemia Carrier Status Report**</h2>



23andMe’s<a target="_blank" href="https://www.23andme.com/topics/carrier/sickle-cell-anemia/" rel="noreferrer noopener"> Sickle Cell Anemia Carrier Status Report</a>, which meets FDA requirements for clinical and analytical validity, looks at the HbS variant in the HBB gene linked to sickle cell anemia.



Sickle cell anemia is the most severe form of sickle cell disease. Three hundred million people worldwide and one in 13 Black and African Americans in the United States have sickle cell trait, making them carriers for sickle cell anemia.



In addition to informing people if they have one copy of the HbS variant and are carriers for sickle cell anemia, <a href="https://blog.23andme.com/articles/23andme-updates-carrier-status-report-on-sickle-cell-anemia">23andMe’s report </a>can also tell individuals if they have two copies of the tested variant and if they are at risk of developing symptoms. However, the report does not describe one’s overall risk of developing symptoms. 



Because the HbS variant is more common in certain populations, the Sickle Cell Anemia report is most relevant to people of African, Middle Eastern, and South Asian descent, as well as people from the Caribbean, the Mediterranean, and parts of Central and South America.



23andMe Health + Ancestry Service customers and 23andMe+ Premium members can see their <a target="_blank" href="https://you.23andme.com/reports/carrier.sickle_cell_anemia/" rel="noreferrer noopener">Sickle Cell Anemia report here</a>.&nbsp;



Not yet a customer? Learn more about <a target="_blank" href="https://www.23andme.com/compare-dna-tests/?_gl=1*11ns9j4*_ga*OTk4NDAyMjA3LjE3MTgzODA2MTg.*_ga_G330GF3ZFF*MTcyNTQxNDcyOS4xNjQuMS4xNzI1NDE0Nzk4LjAuMC4w" rel="noreferrer noopener">all that 23andMe offers here</a>.



<hr class="wp-block-separator has-alpha-channel-opacity"/>



<h2 class="wp-block-heading" id="h-note">Note:</h2>



**The 23andMe PGS test uses qualitative genotyping to detect select clinically relevant variants in the genomic DNA of adults to report carrier status and reporting and interpreting genetic health risks. The relevance of each report may vary based on ethnicity. Our carrier status reports can be used to determine carrier status but cannot determine if you have two copies of any genetic variant. These carrier reports are not intended to tell you anything about your risk for developing a disease in the future, the health of your fetus, or your newborn child’s risk of developing a particular disease later in life. We provide a single report for certain conditions that includes information on carrier status and genetic health risk. For important information and limitations regarding other genetic health risk reports and carrier status reports, click <a target="_blank" href="https://www.23andme.com/test-info/" rel="noreferrer noopener">here</a>.

An illustration for 23andMe's Sickle Cell Carrier Statues Awareness Program.

Learn More About Our Research and Collaborations During Sickle Cell Awareness Month

Editor&#8217;s note 7/8/2024: This post has been updated since 2020. In addition, We do not support uploading DNA data obtained from other testing services to 23andMe. This article explains the risks of uploading your DNA data to third party services.
With all of <a class="waffle-rich-text-link" href="https://www.23andme.com/compare-dna-tests/">23andMe&#8217;s services</a>, you’re in charge of your genetic data. That means we let you decide what information you want to learn and what information you want to share. However, you need to be informed about the risks of sharing your genetic data with other services. This includes understanding the implications if you decide to upload DNA to 23andMe or any third-party service.
After receiving <a class="waffle-rich-text-link" href="https://www.23andme.com/dna-reports-list/">personalized genetic reports</a> from 23andMe, customers can choose to download their raw DNA data. Some customers may do this to upload their data to third-party services, which offer to interpret their raw DNA data to find new genetic relatives or get additional genetic reports. However, 23andMe cannot vouch for the scientific validity or accuracy, or clarity in communication of results of any such third-party services. In fact, only 23andMe offers a consumer genetic test with health reports that have FDA&#8217;s independent assurance of validity and clear results (without requiring a prescription).
Beyond concerns about scientific validity, uploading your raw DNA data to a third-party service can also put <a href="https://www.23andme.com/privacy/">your data privacy</a> at risk. In part, this is why 23andMe provides important warnings to its customers before they choose to download.
<h2>What are some of the risks of uploading your DNA data to a third-party website? </h2>
<div id="attachment_27862" style="width: 310px" class="wp-caption alignright"><a href="https://blog.23andme.com/articles/how-to-be-careful-with-your-raw-dna-data/what-is-dna-upload" rel="attachment wp-att-27862"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-27862" class="size-medium wp-image-27862" src="http://35.88.189.111/wp-content/uploads/2020/01/What-is-DNA-Upload-300x128.jpg" alt="An illustration of the steps for downloading data." width="300" height="128" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/01/What-is-DNA-Upload-300x128.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/01/What-is-DNA-Upload.jpg 512w" sizes="auto, (max-width: 300px) 100vw, 300px" /></a>Most consumer genetics companies, including 23andMe, allow you to download your own raw DNA data. At that point, the customer is free to do what they like with their raw DNA data, such as deciding to upload that raw DNA data to third-party services.</div>
At 23andMe, we’re clear with our users about the risks of using third-party services that provide additional health, wellness or trait insights. This is because only select genotype data used specifically in our Health reports have been individually validated for accuracy. While the rest of your data has undergone a general quality review, it has not been validated to the extent of the data underlying our official 23andMe reports. As a result, raw DNA data should not be used for medical purposes and we do not recommend the use of third-party services that claim to interpret raw DNA data to provide health information.
Consumers also cite concerns about law enforcement uploading crime-scene DNA data to third-party services to crack a cold case. Simply put, uploading crime-scene DNA data into the 23andMe environment is not possible because we do not support the upload of DNA data that has been processed by a third-party laboratory.
Further, 23andMe’s <a href="https://www.23andme.com/transparency-report/">Transparency Report</a> details our policy against releasing customer’s individual DNA data to any third party &#8211; including law enforcement &#8211; without receiving the customer’s explicit consent, unless required by law.
However, this concern about law enforcement upload of crime scene DNA data is a real one that we warn customers about should they choose to upload their DNA data to other third party platforms, including public genealogy services or other third party services that facilitate DNA data upload.
But there’s another form of vulnerability that’s less well-understood: Within databases that allow for raw DNA data uploads with access to relative matching features, people with malicious intent can upload real or fake “<a href="https://en.wikipedia.org/wiki/Trojan_horse_(computing)">Trojan Horse</a>” genetic profiles for access to your personal identifying information. They could even infer your specific DNA variants—such as information about any disease risk variants you might carry. This is one reason why we don&#8217;t support uploading DNA to 23andMe.
<h2>How can that happen?</h2>
<ul>
<li>Many relative-matching services allow you to see the exact section or sections of DNA you share with each relative.*</li>
<li>If uploading DNA data is allowed, it means you no longer know for sure that your relative’s profile is actually controlled by your relative, and a malicious actor could upload real or fake DNA data to deduce information about you based on sections of matching DNA, including any disease risk variants you might have.</li>
<li>Even if shared segments aren’t shown, there are still ways that people with malicious intent can deduce some of your DNA variants.</li>
</ul>
<img loading="lazy" decoding="async" class="size-medium wp-image-27863 alignright" src="https://blog-api.23andme.com/wp-content/uploads/2020/01/How-Uploading-Creates-Risk-300x202.jpg" alt="" width="300" height="202" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/01/How-Uploading-Creates-Risk-300x202.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/01/How-Uploading-Creates-Risk.jpg 512w" sizes="auto, (max-width: 300px) 100vw, 300px" />
This vulnerability was recently described in two reports: one at the University of Washington and another at the University of California, Davis. The authors of these reports explain several ways an “adversary” can deduce people&#8217;s genotypes “either at key positions or at many sites genome-wide” in databases that allow DNA data uploads with relative matching. This highlights the risks associated with uploading DNA to 23andMe or similar services.
Both reports outline specific ways for services to mitigate risk, such as limiting the information displayed in relative-matching features.
While these practices may reduce risk, we believe the simplest and most effective defense is to not allow individuals genotyped through other testing services to upload their DNA data to 23andMe for the purpose of discovering genetic relatives.
In the past, 23andMe has allowed DNA uploads from other consumer genetic testing services in very specific circumstances. Specifically, on DNA Day in April 2018, 23andMe allowed individuals who tested at other companies to upload their results to access a subset of our trait reports, but 23andMe has not enabled the discovery of new relatives for these accounts.
<h2>How does 23andMe ensure that only real, consenting individuals participate in our service? </h2>
In a word, spit.
When you spit into the tube, you’re embarking on the adventure of a lifetime. You’re also trusting 23andMe with some of your most personal information.
Requiring a saliva sample is how 23andMe is able to verify that you’re a real person who chose to participate in the service. While it might be easy to upload fake DNA data, it’s another matter entirely to fake a spit sample, which requires filling a tube with more than two milliliters of spit. It’s how you know that “Linda-your-4th-cousin-who-you-didn’t-know-existed” is a real person who chose to do 23andMe. Linda had to spit in a tube, too.
<h2>What are some key questions you should ask?</h2>
When considering whether or not to upload your raw DNA data to another website, we encourage you to familiarize yourself with their privacy and security policies before you upload your raw DNA data.
Make sure to consider the following questions:
<ol>
<li>Before you upload your DNA data, ask yourself: do I really need to do this? Am I willing to risk the security and privacy of my DNA data by uploading it to a third-party service?</li>
<li>Do your research! Does the third-party service have a track record of strong privacy and data security?</li>
<li>How will the third-party service use your information?  How can your information be further shared with other third parties?</li>
<li>If you are not interested in discovering new relatives but you want additional DNA insights, does the other service explicitly exclude features relating to discovering genetic relatives?</li>
</ol>
An earlier article detailing our stance on protecting customers’ data is available <a href="https://blog.23andme.com/news/our-stance-on-protecting-customers-data/">here</a>. 
<h2>Learn More</h2>
Find out if your <a href="https://www.23andme.com/test-info/genetic-health/">genetics</a> might Increase your risk for any health conditions with 23andMe.
You can also Learn more about common risks associated with uploading raw DNA online and how to protect your DNA information.
*By default, 23andMe does not display your ancestry information or DNA segment information to relatives or connections until you decide to share it with them.

