<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

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

As many as one in 10 women have endometriosis, but diagnosing it can take up to a decade or more. Dive into the science, and learn a bit about a new 23andMe Endometriosis report that looks at the genetic likelihood of developing this painful condition.



<figure class="wp-block-image size-full"><img loading="lazy" decoding="async" width="612" height="252" src="http://35.88.189.111/wp-content/uploads/2025/09/endometriosis_hero-1.jpg" alt="" class="wp-image-34227" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/endometriosis_hero-1.jpg 612w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/endometriosis_hero-1-300x124.jpg 300w" sizes="auto, (max-width: 612px) 100vw, 612px" /></figure>



Have you ever been told your debilitating period pain is &#8220;normal&#8221;? Do you find yourself planning your life around your cycle, canceling plans, or missing work or school due to pain, heavy bleeding, or exhaustion? If so, you&#8217;re not alone; these symptoms could point to endometriosis, a common, yet often misunderstood, condition.



For those with endometriosis, tissue similar to the lining of the uterus grows in other places, like the ovaries, fallopian tubes, or even the bowel and bladder. This can lead to severe pain, heavy periods, and in some cases, may make it harder to become pregnant (between 30–50% of women with endometriosis experience infertility).



If this sounds familiar, it’s important to know that your pain is real and more common than many people think. Endometriosis affects as many as 10% of women in the U.S. Despite this, the journey to a diagnosis can be frustratingly long, sometimes <a href="https://pubmed.ncbi.nlm.nih.gov/39373298/" target="_blank" rel="noreferrer noopener">taking up to 12 years</a>. This delay often happens because symptoms are dismissed as &#8220;just a bad period.&#8221;



To support awareness and help people understand their genetic predisposition to endometriosis, we’ve launched the new Endometriosis* report for female <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a>™ and <a href="https://www.23andme.com/total-health/" target="_blank" rel="noreferrer noopener">Total Health</a>™ members.



<h2 class="wp-block-heading" id="h-what-causes-endometriosis">What causes endometriosis?</h2>



While the exact cause isn&#8217;t known, several factors can increase your likelihood of developing endometriosis:



<figure class="wp-block-image alignright size-full is-resized"><img loading="lazy" decoding="async" width="612" height="720" src="http://35.88.189.111/wp-content/uploads/2025/09/Group-125628.png" alt="" class="wp-image-34211" style="width:259px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/Group-125628.png 612w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/09/Group-125628-255x300.png 255w" sizes="auto, (max-width: 612px) 100vw, 612px" /></figure>



<ul class="wp-block-list">
<li>Age: It most often affects menstruating people and is frequently diagnosed in the 30s and 40s.</li>



<li>Family history: Having a family member with endometriosis increases risk.</li>



<li>Reproductive history: Starting menstruation at a young age, experiencing menopause later in life, and having frequent or heavy periods (short cycles or bleeding lasting more than 7 days) can all increase chances of developing the condition.</li>
</ul>



These factors are associated with a higher risk. On the other hand, having been pregnant or breastfeeding may reduce risk.



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



Endometriosis is what’s known as a <a href="https://www.genome.gov/genetics-glossary/Polygenic-Trait" target="_blank" rel="noreferrer noopener">polygenic</a> condition — meaning that many different genetic variants in many different genes can influence a person’s chances of developing it. In fact, <a href="https://pubmed.ncbi.nlm.nih.gov/26209831/" target="_blank" rel="noreferrer noopener">research suggests</a> that genetics may explain nearly half of the differences in who develops endometriosis across a population.



In 2023, 23andMe collaborated with researchers at Oxford in what was at the time the largest study on <a href="https://blog.23andme.com/articles/largest-genetic-study-to-date-links-endometriosis-with-chronic-pain" target="_blank" rel="noreferrer noopener">endometriosis and its association with chronic pain</a>. Now, to further understand the genetics of this condition, researchers at 23andMe looked at genetic and self-reported data from more than 1.5 million consented research participants. Using this information, they created a Polygenic Risk Score (PRS) — a model that considers thousands of genetic variants to estimate a person’s likelihood of developing endometriosis.



However, this model did not perform as accurately for 23andMe customers with Black or African American ancestry. Due to this limitation, we cannot provide a result for the Endometriosis report to those customers at this time. This is an important reminder that genetics research has historically underrepresented many communities. With continued research and broader participation, we hope to improve this work and reduce these disparities in the future.



<h2 class="wp-block-heading" id="h-what-you-can-do-about-it">What you can do about it</h2>



While the road to getting a diagnosis and managing endometriosis can be long and frustrating, there are proactive steps you can take on your journey to getting answers and feeling better.



<h3 class="wp-block-heading" id="h-advocate-for-yourself">Advocate for yourself</h3>



Track Your Symptoms. Before you see a doctor, consider starting a symptom diary. Being specific can make a big difference. Every day, note:



<ul class="wp-block-list">
<li>Pain: On a scale of 1–10, where is the pain, and what does it feel like (sharp, dull, cramping)?</li>



<li>Timing: When during your cycle do you feel symptoms? (During your period, during ovulation, all month long?)</li>



<li>Bleeding: How heavy is your flow? Are you passing clots?</li>



<li>Other Symptoms: Note any bloating, painful bowel movements, pain with sex, or fatigue.</li>



<li>Impact: How do these symptoms affect your daily life? (e.g., &#8220;Missed two days of work,&#8221; &#8220;Couldn&#8217;t exercise,&#8221; &#8220;Had to leave the party early.&#8221;)</li>
</ul>



Connect with a Doctor. Armed with your symptom diary, make an appointment with a healthcare provider.



<ul class="wp-block-list">
<li>Be clear and confident. Say, &#8220;I am concerned I might have endometriosis because of these specific symptoms.&#8221;</li>



<li>Don&#8217;t be afraid to ask questions. &#8220;What are the next steps for diagnosis?&#8221; or &#8220;Could we explore treatment options for my pain now?&#8221;</li>



<li>If you feel dismissed, get a second opinion. Look for a gynecologist who specializes in endometriosis or pelvic pain.</li>
</ul>



<h3 class="wp-block-heading" id="h-manage-symptoms">Manage symptoms</h3>



There’s no one-size-fits-all approach, but experts agree that certain lifestyle habits can make a difference:



<ul class="wp-block-list">
<li>Exercise: Activities like yoga can improve blood flow, relax muscles, and reduce pain.</li>



<li>Relaxation and self-care: Rest, warmth on the lower stomach (like a heating pad, warm water bottle, or bath), and gentle movement can help ease discomfort.</li>
</ul>



Medical options may include medications to manage pain and hormone levels, pelvic floor physical therapy, and in some cases, surgery. Because endometriosis tissue can respond to estrogen, symptoms may improve after menopause, when estrogen levels remain consistently low.



<h2 class="wp-block-heading" id="h-take-the-next-steps">Take the next steps</h2>



Endometriosis pain is not an exaggeration, and it deserves to be taken seriously. Seeking answers is the first and most powerful step toward managing your health and reclaiming your quality of life.



Ready to learn more about your health and genetics and take the next step in your journey? Learn more about <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium</a> or <a href="https://www.23andme.com/total-health/" target="_blank" rel="noreferrer noopener">Total Health</a> memberships.



Already part of 23andMe? <a href="https://you.23andme.com/" target="_blank" rel="noreferrer noopener">Sign in</a> to view this report with your other Health Predisposition reports or upgrade 23andMe+ Premium or Total Health memberships.



* The 23andMe Endometriosis PRS report is based on a genetic model that includes data and insights from 23andMe consented research participants and incorporates more than 13,000 genetic variants to provide information on the likelihood of developing endometriosis. 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 Endometriosis 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. 



NOTE: Within this blog post, we use the words &#8220;women&#8221; and &#8220;female&#8221; to refer to people whose sex assigned at birth is female. However, we recognize that not everyone who experiences endometriosis will identify as female, and being categorized by birth sex may be an uncomfortable experience for some people. We do not mean to delegitimize anyone’s gender identity. Learn more about why we made this decision in this <a href="https://customercare.23andme.com/hc/en-us/articles/360010964373-How-23andMe-Uses-Your-Genetic-Sex-Birth-Sex-and-Gender" target="_blank" rel="noreferrer noopener">help article</a>.

Could Your Painful Periods Be Endometriosis? Here’s What You Should Know

This week, 23andMe added a new genetic report to help us all be more aware of an often overlooked contributor to health disparities.