Can You Upload DNA Data to 23andMe? 

<h5 class="wp-block-heading" id="h-fda-now-recommends-genetic-testing-before-prescribing-specific-chemotherapy-medications">FDA Now Recommends Genetic Testing Before Prescribing Specific Chemotherapy Medications</h5>



For years, patient advocates have been calling for stronger safeguards against preventable toxicity from chemotherapy. Last week, the FDA took a major step forward, updating the label for a drug called <a href="https://medlineplus.gov/druginfo/meds/a699003.html" target="_blank" rel="noreferrer noopener">capecitabine</a> to explicitly recommend testing for variants in the DPYD gene before starting treatment. This is more than just a label change—it&#8217;s a long-awaited acknowledgment that genetics matter when it comes to patient safety.



<h2 class="wp-block-heading">What is DPYD?</h2>



The <a href="https://medlineplus.gov/genetics/gene/dpyd/" target="_blank" rel="noreferrer noopener">DPYD gene</a> provides instructions for making an enzyme called DPD (dihydropyrimidine dehydrogenase), which helps the body break down certain chemotherapy drugs like capecitabine and <a href="https://medlineplus.gov/druginfo/meds/a682708.html" target="_blank" rel="noreferrer noopener">5-fluorouracil</a>. These medications are commonly used to treat breast, colorectal, and other cancers. People with certain changes in this gene may not process these drugs properly, causing the drugs to build up in the body and, in some cases, leading to severe or even life-threatening <a href="https://medlineplus.gov/genetics/condition/dihydropyrimidine-dehydrogenase-deficiency/" target="_blank" rel="noreferrer noopener">reactions</a>.



<figure class="wp-block-image alignleft size-full is-resized"><img loading="lazy" decoding="async" width="508" height="531" src="http://35.88.189.111/wp-content/uploads/2025/10/drug-bottle.png" alt="" class="wp-image-34304" style="width:126px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/drug-bottle.png 508w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/drug-bottle-287x300.png 287w" sizes="auto, (max-width: 508px) 100vw, 508px" /></figure>



These reactions can include painful mouth sores, severe diarrhea, low white blood cell counts, and nerve problems. <a href="https://medlineplus.gov/genetics/condition/dihydropyrimidine-dehydrogenase-deficiency/#frequency" target="_blank" rel="noreferrer noopener">Up to 8%</a> of people have a variant in the DPYD gene that affects how well they process these medications. Sadly, some patients with DPYD variants have died after receiving these drugs. Such experiences have fueled years of advocacy calling for genetic testing before treatment, not after. 



<h2 class="wp-block-heading" id="h-a-change-in-the-recommendations">A change in the recommendations</h2>



Until now, the FDA advised doctors they could &#8220;consider testing&#8221; patients before giving capecitabine or similar drugs. The <a href="https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/020896s052lbl.pdf" target="_blank" rel="noreferrer noopener">new label</a> goes much further, adding a warning that says, &#8220;serious adverse reactions or death may occur in patients with complete DPD deficiency&#8221; and telling doctors to test for DPYD variants before prescribing the medication. (Experts predict a similar change to the 5-fluorouracil drug label soon.) It&#8217;s a major win for patient safety and for the <a href="https://test4dpd.org/" target="_blank" rel="noreferrer noopener">advocacy groups</a> who have pushed tirelessly for this change. Organizations that have long advocated for universal DPYD testing hope this update will encourage hospitals and cancer centers across the U.S. to make pretreatment genetic testing standard care.



<figure class="wp-block-image alignright size-large is-resized"><img loading="lazy" decoding="async" width="790" height="1024" src="http://35.88.189.111/wp-content/uploads/2020/09/PGt-Home-790x1024.png" alt="23andMe mobile pharmacogenomics" class="wp-image-28527" style="width:256px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home-790x1024.png 790w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home-231x300.png 231w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home-768x996.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home-679x880.png 679w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home-910x1180.png 910w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2020/09/PGt-Home.png 1583w" sizes="auto, (max-width: 790px) 100vw, 790px" /></figure>



We share the belief that genetic insights can empower individuals and help improve outcomes. The 23andMe® <a href="https://www.23andme.com/topics/pharmacogenetics/dpyd/" target="_blank" rel="noreferrer noopener">DPYD Drug Metabolism Pharmacogenetics report</a>*, available to <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members, provides information about two variants associated with reduced DPD enzyme activity. While this report isn&#8217;t a substitute for clinical testing, it can help people learn whether they carry certain DPYD variants and start a conversation with their healthcare provider. 



The FDA&#8217;s new label is an important step toward safer, more personalized cancer treatment and a long-awaited victory for the patients and advocates who made their voices heard.



<hr class="wp-block-separator has-alpha-channel-opacity"/>



 * 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 <a href="http://23andme.com/test-info/pharmacogenetics/" target="_blank" rel="noreferrer noopener">23andme.com/test-info/pharmacogenetics/</a>

A Big Step Forward for Patient Safety

Every year on the third Saturday in October, the world celebrates International Archaeology Day, recognizing the important contributions archaeological research makes to society. This year, to celebrate, we&#8217;re spotlighting one of our favorite archaeological mysteries in the <a href="https://blog.23andme.com/articles/23andmes-historic-matches" target="_blank" rel="noreferrer noopener">Historical Matches</a>SM feature—the skeletons of Roopkund Lake.



<h2 class="wp-block-heading" id="h-about-roopkund-lake">About Roopkund Lake</h2>



Roopkund Lake is a small glacial lake located over 5,000 meters (over 16,000 ft) above sea level in the Nanda Devi National Park, in the Indian Himalayas. In 1942, a forest ranger patrolling the park stumbled upon a chilling scene: hundreds of skeletal remains strewn around the lake. The site has captivated researchers and locals alike ever since.



The mystery of who these individuals were, how they died, and why they were in such a remote and inhospitable location has sparked decades of speculation. Some early researchers proposed that the remains belonged to an army that had lost its way in the mountains, while others suggested they might have been traders following a trans-Himalayan route that had since vanished. A few archaeologists posited that they were pilgrims traveling to nearby shrines, possibly part of the ancient Nanda Devi Raj Jat, a religious procession spanning ~290 kilometers (~180 miles) that is still undertaken in the region every 12 years.



The identification of women and children among the dead, however, made some of the proposed explanations less plausible–especially the claim that they may have been members of an army. Without weapons, trade goods, or written records, no single theory could fully account for the diversity and composition of the group. Local folklore offered its own interpretation: a king, his family, and attendants on a pilgrimage to honor the mountain goddess Nanda Devi had violated sacred protocol and were struck down by a deadly hailstorm in divine retribution.



<h2 class="wp-block-heading" id="h-an-exciting-23andme-connection">An exciting 23andMe connection</h2>



<a href="https://pubmed.ncbi.nlm.nih.gov/31431628/" target="_blank" rel="noreferrer noopener">In 2019</a>, scientists sequenced the genomes of 38 individuals from Roopkund Lake in an effort to better understand the origins of the mysterious remains. But instead of resolving this longstanding mystery, their findings uncovered an even more complex puzzle. 



So what makes this story one of 23andMe’s favorite archaeological mysteries? That 2019 research study was actually led by our very own Dr. Éadaoin Harney—a Scientist on the Population Genetics R&amp;D Team and 23andMe’s “resident ancient DNA expert.” She worked on this study during her PhD at Harvard University where she was a member of Prof. David Reich’s ancient DNA laboratories–one of the largest ancient DNA research laboratories in the world.



“When I first started working with the Roopkund ancient DNA data, I thought that genetics would be a simple and straightforward way to finally help solve the mystery of who they were,” said Dr. Harney. But she was in for a big surprise! “The first hint that this wasn’t going to be as simple as I initially thought was when we discovered how ancestrally diverse the Roopkund individuals were. Then we learned that they didn’t all die at the same time, as had previously been believed. Instead radiocarbon dates generated from the bones spanned over 1,000 years.”



<h2 class="wp-block-heading" id="h-how-dna-adds-to-the-mystery">How DNA adds to the mystery</h2>



The 2019 genetic analysis showed that the individuals fell into three distinct genetic groups, with ancestries from across the globe.



The largest group (which we’ll refer to as Roopkund A) consisted of 23 individuals who died between the 7th and 10th centuries CE, likely during multiple distinct events. Genetically, all appeared South Asian, but with remarkably diverse ancestries–each individual appeared most closely related to different present-day South Asian populations. This finding suggests that they may have traveled to the lake from multiple locations across the subcontinent. Although the exact purpose of their journey to Roopkund Lake remains uncertain, some researchers speculate that they may have been early participants in the Nanda Devi Raj Jat, a traditional pilgrimage that still passes by the lake every 12 years.



The other two groups were even more surprising. One group (Roopkund B) consisted of 14 individuals whose DNA connected them to present-day populations from the eastern Mediterranean—particularly populations in Greece and neighboring regions. The third group (Roopkund C) was represented by a single individual with genetic ancestry most similar to Southeast Asian populations. Radiocarbon dating revealed that these individuals likely died in a single event some time between the 17th and 20th centuries. Why people with ancestry from such distant regions were traveling together in one of the most remote parts of the Himalayas remains a mystery to this day.



Dr. Harney joined 23andMe in 2020 with the goal of creating an approach to identify direct genetic connections between historical and living people. She and her colleagues on the Population Genetics R&amp;D Team succeeded! This technology was first described in their <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC10958645/" target="_blank" rel="noreferrer noopener">2023 study of African Americans from Catoctin Furnace</a>, which was published in (and featured on the cover of) Science. She then helped spearhead the creation of the 23andMe Historical Matches feature, enabling customers to learn how they connect to different historical and ancient individuals.



Over the last five years, one of her secret ambitions was to use this technology to try and finally solve the mystery of the Roopkund individuals&#8217; identities. Could identifying any close genetic relatives of the Roopkund individuals in the 23andMe genetic database help us learn about their identities and answer what brought them to Roopkund?



<h2 class="wp-block-heading" id="h-did-we-solve-the-mystery">Did we solve the mystery?</h2>



We compared the Roopkund individuals to over 11 million research consenting participants in the 23andMe genetic database. While we were hoping this analysis would reveal a number of close genetic relatives, unfortunately, the mystery of Roopkund Lake lives on.



We found that only about 1,240 research participants—less than 0.011% of the individuals included in our analysis—share any sort of genetic connection to the Roopkund individuals. And of those participants, we can count the number of individuals who share over 30 cM of DNA (what we label a “significant genetic connection” in the Historical Matches feature) on just one hand. In fact, we found so few &#8220;significant relatives” that the chances any of those connections trace back to a recent shared common ancestor on a genealogical family tree are extremely slim.



(Although if you happen to be one of those lucky individuals who sees a “significant connection” listed to one of the Roopkund individuals in your 23andMe report, please <a href="https://customercare.23andme.com/hc/en-us/requests/new" target="_blank" rel="noreferrer noopener">reach out to us</a>, as we’d love to learn more!)



<h2 class="wp-block-heading" id="h-what-else-did-we-discover">What else did we discover?</h2>



So, we didn’t solve the mystery of who the Roopkund individuals were, but we did gather fascinating data about their connections to the present day.



First, here is a breakdown of the 17 Roopkund individuals whose DNA was well preserved enough to include in our analyses:



<ul class="wp-block-list">
<li>8 from Roopkund A (South Asian ancestry)</li>



<li>8 from Roopkund B (Eastern Mediterranean ancestry)</li>



<li>1 from Roopkund C (Southeast Asian ancestry)</li>
</ul>



As we mentioned, about 1,240 23andMe research participants shared a genetic connection to the Roopkund individuals. The figure below shows the number of matches each Roopkund group received and highlights the amount of DNA shared. As you can see, the vast majority of the connections we discovered involve less than 20 cM of DNA, meaning that they likely trace back to a shared common ancestor who lived long before any of the Roopkund individuals.



<figure class="wp-block-image size-full is-resized"><img loading="lazy" decoding="async" width="411" height="252" src="http://35.88.189.111/wp-content/uploads/2025/10/image-3.png" alt="" class="wp-image-34359" style="width:625px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/image-3.png 411w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/image-3-300x184.png 300w" sizes="auto, (max-width: 411px) 100vw, 411px" /><figcaption class="wp-element-caption">This figure shows the distribution of total shared DNA that we detected between 23andMe research participants and each of the Roopkund groups (A, B and C). It shows that the vast majority of the connections we identified are to individuals in the Roopkund B group, and the DNA segments they share are shorter than 15 cM. In order to protect participant privacy, all counts less than or equal to 5 are masked and appear equal to 5. </figcaption></figure>



Of those who share a genetic connection, the majority (~1,160) shared a connection to one or more individuals in the Roopkund B group—the one with Eastern Mediterranean-related ancestry. This didn&#8217;t surprise us, since the majority of 23andMe research participants have European ancestry, making them more likely to be related to the Roopkund B individuals.



In addition to occurring more frequently, the Roopkund B individuals also shared some of the strongest genetic connections to 23andMe research participants, as shown in the figure below which depicts the maximum amount of DNA that each Roopkund individual shared with a research participant.



<figure class="wp-block-image size-full"><img loading="lazy" decoding="async" width="643" height="448" src="http://35.88.189.111/wp-content/uploads/2025/10/image-4.png" alt="" class="wp-image-34360" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/image-4.png 643w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/image-4-300x209.png 300w" sizes="auto, (max-width: 643px) 100vw, 643px" /><figcaption class="wp-element-caption">This figure shows the maximum amount of shared DNA that we detected between 23andMe research participants and each of the Roopkund individuals. The individuals are arranged along the x-axis by when they lived, as measured by radiocarbon dating. We masked this result for Roopkund individuals who shared DNA with 5 or fewer 23andMe research participants in order to protect participant privacy, and reported maximum DNA sharing as equal to 0.</figcaption></figure>



We decided to see what Genetic Groups the Roopkund individuals could be connected to, using the same approach that we use to connect customers to these Genetic Groups.&nbsp;&nbsp;&nbsp;



Many of the Roopkund B individuals received matches to Genetic Groups in south eastern Europe, with the strongest connections to groups in Greece and Crete–exactly mirroring the findings of the original study!



<figure class="wp-block-image size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="849" src="http://35.88.189.111/wp-content/uploads/2025/10/roopkund_b_2-1024x849.png" alt="" class="wp-image-34352" style="width:575px" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_b_2-1024x849.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_b_2-300x249.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_b_2-768x636.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_b_2-880x729.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_b_2-1180x978.png 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /><figcaption class="wp-element-caption">This map shows the location of the different Genetic Groups that we compared the Roopkund B individuals to. Groups shown in darker colors shared the strongest genetic matches to one or more of the Roopkund B individuals.</figcaption></figure>



Since the Roopkund A and Roopkund C individuals shared far fewer genetic connections to 23andMe research participants, it was hard to localize their ancestry in the same way. But we were able to connect the Roopkund C individual to a single Genetic Group, located in China. This finding is generally consistent with the original study, where this individual exhibited connections to populations in East and Southeast Asia.&nbsp;



<figure class="wp-block-image size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="874" src="http://35.88.189.111/wp-content/uploads/2025/10/roopkund_c_2-1024x874.png" alt="" class="wp-image-34353" style="width:592px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_c_2-1024x874.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_c_2-300x256.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_c_2-768x655.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_c_2-880x751.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/roopkund_c_2-1180x1007.png 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /><figcaption class="wp-element-caption">This map shows the location of the different Genetic Groups that we compared the Roopkund C individual to. Groups shown in darker colors shared the strongest genetic matches to the Roopkund C individual.</figcaption></figure>



We couldn’t connect the Roopkund A individuals to any of the Genetic Groups that we have identified. That doesn’t mean they aren’t genetically related to any of these groups. Instead it is likely just because the original research team was only able to sequence a small amount of DNA from these individuals, making it harder to connect them to research participants in the 23andMe database.&nbsp;



<h2 class="wp-block-heading" id="h-what-s-next">What’s Next?</h2>



So for now, all we can say is that the mystery of Roopkund Lake continues. But we promise this archaeological site is one that is close to our hearts. If we have any updates in the future, we’ll be sure to let you know.