<figure class="wp-block-image alignright size-large is-resized"><img loading="lazy" decoding="async" width="1024" height="763" src="http://35.88.189.111/wp-content/uploads/2025/08/duffy-statistic-1024x763.png" alt="" class="wp-image-34101" style="width:309px;height:auto" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/duffy-statistic-1024x763.png 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/duffy-statistic-300x224.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/duffy-statistic-768x572.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/duffy-statistic-880x656.png 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/duffy-statistic-1180x879.png 1180w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/duffy-statistic.png 1224w" sizes="auto, (max-width: 1024px) 100vw, 1024px" /></figure>



<a href="https://pubmed.ncbi.nlm.nih.gov/35994632/" target="_blank" rel="noreferrer noopener">Nearly 70%</a> of Black and African Americans have two copies of a variant in the Duffy antigen gene that can cause them to have white blood cell (WBC) counts that are lower than most standard reference ranges.&nbsp;



People who have this genotype — called Duffy null status — do not have an increased risk for <a href="https://pubmed.ncbi.nlm.nih.gov/32959868/" target="_blank" rel="noreferrer noopener">infection</a> or <a href="https://pubmed.ncbi.nlm.nih.gov/39825822/" target="_blank" rel="noreferrer noopener">other health problems</a>. But they may be flagged incorrectly as having abnormally low WBC counts, which can negatively impact the healthcare they receive.&nbsp;



&#8220;I&#8217;ve seen patients that are told that they might have cancer, go through painful bone marrow biopsies, miss out on joining clinical trials, or have critical medications like chemotherapy discontinued simply because their white blood cell counts were interpreted without understanding their Duffy status,&#8221; says Dr. Lauren Merz, Assistant Professor of Medicine, Division of Hematology/Oncology at the University of Michigan, who is leading efforts to raise awareness about Duffy null status and develop Duffy null-specific reference ranges and who provided expert feedback on 23andMe&#8217;s new report.



<h2 class="wp-block-heading" id="h-when-a-one-size-fits-all-blood-test-falls-short">When a one-size-fits-all blood test falls short</h2>



When we have our blood drawn, testing labs use reference ranges to determine whether our results fall in the range considered &#8220;normal&#8221; or are too high or too low, which can flag the need for clinical follow-up. One common blood test measures neutrophils, which are a type of white blood cell that helps the body fight infections.



Most neutrophil reference ranges are defined based on populations where Duffy null status is rare, such as people with European or Asian genetic ancestry. And blood testing labs don&#8217;t usually take into account Duffy status. As a result, <a href="https://pubmed.ncbi.nlm.nih.gov/35994632/" target="_blank" rel="noreferrer noopener">nearly 25%</a> of healthy Black and African Americans with Duffy null status — and more than 15% of all Black and African Americans — have neutrophil counts below the standard reference range.



These individuals may be misdiagnosed with neutropenia (low neutrophil counts), which can lead to a number of downstream harms, including <a href="https://pubmed.ncbi.nlm.nih.gov/34180972/" target="_blank" rel="noreferrer noopener">unnecessary specialty referrals and follow-up tests</a> like bone marrow biopsies; <a href="https://pubmed.ncbi.nlm.nih.gov/39259539/" target="_blank" rel="noreferrer noopener">exclusion from clinical trials</a> (because many trials require a minimum number of neutrophils that is higher than the normal range for people with the Duffy null genotype); and delayed or reduced access to medications for <a href="https://pubmed.ncbi.nlm.nih.gov/39259539/" target="_blank" rel="noreferrer noopener">cancer</a>, <a href="https://pubmed.ncbi.nlm.nih.gov/34645395/" target="_blank" rel="noreferrer noopener">mental health conditions</a>, and <a href="https://pubmed.ncbi.nlm.nih.gov/35724382/" target="_blank" rel="noreferrer noopener">autoimmune disorders</a>. (See the sidebar at the bottom for more details.)



<h2 class="wp-block-heading" id="h-what-is-the-duffy-antigen-and-how-does-it-impact-white-blood-cells">What is the Duffy antigen, and how does it impact white blood cells?</h2>



<figure class="wp-block-image alignleft size-large is-resized"><img loading="lazy" decoding="async" width="87" height="138" src="http://35.88.189.111/wp-content/uploads/2021/11/research.b57972a5e8fa.svg" alt="an icon representing research" class="wp-image-29284" style="width:117px;height:auto"/></figure>



The Duffy antigen is a protein found on the surface of red blood cells and certain other cells in the body. People with two copies of a specific <a href="https://www.cincinnatichildrens.org/health/d/duffy-null-associated-neutrophil-count" target="_blank" rel="noreferrer noopener">genetic variant in the ACKR1 (Duffy antigen) gene</a> don&#8217;t express this protein on their red blood cells — giving rise to the name &#8220;Duffy null.&#8221;



Being Duffy null can also impact infection-fighting white blood cells called neutrophils. People who are Duffy null tend to have naturally lower levels of circulating neutrophils in the peripheral blood — <a href="https://pubmed.ncbi.nlm.nih.gov/37338884/" target="_blank" rel="noreferrer noopener">about 40% lower, on average</a>. But they don&#8217;t have an increased risk for infection, because the total number of neutrophils in their bodies remains the same. (Their neutrophils just move from the blood into other tissues like the spleen more easily.)



In the past, healthy people with low neutrophil counts were said to have &#8220;benign ethnic neutropenia,&#8221; because the Duffy null variant is more common in certain populations. But the preferred name is now <a href="https://www.cincinnatichildrens.org/health/d/duffy-null-associated-neutrophil-count" target="_blank" rel="noreferrer noopener">Duffy null-associated neutrophil count (DANC)</a>, as this refers to the biological driver of Duffy status rather than the social construct of race or ethnicity — and highlights that lower neutrophil counts are normal for people who are Duffy null.



<h2 class="wp-block-heading" id="h-is-duffy-null-status-associated-with-any-health-conditions">Is Duffy null status associated with any health conditions?</h2>



To date, there is no robust evidence that people with Duffy null status are at increased risk for any health conditions. In fact, a <a href="https://pubmed.ncbi.nlm.nih.gov/39825822/" target="_blank" rel="noreferrer noopener">recent, large phenome-wide association study (PheWAS)</a> — which looked for potential associations between the Duffy null variant and 1,400 possible health conditions using the National Institutes of Health&#8217;s All of Us initiative and other cohorts — did not report any associations with disease. However, this is an active area of research.



<h2 class="wp-block-heading" id="h-why-is-duffy-null-status-most-common-in-certain-populations">Why is Duffy null status most common in certain populations?</h2>



Although anyone can have Duffy null status, it is most common among people with African or Middle Eastern ancestry. In the U.S., two-thirds of people who identify as Black or African American have the Duffy null genotype, which means they do not express the Duffy antigen on their red blood cells.&nbsp;



Scientists believe this variant became common in certain populations because it <a href="https://pubmed.ncbi.nlm.nih.gov/21468018/" target="_blank" rel="noreferrer noopener">helps protect against Plasmodium vivax</a>, a malaria parasite that relies on the Duffy antigen to infect red blood cells. (The variant does not protect against other types of malaria.) Over generations, people in regions where this malaria parasite was widespread were more likely to inherit this protective variant, and it remains common today in people with ancestry from some malaria-endemic regions.



<figure class="wp-block-image size-full"><img loading="lazy" decoding="async" width="934" height="597" src="http://35.88.189.111/wp-content/uploads/2025/08/af_rs2814778_C.png" alt="" class="wp-image-34139" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/af_rs2814778_C.png 934w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/af_rs2814778_C-300x192.png 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/af_rs2814778_C-768x491.png 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2025/08/af_rs2814778_C-880x562.png 880w" sizes="auto, (max-width: 934px) 100vw, 934px" /><figcaption class="wp-element-caption">23andMe data also show that the Duffy null genetic variant is most common in people with ancestry from parts of the world where Plasmodium vivax malaria is common.</figcaption></figure>



<h2 class="wp-block-heading" id="h-the-importance-of-raising-awareness">The importance of raising awareness</h2>



Last year, the American Society of Hematology (ASH) launched the <a href="https://www.hematology.org/education/danc/danc-project" target="_blank" rel="noreferrer noopener">Absolute Neutrophil Count (ANC) by Duffy Status Project</a>, aimed at creating specific neutrophil reference ranges for people with the Duffy null genotype and advocating for broader awareness and testing.



&#8220;The Duffy null genotype is a perfect example of how well-meaning systems can fall short when they don&#8217;t reflect the full diversity of the people they serve,&#8221; says Dr. Merz. &#8220;Raising awareness — among both clinicians and patients — is essential to prevent misdiagnosis and ensure more equitable and personalized care.&#8221;



You can become your own advocate by learning about your Duffy status and sharing that information with your doctor.&nbsp;



The White Blood Cell Count (Duffy Antigen-Related) report is available to <a href="https://www.23andme.com/membership/" target="_blank" rel="noreferrer noopener">23andMe+ Premium™ members</a> with their other Wellness reports.