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



Want to see if you share a genetic connection with any of the individuals who died at Roopkund Lake—or hundreds of other historical people? The Historical Matches feature is available to <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members.



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 <a href="https://www.archaeological.org/events/category/international-archaeology-day/list/" target="_blank" rel="noreferrer noopener">calendar of Archaeology-related events</a>.

New Historical Matches Could Connect You to the Mysterious Skeletons of Roopkund Lake

Late in the first quarter in only his third game this season, one professional football team’s star edge-rusher limped off the field, gesturing to his trainers with his thumb down. Apparently, he already knew what he&#8217;d find out a short time later with an MRI: he&#8217;d again torn his ACL, the anterior cruciate ligament.



While a hard tackle or awkward fall can tear an ACL, some people may be more prone to an ACL tear than others, and their genetics may explain why.



A new 23andMe polygenic risk score (PRS) report sheds light on that genetic connection. The report examines how a person&#8217;s genetics may impact their likelihood of experiencing an ACL tear, an injury particularly common among those involved in high-impact sports.



<h2 class="wp-block-heading" id="h-how-genetics-may-influence-acl-tear-risk">How Genetics May Influence ACL Tear Risk</h2>



First, it&#8217;s important to note that your genetics is only one part of the story – many other factors can influence the risk of an ACL tear. 



<figure class="wp-block-image alignright size-full"><img loading="lazy" decoding="async" width="306" height="126" src="http://35.88.189.111/wp-content/uploads/2025/10/ACL-tear-PRS-Hero.png" alt="" class="wp-image-34316" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/ACL-tear-PRS-Hero.png 306w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/10/ACL-tear-PRS-Hero-300x124.png 300w" sizes="auto, (max-width: 306px) 100vw, 306px" /></figure>



Tears typically occur when the knee twists or extends beyond its normal range, often seen in sports that involve jumping and sudden stops, pivots, or changes in direction. That might be in sports such as football, soccer, basketball, or downhill skiing. The ACL is the most commonly injured ligament in the knee.&nbsp;&nbsp;



We also know that ACL tears are more common in female athletes. However, because more males participate in high-risk sports, the total number of ACL tears may actually be higher in males. They are also more likely in people with a family history of an ACL injury or a personal history of an ACL tear. Indeed, genetics plays an important role, with one 2020 sports medicine journal study estimating the <a href="https://bjsm.bmj.com/content/55/7/385" target="_blank" rel="noreferrer noopener">genetic contribution to an ACL tear at approximately 69 percent</a>. 



While the exact biological mechanism involved is not yet known, the genetic associations do offer some hints. Among the many genetic variants associated with ACL tears are variants in or near genes involved in the formation of collagen, a building block for ligaments. Scientists have discovered other variants linked to tears, but most of those associations are inconclusive, and more research is needed.&nbsp;



<h2 class="wp-block-heading" id="h-23andme-s-new-acl-tear-prs-report">23andMe&#8217;s New ACL Tear PRS Report</h2>



Knowing how genetics influences the risk for an ACL tear can empower athletes, who are at the highest risk, train smarter and work toward preventing them.&nbsp;



To create the new ACL Tear PRS Report* 23andMe scientists analyzed data from people who consented to participate in research to identify thousands of variants associated with ACL tears. The 23andMe scientists then created a genetic model that incorporated those variants to calculate the genetic likelihood of an ACL tear.



This PRS report, like other 23andMe PRS reports, is research-based and not validated for medical diagnostic use; it may have limitations for people with mixed or less-studied ancestries and does not account for every possible factor influencing ACL health. In addition, polygenic risk scores integrate many common variants, but they do not account for rare genetic variants or lifestyle factors that can heavily impact risk.&nbsp;



For individuals with an elevated genetic or family risk, creating a personalized prevention plan and scheduling regular check-ins with sports medicine professionals are great ways to keep knees healthy.&nbsp;



<h2 class="wp-block-heading" id="h-mitigating-the-risk-of-acl-tears">Mitigating the Risk of ACL Tears</h2>



Whether you’re a pro athlete or not, and especially if you’ve already had an ACL tear before, proper training and technique&nbsp; are simple ways to help lower the likelihood of injury.



Here are a few things you can do to help lower the risk of an ACL tear:



<ul class="wp-block-list">
<li>Build muscle strength in the hamstrings, and core to stabilize the knee.</li>



<li>Maintain proper technique for movements such as jumping, pivoting, and squatting — like landing on the balls of your feet with knees bent and keeping knees aligned over your toes.</li>



<li>Warm up and cool down before and after physical activity to increase flexibility.</li>



<li>Wear supportive, activity-appropriate footwear for correct alignment.</li>



<li>Consulting with physical therapists or trainers for form and strength assessments can further reduce the risk, regardless of one&#8217;s genetic background.</li>
</ul>



We continue to learn about the role genetics plays in sports-related injuries, including ACL tears, but genetics is just one factor.&nbsp;



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



<a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members can view this report with their other Wellness reports.



<a href="https://you.23andme.com/" target="_blank" rel="noreferrer noopener">Sign in</a> to learn more about what 23andMe&#8217;s ACL Tear PRS can tell you. 



* The 23andMe ACL Tear PRS report is based on a genetic model that includes data and insights from 23andMe consented research participants and incorporates more than 6,000 genetic variants to provide information on the likelihood of experiencing an ACL tear. 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 ACL Tear 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.

Genetics May Explain Why Some Athletes Are More Prone to ACL Tears

<div class="wp-block-group is-nowrap is-layout-flex wp-container-core-group-is-layout-6c531013 wp-block-group-is-layout-flex">
This October, for Breast Cancer Awareness Month, we will be sharing some of the latest research on this important topic.
</div>



What if the same genetic factors that put you at higher risk for developing cancer could potentially increase the chances you&#8217;d survive longer if you do get cancer? This counterintuitive possibility is exactly what researchers discovered in a groundbreaking collaboration between the 23andMe Research Institute and the Dana-Farber Cancer Institute.



<h2 class="wp-block-heading" id="h-understanding-cancer-risk-and-polygenic-scores">Understanding cancer risk and polygenic scores</h2>



Like most common diseases, cancer is multifactorial – it&#8217;s caused by a combination of genetic factors and non-genetic factors like environmental exposures and lifestyle. Polygenic risk scores are tools that can estimate an individual&#8217;s inherited genetic risk of developing many common conditions, such as cancers.&nbsp;



A <a href="https://pubmed.ncbi.nlm.nih.gov/40877800/" target="_blank" rel="noreferrer noopener">recent study</a> conducted at the Dana-Farber Cancer Institute investigated whether  polygenic risk scores may be associated not just with risk of disease, but with clinical outcomes. The study analyzed nearly 24,000 cancer patients to ask whether having a high <a href="https://blog.23andme.com/articles/three-new-prs-cancer-reports" target="_blank" rel="noreferrer noopener">polygenic risk score, predicting a high likelihood of cancer</a>, also could tell you anything about the prognosis for a person who does go on to develop cancer.



In collaboration with 23andMe, researchers looked at polygenic risk scores for more than 200 diseases to see if any could also predict the prognosis of six common cancer types: non-small cell lung cancer, colorectal cancer, breast carcinoma, glioma, ovarian cancer, and prostate cancer.&nbsp;



<h2 class="wp-block-heading" id="h-an-unexpected-finding">An unexpected finding</h2>



Surprisingly, they found that among breast cancer patients, those with high polygenic risk scores for breast cancer actually showed longer average survival times than those with low scores. This finding held up even when accounting for other factors like a patient&#8217;s age, treatment, or different kinds of tumors.



Why might this be the case?&nbsp;



Cancer-causing genetic changes come in two types: those you&#8217;re born with (germline mutations) that appear in every cell, and those that develop over time in specific tissues (somatic mutations) due to factors like smoking or aging. Polygenic risk scores measure only germline mutations.



The researcher&#8217;s results raise the possibility that tumors driven more by germline mutations — and corresponding high polygenic risk scores — may tend to be less aggressive compared to tumors that are more driven by somatic mutations.&nbsp;



<h2 class="wp-block-heading" id="h-what-comes-next">What comes next</h2>



While these results are statistically robust, they&#8217;ll need to be confirmed in other studies before changing how doctors might treat cancer patients. With additional investigation, these findings could eventually help doctors provide more personalized prognoses and potentially identify patients who might benefit from different treatment approaches based on their genetic risk profiles.