<div style="float: left; text-align: justified; width: 700px; background-color: #eee; padding: 15px; margin-left: 5px;">
 
<h3>A deeper dive: How lack of awareness of Duffy null status can lead to downstream harm</h3>


Although Duffy null status does not usually cause health problems, harms can arise when Duffy null individuals are misdiagnosed with abnormally low neutrophil counts. These harms can include:
<ul>
<li>
Unnecessary follow-up testing. In general, low neutrophil counts can prompt concern from doctors, because they can be caused by blood cancers like leukemia. Follow-up testing involves a bone marrow biopsy, which is an invasive and sometimes painful test. 
 Because their neutrophil counts may be naturally lower than standard reference ranges, people with Duffy null status are much more likely to receive <a href="https://pubmed.ncbi.nlm.nih.gov/34180972/" target="_blank" rel="noreferrer noopener">unnecessary bone marrow biopsies</a>. And one study reported that Duffy null status was the <a href="https://pubmed.ncbi.nlm.nih.gov/37419240/" target="_blank" rel="noreferrer noopener">most common reason</a> for children to be referred to a children&#8217;s hospital for low neutrophil counts.
</li>
 
<li>
Exclusion from clinical trials. Many chemotherapy drugs reduce WBC production, which can make patients more susceptible to infections. As a result, most cancer clinical trials require patients to have a minimum neutrophil count before starting the trial, to help keep patients safe. 
 But a recent study found that more than 75% of cancer clinical trials have neutrophil thresholds that <a href="https://pubmed.ncbi.nlm.nih.gov/39259539/" target="_blank" rel="noreferrer noopener">exclude some people with Duffy null status</a>. Researchers have suggested these exclusion criteria may be one reason that Black Americans are <a href="https://pubmed.ncbi.nlm.nih.gov/37477920/" target="_blank" rel="noreferrer noopener">less likely to be included in cancer clinical trials</a>.
</li>
 
<li>
Delayed or reduced access to medications. Because some medications reduce WBC production, patients often have their neutrophils counted before and during treatment, so that their clinicians can adjust the dose, delay the start of treatment, or discontinue medications if counts become too low. 
 Because people with Duffy null status tend to have lower starting neutrophil counts, they may experience reduced or delayed access to important medications for <a href="https://pubmed.ncbi.nlm.nih.gov/39259539/" target="_blank" rel="noreferrer noopener">cancer</a>, <a href="https://pubmed.ncbi.nlm.nih.gov/34645395/" target="_blank" rel="noreferrer noopener">mental health conditions</a>, and <a href="https://pubmed.ncbi.nlm.nih.gov/35724382/" target="_blank" rel="noreferrer noopener">autoimmune disorders</a>, or inappropriate dose adjustments. Because chemotherapy dose often increases the chance of survival, some scientists think that inappropriate chemotherapy dosing related to Duffy null status could help explain, in part, why <a href="https://www.cancer.org/about-us/what-we-do/health-equity/cancer-disparities-in-the-black-community.html" target="_blank" rel="noreferrer noopener">breast cancer mortality is higher in Black than white Americans</a>.
</li>
</ul>