Study Reveals an Unexpected Link Between Genetic Cancer Risk Scores and Survival

This update is currently available to all eligible customers on the latest, V5, genotyping chip. 



The 23andMe Ancestry Team has been working hard on <a href="https://blog.23andme.com/articles/a-major-update-to-ancestry-composition-is-coming-soon" target="_blank" rel="noreferrer noopener">a major update to the Ancestry Composition report</a>, and results are now available! Our goal is to provide the most accurate and meaningful genetic ancestry results in the industry. We ground our models in rigorous science, guided by established population genetics research, to ensure your results are consistent, reliable, and can help guide your personal journey of discovery.



<h2 class="wp-block-heading" id="h-what-changes-you-ll-see">What changes you&#8217;ll see</h2>



<ul class="wp-block-list">
<li>New granularity in your ancestry percentages: 33 new populations in Europe and 6 in the Americas to explore. Plus we&#8217;ve updated our algorithm to eliminate “Broadly” and “Unassigned” categories in the default results view.&nbsp;</li>



<li>More accurate results: A new state-of-the-art DNA phasing pipeline reduces errors and gives a more accurate estimate of your percentages, even if your ancestry isn&#8217;t from Europe or the Americas.&nbsp;</li>



<li>New features: A new “Version History” section lets you compare your new results to your previous result, and <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members can also access all previous versions of their results at different confidence thresholds.</li>
</ul>



This update powers your Ancestry Composition, Ancestry Timeline, Parental Inheritance, DNA Painting, and more.



<h2 class="wp-block-heading" id="h-our-focus-for-this-update">Our focus for this update</h2>



For this update we focused on improving the entire Ancestry Composition pipeline integrating the latest research. Throughout the rounds of development we look at two major metrics: precision and recall. Precision lets us know how often we correctly predict that a piece of DNA is from a specific population. Recall tells us how much DNA from a specific population we can correctly identify. Working to maximize both precision and recall is critical to making Ancestry Composition and other ancestry features as accurate as possible.



<figure class="wp-block-image alignleft size-full is-resized"><img loading="lazy" decoding="async" width="366" height="368" src="http://35.88.189.111/wp-content/uploads/2025/09/AC78_wheel.png" alt="" class="wp-image-34276" style="width:170px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/AC78_wheel.png 366w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/AC78_wheel-298x300.png 298w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/AC78_wheel-150x150.png 150w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/AC78_wheel-271x271.png 271w" sizes="auto, (max-width: 366px) 100vw, 366px" /></figure>



The final models in this update had good precision and recall across the new populations, ensuring the accuracy of the ancestry breakdown predictions while also expanding the specificity and granularity of the populations. One example of the improvements gained by this update is the reduced amount of North Asian ancestry predicted for some Indigenous North American customers. You can learn more about the development process and see precision and recall metrics for each population in the <a href="https://www.23andme.com/ancestry-composition-guide/" target="_blank" rel="noreferrer noopener">Ancestry Composition Guide</a>.



While this update focused on increasing granularity in Europe and the Americas, customers from other parts of the world will still benefit thanks to the improvements to the science and the removal of broadly and unassigned ancestry.



<a href="https://you.23andme.com/" target="_blank" rel="noreferrer noopener">Sign in</a> and check out your new results.&nbsp;



Not yet a 23andMe member? Learn more about what <a href="https://www.23andme.com/compare-dna-tests/" target="_blank" rel="noreferrer noopener">23andMe has to offer</a>.



<h2 class="wp-block-heading" id="h-some-questions-you-might-be-wondering-about">Some questions you might be wondering about</h2>



Why are certain populations combined?



To define the 78 Ancestry Composition populations, we analyzed the reference datasets, chose candidate populations that appeared to cluster together, and then evaluated whether we can distinguish those groups in practice. Some populations tend to cluster on their own, but most country-level populations overlap to some degree. In these cases, we experiment with different groupings of country-level populations to find combinations that we can distinguish with high confidence. Check out the <a href="https://www.23andme.com/ancestry-composition-guide/" target="_blank" rel="noreferrer noopener">Ancestry Composition Guide</a> to learn more.



Does this mean that the people in those groups are the same? No. Each group has its own history, culture, and often different languages. These groupings are a reflection of our current genetic understanding and scientific methods, not a statement about cultural identity.



Does this mean DNA that is assigned to these populations is from all groups? Not necessarily. For example, DNA assigned to the Belarusian, Polish &amp; Ukrainian group might mean your ancestors were from one, two, or all three of those country-level populations. Sometimes other information from your DNA, such as your Genetic Groups, might help you identify more specific locations your ancestors may have come from.&nbsp;



Why are some reference panels smaller than before?



A reference panel, or a reference population or reference dataset, is a collection of DNA samples from people with some common connection. We compare your DNA to these reference panels to determine which ancestry most closely corresponds to your DNA. We often use 23andMe research participants who tell us they have four grandparents all born in the same country for reference panels.



However, sometimes when we look at the ancestry prediction for individuals in a reference panel for a specific population a few individuals don&#8217;t end up being predicted to have a reasonably large percentage of their DNA from that population. These individuals are considered outliers. As part of this update we systematically reviewed our reference panels around the world to remove these outliers. But don&#8217;t worry; even though some reference panels might be smaller, we still check that the models perform as well as (or better than) before for people with ancestry from these regions.&nbsp;



Why is there no Indigenous Caribbean population?



To define a new ancestry population we need reference panels made up of individuals who have deep genetic roots from one place. However, many individuals from the Caribbean are highly admixed (“admixture” refers to places where there was mixing of previously separate populations). This makes it incredibly difficult to identify a sufficient number of individuals with primarily indigenous DNA from the Caribbean. The reference panels for the new Indigenous American populations are almost entirely unadmixed, which is why we are able to provide ancestry percentages for these populations.&nbsp;



<figure class="wp-block-image alignright size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="502" src="http://35.88.189.111/wp-content/uploads/2019/08/avg_ancestry_caribbean-1024x502.png" alt="" class="wp-image-27359" style="width:371px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/08/avg_ancestry_caribbean-1024x502.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/08/avg_ancestry_caribbean-300x147.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/08/avg_ancestry_caribbean-768x376.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/08/avg_ancestry_caribbean-880x431.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/08/avg_ancestry_caribbean-1180x578.png 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



So where does Indigenous Caribbean ancestry show up? We tend to see that Indigenous American ancestry in individuals from the Caribbean is spread among several of the new Indigenous American populations (especially North American, Southern Mesoamerican, Central Andean &amp; Amazonian, and Northern Andean).



Does this mean Indigenous Caribbean ancestors came from those places? Not necessarily. It simply means that of the options available today, those populations are the closest genetic match.&nbsp;



Why weren&#8217;t other parts of the world updated?



While we would love to be able to make major updates around the world more frequently, each new population requires new reference data and major updates in the prediction models. Throughout the years we have increased the number of populations across the rest of the world; however, we have not updated the populations in Europe since 2012. This update was an important opportunity to provide more detail in Europe and the Americas.



We will continue to work towards providing more specificity and granularity around the world in your ancestry percentages as well as Genetic Groups (keep an eye out over the next few months for new Genetic Groups in Africa), <a href="https://blog.23andme.com/articles/23andmes-historic-matches" target="_blank" rel="noreferrer noopener">Historical Matches</a>SM, and other features.



Why did the colors change?



Adding 39 new colors to the color palette was quite the task for the 23andMe Design Team. The team took this opportunity to think about the colors holistically, coming up with a new system that provides a gradient across the world, allowing for nearby populations that are closer together geographically to be represented by more similar colors, while at the same time providing a system that can work for more populations in the future.



Who will get this update?



All customers genotyped on the current (V5) chip and with access to the ancestry service will see this update. A genotyping chip (or array) tests for a fixed set of genetic variants (SNPs) across the genome. Different chip versions (V1, V2, V3, V4, V5, etc.) test for different sets of SNPs. More recent chips often include better coverage for certain populations, recently discovered variants, or better genetic markers that help improve ancestry?composition algorithms or detect health?associated variants.



Ancestry Composition is trained on specific genotyping chip versions, and these latest models were only trained on the latest chip version. The models are incompatible with data from older genotyping chips, as older chips don’t include most of the genetic markers used by these new ancestry models. More recent chip versions are also designed with better coverage for diverse populations. If you&#8217;re on an older chip version (or not sure which chip version you have) learn about chip upgrades <a href="https://customercare.23andme.com/hc/en-us/articles/360025014494-How-Do-I-Upgrade-My-Genotyping-Chip" target="_blank" rel="noreferrer noopener">here</a>.



What happens if my family deleted data and I want to connect with them?



When you connect with a biological parent through Your Connections, we use the additional information we learn from your parents&#8217; DNA to improve the resolution of your Ancestry Composition results. You will also be able to see the proportions of each ancestry that you inherited from each parent in the Parental Inheritance section in your Ancestry Composition report. If a family member has deleted their account they will need to purchase a new kit and create a new account before you can connect with them.

It’s Finally Here: A New Version of Ancestry Composition

Obsessive-compulsive disorder (OCD) is a complex and often debilitating condition that affects up to three percent of people, but the biological basis of the disorder has remained largely elusive. While we’ve known that genetics play a role, previous genetic studies have been limited by their relatively small sample size and have only identified a few of the specific genetic variants involved.



But that is now changing.



<a href="https://pubmed.ncbi.nlm.nih.gov/40360802/" target="_blank" rel="noreferrer noopener">In a recent study</a>, the largest of its kind ever conducted for OCD, researchers identified dozens of genetic variants associated with the disorder, offering unprecedented insight into its underlying biology.



<h2 class="wp-block-heading" id="h-the-power-of-numbers">The Power of Numbers</h2>



For complex conditions like OCD, genetic discovery is a numbers game. To find the subtle genetic variations that contribute to risk, scientists need to compare the DNA of vast numbers of people with and without the condition. This is where the research model of the 23andMe Research Institute makes a world of difference.



<figure class="wp-block-image alignright size-full is-resized"><img loading="lazy" decoding="async" width="600" height="600" src="http://35.88.189.111/wp-content/uploads/2017/05/your_dna_family.png" alt="" class="wp-image-25345" style="width:141px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family.png 600w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family-150x150.png 150w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family-300x300.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family-271x271.png 271w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family-372x372.png 372w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/05/your_dna_family-574x574.png 574w" sizes="auto, (max-width: 600px) 100vw, 600px" /></figure>



This study combined data from 28 different cohorts. The result was a dataset of incredible scale, including 53,660 individuals with OCD and more than 2 million controls. Consented 23andMe research participants made up about half of the entire cohort in this study. This immense contribution, made possible by those who choose to participate in research, was critical to achieving the statistical power needed to make these new discoveries.



<h2 class="wp-block-heading" id="h-what-the-study-found">What the Study Found</h2>



By scanning the genomes of millions of individuals, the researchers identified 30 independent genetic variants that were significantly associated with OCD. Of these 30 genetic variants, half are entirely new discoveries, while the others confirm and strengthen findings from previous, smaller studies. Researchers mapped these genetic variants to 25 genes that are likely impacted by those variants.



<h3 class="wp-block-heading" id="h-zeroing-in-on-the-brain">Zeroing In on the Brain</h3>



Identifying the genes is just the first step. The next question is: where in the body do these genes do their work?



<figure class="wp-block-image alignleft size-full is-resized"><img loading="lazy" decoding="async" width="438" height="458" src="http://35.88.189.111/wp-content/uploads/2015/06/Brain-Logo.jpg" alt="Brain Logo" class="wp-image-22635" style="width:157px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/Brain-Logo.jpg 438w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2015/06/Brain-Logo-287x300.jpg 287w" sizes="auto, (max-width: 438px) 100vw, 438px" /></figure>



To find out, the researchers performed tissue and single-cell enrichment analyses. The results were striking. The genetic signals for OCD were highly enriched in six different types of human brain tissue. In contrast, there was no enrichment found in tissues outside the brain.



The study drilled down even further, pinpointing specific cell types and found that these genes are at work in the same cells identified by neuroimaging and deep brain stimulation studies of OCD. By independently identifying these precise brain regions and cell types through genetics, this study provides additional supporting evidence that these genes and neurons play a direct role in the biology of OCD.



<h3 class="wp-block-heading" id="h-shared-genetics">Shared Genetics</h3>



The study also investigated the genetic relationship between OCD and other psychiatric and behavioral conditions. The researchers found statistically significant positive genetic correlations between OCD and a range of other disorders, including anxiety, depression, anorexia nervosa, and Tourette syndrome



This finding reinforces a growing body of evidence that many psychiatric conditions, while appearing different on the surface, are likely to share some underlying genetic susceptibility factors. Understanding this genetic overlap may be key to understanding mental health as a whole.



<h2 class="wp-block-heading" id="h-a-foundation-for-the-future">A Foundation for the Future</h2>



This study represents a pivotal moment for OCD research. By dramatically expanding the list of known genetic variants associated with OCD and grounding them in the specific biology of the brain, this work opens doors for researchers to explore the precise mechanisms by which these genes influence brain circuits and contribute to OCD symptoms.



Ultimately, these findings may be a critical step toward developing novel and more effective treatments for a disorder that has long been misunderstood.



And once again, we want to extend our deepest gratitude to 23andMe research participants. Your contribution to this landmark study has advanced our understanding of OCD and paved the way for a healthier future.

A Major Leap Forward in Understanding the Genetics of OCD

Each year from September 15–October 15, National Hispanic Heritage Month celebrates the histories, cultures, and contributions of people from Spain, Latin America, and other Spanish-speaking communities. To mark the occasion, we’re highlighting a remarkable ancient DNA study from Las Gobas, a medieval site in northern Spain that sheds new light on life in early Iberia, which comprises present-day Spain and Portugal.



<h2 class="wp-block-heading" id="h-setting-the-scene-iberia-in-the-early-medieval-period">Setting the Scene: Iberia in the Early Medieval Period</h2>



From the 5th to 8th centuries CE, Iberia was ruled by the Visigoths, a Germanic people who established power after the fall of the Western Roman Empire. In 711 CE, their kingdom collapsed after the Umayyads—an Islamic dynasty with roots in Arabia and North Africa—invaded and established the Emirate (and later the Caliphate) of Córdoba. This new state controlled much of Iberia, along with the Balearic Islands and parts of North Africa.



In the mountainous north, however, many communities retained their independence and Christian traditions, even as the rest of the Iberian peninsula underwent profound cultural and political change.



<h2 class="wp-block-heading" id="h-life-at-las-gobas">Life at Las Gobas</h2>



Las Gobas, located in today’s province of Burgos in northern Spain, consists of 13 rock-cut caves and several freestanding structures. Beginning in the 7th century, it served as a mixed-use settlement with homes, a Christian church, and a cemetery. By the late 9th century, the residential area was abandoned, but the site continued to be used as a burial ground and place of worship until the 11th century.



<a href="https://pubmed.ncbi.nlm.nih.gov/39196943/" target="_blank" rel="noreferrer noopener">In 2024</a>, researchers analyzed DNA from 33 individuals buried at Las Gobas. They discovered that the community’s ancestry remained surprisingly stable over the centuries, with little evidence of genetic influence from the Islamic expansion that reshaped much of Iberia.



Why was Las Gobas different? Their DNA offered a clue. Many individuals carried stretches of identical DNA inherited from both parents—patterns that often occur in small, insular populations with limited outside contact. This genetic isolation likely helped shield the community from broader population shifts happening elsewhere.



The study also revealed striking details about life at Las Gobas:



<ul class="wp-block-list">
<li>Inbreeding: The DNA of several individuals showed evidence that their parents were close relatives; likely first cousins or closer.</li>



<li>Disease: DNA evidence showed infections from multiple pathogens, including what may be one of the earliest documented cases of smallpox in northern Iberia.</li>



<li>Violence: Skeletal remains showed signs of traumatic injuries, likely from swords—evidence of interpersonal conflict or warfare.</li>
</ul>



Taken together, the findings paint a vivid—and sometimes harsh—picture of life more than a thousand years ago in a small, tightly knit community in northern Spain.



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



Want to see if you share a genetic connection with these newly added individuals from Las Gobas—or hundreds of other historical people? The <a href="https://blog.23andme.com/articles/23andmes-historic-matches" target="_blank" rel="noreferrer noopener">Historical Matches</a>SM feature is available to <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members.

New Historical Matches Could Connect You to the Medieval Iberian Site of Las Gobas

<a href="https://blog.23andme.com/articles/ancestry-composition-version-7-is-here" target="_blank" rel="noreferrer noopener">This update</a> is currently available to all eligible customers on the latest, V5, genotyping chip.



23andMe’s flagship Ancestry Composition algorithm was last updated in 2022, when three new reference populations were added in China. Since then, the 23andMe Ancestry Team has focused on improving the specificity of reference populations and updating the methods underlying this state-of-the art algorithm. The result? More specificity and accuracy in the ancestry breakdowns we provide.&nbsp;



<figure class="wp-block-image size-large"><img loading="lazy" decoding="async" width="1024" height="508" src="http://35.88.189.111/wp-content/uploads/2025/09/Ac-omega-map-correc-1024x508.png" alt="" class="wp-image-34246" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/Ac-omega-map-correc-1024x508.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/Ac-omega-map-correc-300x149.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/Ac-omega-map-correc-768x381.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/Ac-omega-map-correc-880x437.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/Ac-omega-map-correc-1180x585.png 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



The project, Version 7 of Ancestry Composition, is the most significant update to the feature ever.



<h2 class="wp-block-heading" id="h-improved-algorithm-expanded-populations-better-results">Improved algorithm, expanded populations, better results</h2>



Over the last few months, we’ve been hard at work finalizing the details on this major update to your favorite report: Ancestry Composition.&nbsp;



<figure class="wp-block-image size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="499" src="http://35.88.189.111/wp-content/uploads/2025/09/image-3-1024x499.png" alt="" class="wp-image-34237" style="width:537px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/image-3-1024x499.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/image-3-300x146.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/image-3-768x374.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/image-3-880x429.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/image-3-1180x575.png 1180w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/image-3.png 1600w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



Here’s what we&#8217;ve been working on:



<ul class="wp-block-list">
<li>Better breakdowns in Europe and the Americas: Thanks mainly to consented 23andMe research participants we&#8217;ve been able to expand the number of unique populations in our reference datasets. Reference datasets are collections of DNA samples from people with deep roots in a specific part of the world. It&#8217;s what is needed to compare each piece of your DNA to in order to determine where in the world that DNA most likely came from. What this means is we’re launching with nearly four times the resolution in Europe and six new populations in the Americas. We also took the opportunity to refine reference datasets from around the world, making them more specific to each global population.</li>



<li>Enhanced Accuracy: The accuracy of these new ancestry results are greatly improved by using our <a href="https://www.cell.com/hgg-advances/fulltext/S2666-2477(25)00082-X" target="_blank" rel="noreferrer noopener">recently published</a>, state-of-the-art DNA phasing method. You could think of phasing as sorting which DNA you inherited from each parent. Reducing errors in phasing means a more accurate estimate of your ancestry percentages and better <a href="https://customercare.23andme.com/hc/en-us/articles/212860507-Chromosome-Painting-23andMe-Ancestry-Results" target="_blank" rel="noreferrer noopener">DNA Painting</a>.&nbsp;</li>



<li>Elimination of Broadly and Unassigned DNA: We are updating our algorithm to report the most likely assignment for a given stretch of DNA rather than at a fixed confidence threshold. This will have the benefit of eliminating &#8220;Broadly&#8221; and &#8220;Unassigned&#8221; categories in the default results view. You will still be able to view your results at different confidence thresholds in the Version History section.</li>



<li>Better Error Detection: We&#8217;ve upgraded our smoother to better filter out erroneous trace ancestries between two larger blocks of ancestry. See our <a href="https://www.23andme.com/ancestry-composition-guide/" target="_blank" rel="noreferrer noopener">Ancestry Composition Guide</a> for more information about the current smoother.</li>



<li>Version History: Compare your new results to your old ones in a new &#8220;Version History&#8221; section. <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ members will also be able to access previous versions at different confidence settings.</li>
</ul>



<h2 class="wp-block-heading" id="h-what-are-the-new-reference-populations-nbsp">What are the new reference populations?&nbsp;</h2>



<ul class="wp-block-list">
<li>33 new ancestry populations in Europe are coming: Albanian &amp; Macedonian; Andalusian, Asturian &amp; Castilian; Aragonese &amp; Catalan; Austrian &amp; Southern German; Basque; Belarusian, Polish &amp; Ukrainian; Belgian, Rhinelander &amp; Southern Dutch; Bosnian, Croatian, Montenegrin &amp; Serbian; Bulgarian, Moldovan &amp; Romanian; Canary Islander; Czech, Hungarian, Slovak &amp; Southern Polish; Danish; Dutch &amp; Northern German; English; Estonian; Finnish; French; Greek; Icelandic; Irish; Kosovar &amp; Northern Albanian; Latvian; Lithuanian; Maltese; Northern Italian; Norwegian; Portuguese &amp; Galician; Russian; Sardinian; Scottish; Slovenian; Southern Italian; Swedish; Swiss, Southwestern German &amp; Western Austrian; Welsh</li>
</ul>



<figure class="wp-block-image size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="840" src="http://35.88.189.111/wp-content/uploads/2025/09/europe_map-1024x840.png" alt="" class="wp-image-34262" style="width:523px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/europe_map-1024x840.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/europe_map-300x246.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/europe_map-768x630.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/europe_map-880x722.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/europe_map.png 1101w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



<ul class="wp-block-list">
<li>Indigenous American will be broken into 6 new ancestry populations: Arctic North American, Central Andean &amp; Amazonian, North American, Northern Andean, Southern Mesoamerican, and Western North American</li>
</ul>



<figure class="wp-block-image size-full"><img loading="lazy" decoding="async" width="562" height="393" src="http://35.88.189.111/wp-content/uploads/2025/09/image-2.png" alt="" class="wp-image-34236" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/image-2.png 562w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/image-2-300x210.png 300w" sizes="auto, (max-width: 562px) 100vw, 562px" /></figure>



<h2 class="wp-block-heading" id="h-your-dna-story-now-clearer-across-time-place-and-family">Your DNA story, now clearer across time, place, and family</h2>



These updates, drawn from sharper science and richer data, power everything you use to explore your ancestry, including Ancestry Timeline, Parental Inheritance, DNA Painting, and more. This builds on the world’s most comprehensive ancestry breakdown on the market with over 4,000 regions, helping you experience the life-changing power of DNA by tracing where your ancestors lived and what they passed on to you.



Ancestry Composition, Version 7. More precision. More connection. More you.



This is a massive project for us and a chance to get back to our roots by digging deeper into yours. We’re thrilled you’re as excited as we are.



The 23andMe Ancestry Team

A Major Update to Ancestry Composition

For many of us, reading is second nature, but it&#8217;s an arduous challenge for 5–10% of school-aged children with dyslexia. <a href="https://pubmed.ncbi.nlm.nih.gov/40825760/" target="_blank" rel="noreferrer noopener">A new genetic study</a>—the largest of its kind to date—is helping scientists to expand our understanding of the genetic foundations of reading and dyslexia, uncovering dozens of previously unknown genetic factors. 



<h2 class="wp-block-heading" id="h-what-we-already-knew">What We Already Knew</h2>



<figure class="wp-block-image alignright size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="683" src="http://35.88.189.111/wp-content/uploads/2025/08/open_book-1024x683.jpg" alt="" class="wp-image-34166" style="width:364px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/open_book-1024x683.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/open_book-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/open_book-768x512.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/open_book-880x587.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/open_book-1180x786.jpg 1180w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/open_book.jpg 2048w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



<a href="https://blog.23andme.com/articles/study-identifies-genetic-links-to-dyslexia" target="_blank" rel="noreferrer noopener">Previous research</a>, using data from consented 23andMe research participants, had already successfully identified 42 genetic variants linked to a self-reported diagnosis of dyslexia and demonstrated that many of these genetic variants are also linked to cognitive ability and educational attainment.



This earlier work also supported a key idea: dyslexia isn&#8217;t a biologically distinct condition, but rather represents the lower end of a continuous spectrum of reading ability that varies naturally across the population.



<h2 class="wp-block-heading" id="h-a-bigger-bolder-approach">A Bigger, Bolder Approach</h2>



So, how do you find even more subtle genetic clues? You build a more powerful magnifying glass.



In this latest effort, researchers used a method, called multi-trait analysis of GWAS (MTAG), to combine the statistical power of two massive datasets:



<ol class="wp-block-list">
<li>The GenLang Consortium&#8217;s study on reading skill (involving ~27,000 people).</li>



<li>The 23andMe study on dyslexia (involving over 1.1 million research participants).</li>
</ol>



By merging the results, scientists created an effective sample size of over 1.2 million individuals, dramatically boosting their power to detect genetic variants associated with dyslexia.



<h2 class="wp-block-heading" id="h-landmark-discoveries">Landmark Discoveries</h2>



The results from this powerful analysis represent a leap forward in our understanding of the genetics of dyslexia and reading ability.



<h3 class="wp-block-heading" id="h-dozens-of-new-genetic-loci">Dozens of New Genetic Loci</h3>



The study found 80 independent genome-wide significant regions linked to dyslexia. Of those, 36 had never been found by previous studies. Even more exciting, 13 of these regions were completely novel, with no prior known association with dyslexia.



<h3 class="wp-block-heading" id="h-clues-in-brain-development">Clues in Brain Development</h3>



Digging deeper, many of the genes located in these newly identified regions play a role in early brain development. Specifically, they are highly active in neuronal pathways, especially during embryonic brain development. This provides new insights into how the brain may be wired for reading ability.



<h3 class="wp-block-heading" id="h-an-evolutionary-angle">An Evolutionary Angle</h3>



Interestingly, the researchers looked to see if there was evidence that the genetic factors influencing dyslexia have been subject to recent evolutionary pressure and found none. In other words, there does not appear to be any evolutionary advantage from the genetic variants associated with dyslexia for humans as we transitioned from hunter-gatherer societies to agricultural ones in Europe.



<h2 class="wp-block-heading" id="h-the-big-picture-and-what-s-next">The Big Picture and What&#8217;s Next</h2>



This research expands our map of the genetic landscape of dyslexia. By identifying the biological pathways involved, new avenues for future research into why reading is difficult for some people and how to develop better support strategies are opened.



It’s crucial to remember that genes are not destiny. The research team created a polygenic index—also known as a polygenic score—that tallies the effects of multiple genetic variants. This index was able to predict between 2.3% and 4.7% of the variance in reading skills in a separate, independent group of individuals. Meaning that there may be other genetic factors, but also education, environment, and support systems that help determine reading skills.



Finally, like much genetic research, this work was conducted primarily in people of European descent. A critical next step is to conduct similar large-scale studies in more diverse populations to ensure that the insights and potential benefits of this research can apply to everyone.

New Study Expands Our Understanding of the Genetics of Dyslexia

Have you ever wondered why some people stutter? You’re not alone. Developmental stuttering—disruptions in the normal flow of speech, like repeating sounds or involuntary pausing on words— affects more than 400 million people worldwide. <a href="https://pubmed.ncbi.nlm.nih.gov/40721530/" target="_blank" rel="noreferrer noopener">A new genetic study</a>, powered in part by data from more than one million consented 23andMe research participants, offers exciting insights into the genetics behind stuttering.



<h2 class="wp-block-heading" id="h-stuttering-often-starts-young-and-many-kids-recover">Stuttering Often Starts Young—And Many Kids Recover</h2>



Most people who stutter begin showing signs between ages 2 and 5. For many, it’s temporary—about 80% of children who stutter will recover, often naturally and sometimes with the help of speech therapy. Interestingly, boys and girls are about equally likely to start stuttering, but by the time they reach adulthood, men are four times more likely to continue stuttering compared to women.



<h2 class="wp-block-heading" id="h-the-genetics-of-stuttering-a-new-look">The Genetics of Stuttering: A New Look</h2>



Until recently, research into the genetics of stuttering has been limited to a handful of rare genetic variants identified in families. But a new large-scale study is changing that. By combining genetic data from over a million individuals, researchers identified 57 genetic variants (in or near 48 unique genes) linked to self-reported stuttering.



<figure class="wp-block-image size-full"><img loading="lazy" decoding="async" width="616" height="378" src="http://35.88.189.111/wp-content/uploads/2022/11/Visualize-GWAS.jpg" alt="" class="wp-image-30872" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/11/Visualize-GWAS.jpg 616w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2022/11/Visualize-GWAS-300x184.jpg 300w" sizes="auto, (max-width: 616px) 100vw, 616px" /></figure>



Some of these genetic signals were ancestry- or sex-specific, meaning they were only significant associations in certain populations. Others were shared across groups, highlighting the complex nature of the genetics behind stuttering.



And there’s more: while most previously reported variants were too rare or not included in the dataset, this study still found strong genetic signals in three of the six candidate genes previously linked to stuttering—GNPTAB, GNPTG, and AP4E1—adding new weight to past findings.



Some of the genetic findings in this study also overlap with traits like depression, autism, and even beat synchronization (your ability to accurately synchronize your movements with a musical beat). These overlaps suggest that stuttering might share some genetic similarity with these other traits.



<h2 class="wp-block-heading" id="h-the-value-of-diversity-in-genetic-research">The Value of Diversity in Genetic Research</h2>



<figure class="wp-block-image alignright size-full is-resized"><img loading="lazy" decoding="async" width="406" height="444" src="http://35.88.189.111/wp-content/uploads/2024/02/CRC-Group.jpg" alt="An image to represent African Americans participating in 23andMe's colorectal cancer research." class="wp-image-32581" style="width:240px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/02/CRC-Group.jpg 406w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2024/02/CRC-Group-274x300.jpg 274w" sizes="auto, (max-width: 406px) 100vw, 406px" /></figure>



One important takeaway from this study is the value—and the current limits—of genetic diversity in research. Researchers were able to create a polygenic risk score (PRS) for stuttering using data from people of European descent and found that it predicted stuttering risk well in both independent clinical and self-reported datasets. However, a lack of large, diverse datasets meant that the team couldn’t validate similar scores for people from other ancestry groups.



That’s why increasing diversity in genetic studies is so important. It helps ensure that the insights we gain are applicable to everyone.



<h2 class="wp-block-heading" id="h-what-this-means-for-the-future">What This Means for the Future</h2>



This study marks a major step forward in understanding the genetic contribution to stuttering. It confirms that stuttering, like many other traits, is influenced by a complex mix of genetic factors. And it highlights the importance of building inclusive, diverse research databases to ensure that discoveries can benefit as many people as possible.



Whether you’ve experienced stuttering yourself, know someone who has, or are just curious about the science of speech, studies like this help us better understand the fascinating interplay between genetics and communication.



Learn more about this study from our collaborators at <a href="https://news.vumc.org/2025/07/28/large-scale-study-defines-genetic-architecture-of-stuttering/" target="_blank" rel="noreferrer noopener">Vanderbilt University Medical Center</a> and learn more about <a href="https://www.23andme.com/research/" target="_blank" rel="noreferrer noopener">research at 23andMe</a>.

Why Do People Stutter? Genetics Holds Some Clues

A <a href="https://pubmed.ncbi.nlm.nih.gov/40691366/" target="_blank" rel="noreferrer noopener">new study</a> published this week demonstrates just how powerful large-scale genetic research can be when it comes to predicting health traits—like body weight. By combining data from consented 23andMe research participants with the GIANT consortium, an international group of scientists have created the most predictive polygenic score for body mass index (BMI) to date. The study used genetic data from up to 5.1 million individuals from diverse backgrounds, helping push the science forward in important and inclusive ways.



<h2 class="wp-block-heading" id="h-what-s-a-polygenic-score">What’s a Polygenic Score?</h2>



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Think of a polygenic score (sometimes called a polygenic risk score or PRS) as a genetic summary. It adds up the small effects of many different genetic variants—often thousands or even millions—that are each linked to a trait, like BMI. The higher your score, the higher your predicted BMI. These scores are increasingly used in research, and even clinical settings, to better understand traits and potential health risks.



<h2 class="wp-block-heading" id="h-why-this-study-matters">Why This Study Matters</h2>



One of the big takeaways from this research? The more data we include in building a polygenic score, the more accurate the predictions become. Thanks to the massive dataset, this new BMI polygenic score is one of the most accurate developed so far—and it&#8217;s also more applicable to people of diverse ancestries than previous versions.



Still, it’s important to note that while this polygenic score performs better across different populations, its accuracy is still highest in individuals of European descent. That’s because most genetic research to date has been heavily based on European-ancestry populations. Studies like this one help move the field toward more inclusive and equitable research.



<h2 class="wp-block-heading" id="h-what-the-study-found">What the Study Found</h2>



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<li>Childhood weight gain: A higher BMI polygenic score was linked to faster weight gain starting from age 2.5 onwards and an earlier “adiposity rebound”—a key moment in childhood growth when BMI dips and then begins to increase again. This could help identify children at higher risk of becoming overweight before other warning signs appear. </li>



<li>Adult weight change: Between ages 20 and 50, people with higher BMI polygenic scores were more likely to gain weight. Interestingly, this was especially true for those who started adulthood at a weight lower than what their genetics might predict. It suggests that individuals with a genetic predisposition to higher weight may eventually &#8220;catch up&#8221; to their genetic set point over time. </li>



<li>Lifestyle changes: In lifestyle intervention studies (think: intensive diet and exercise programs), people with a higher genetic predisposition to obesity tended to lose more weight during the first year—but they were also more likely to regain it. This pattern fits with previous research showing that people who are genetically predisposed to obesity often respond more dramatically to environmental changes, both positive and negative. </li>
</ul>



<h2 class="wp-block-heading" id="h-what-this-study-doesn-t-say">What This Study Doesn’t Say</h2>



This research doesn’t mean that lifestyle doesn’t matter. In fact, it’s just the opposite. Even with a high genetic predisposition to obesity, lifestyle choices—like diet, physical activity, sleep, and stress management—still have a meaningful impact. What polygenic scores offer is insight into who may be at higher risk and might benefit most from early interventions or targeted prevention strategies.



<h2 class="wp-block-heading" id="h-final-thoughts">Final Thoughts</h2>



Your genes are only one part of the story. While this research gives us a clearer picture of how genetics influence weight over time, it also highlights the importance of using that information wisely. At 23andMe, we believe that understanding your genetics can empower you to make informed health decisions—not define your destiny. As science continues to evolve, so do the tools we have to support healthier, more personalized approaches to wellness.

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