</div>

The Duffy Antigen Gene: A Clue Behind White Blood Cell Differences

A massive new study, the largest genome-wide association study ever done, has found nearly all the common genetic variants that explain the heritability of height among people of European ancestry, and in the process may have set the framework for future genetic research into other traits and diseases.<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/04/tallshadow-225x300.jpg" alt="" width="225" height="300" class="alignright size-medium wp-image-180" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2008/04/tallshadow-225x300.jpg 225w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2008/04/tallshadow.jpg 300w" sizes="auto, (max-width: 225px) 100vw, 225px" />
Using data from about 5.4 million individuals, almost half of whom were 23andMe customers who consented to participate in research, the study identified 12,111 variants or single nucleotide polymorphisms (SNPs) that help explain differences in height.
“We feel that this is really a milestone,” said&nbsp;<a href="https://www.broadinstitute.org/node/7053">Joel Hirschhorn</a>, senior author on the study, an institute member at the Broad, and also a professor of genetics and Concordia Professor of Pediatrics at Boston Children’s Hospital and Harvard Medical School. “We’d been studying height for a while but had only identified a small fraction of common variant heritability. We’re now basically done mapping this heritability to specific genomic regions, and that highlights what increasing sample size can tell us about traits controlled by multiple genes.”
<h6>GIANT</h6>
Published in the journal <a href="https://www.nature.com/articles/s41586-022-05275-y">Nature</a>, the study, led by researchers at the <a href="https://www.broadinstitute.org/news/largest-genome-wide-association-study-ever-uncovers-nearly-all-genetic-variants-linked-height">Broad Institute</a> and the international <a href="https://portals.broadinstitute.org/collaboration/giant/index.php/GIANT_consortium">Genetic Investigation of ANthropometric Traits (GIANT) Consortium</a>, is the culmination of a multi-year effort to foster collaboration between academic, non-profit, government, and commercial partners. In their effort, the researchers collected, merged, and analyzed numerous independently generated genome-wide association studies into a single data set. In all, there are more than 200 different datasets incorporated into this study, which included contributions from hundreds of scientists from around the world.
<h6>The Power of Scale</h6>
What they found is important not just because of what it says about height, syndromes, and abnormalities affecting stature, but what it says about the potential of using very, very large amounts of data to generate insights into the genetics of different traits and conditions. Because height is so heritable, and because it is easy to measure someone’s height, it offers a very straightforward way to conduct a genetic study into a trait.
&#8220;This study highlights the ability of large-scale genetic studies to reveal the underlying biology of human phenotypes,” said Adam Auton, 23andMe’s Vice President of Human Genetics. 23andMe was one of a long list of institutions and organizations involved in the study.
“With this 5.4 million person study, we&#8217;re now at the stage where we&#8217;re starting to saturate our genetic understanding of height,” Auton said. “However, for other phenotypes — particularly human diseases — we&#8217;re a long way from saturation, and there is a lot we don&#8217;t yet understand.&#8221;
<h6>Heritability of Height</h6>
Heritability is the measure of how much our DNA explains the differences in specific traits or conditions. A SNP is a one-letter variation in the genetic code at a single point along the genome. These common variants are associated with differences in everything from traits like the color of our eyes or our height, or our risk for certain diseases.
Along with genetics, one’s environment — diet, for instance — also plays a role in these different traits and conditions. In the case of height, genetics has an outsized role in explaining about 80 percent of the variation. Because researchers included more than twice the number of individuals in this study from the next largest height study, they were able to discern almost all the heritability for height. So, size matters in genetic studies.
Previous height studies were large but just not large enough. According to the authors, this study was big enough to discern almost all of the heritability for height. In finding most of the variants that explain the heritability for height, the authors estimate that they’ve now identified variants that account for 40 percent of all variation in height in people with European ancestry. But they’ve identified only around 10–20 percent of the variation in people of other ancestries.
<h6>Diversity Matters</h6>
Also significant is that the study found that the genetic variants associated with height clustered within or near genes or gene regions associated with growth and development. That makes sense, but scientists were not so sure that is what they’d find. Many scientists thought that perhaps the variants they’ve identified could be found randomly sprinkled throughout the genome. But seeing that there is clustering will allow researchers to focus more on the clues around the biology and processes involved in individual traits like height.
In addition, the study illustrates something we already know about genetic research: diversity matters.&nbsp;
Although there were large numbers of individuals – more than a million – with African, Asian, and Latino ancestry included in this study, the vast majority of the data came from people of European ancestry. Some of the variants associated with height were associated with individuals of all different ancestries, but the findings were most applicable to those of European ancestry.&nbsp;
The researchers concluded that their study would benefit from data from a more diverse pool of individuals, especially those of African ancestry since people of African ancestry have the most genetic diversity of all populations. Not only would it improve the predictive power of the models developed to predict height for non-Europeans,&nbsp; it would also help in identifying causal genes and rare variants involved in height.
Read the full paper <a href="https://www.nature.com/articles/s41586-022-05275-y">here</a>.
&nbsp;

Giant Study Offers Insights into the Genetics of Height

<img loading="lazy" decoding="async" class="alignnone size-medium wp-image-13464" src="https://blog-api.23andme.com/wp-content/uploads/2012/06/thumbnail-300x200.jpg" alt="" width="300" height="200" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/06/thumbnail-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/06/thumbnail-768x513.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/06/thumbnail-1024x684.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/06/thumbnail-880x588.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2012/06/thumbnail-1180x789.jpg 1180w" sizes="auto, (max-width: 300px) 100vw, 300px" />
(Editor&#8217;s note: This post originally ran in June, but we thought it was worth a second look on the eve of the election.) 
As Americans approach the elections this November, discussions of what influences economic and political preferences will surely flood our television sets and news feeds. Pundits use factors like income, gender, and education level to make predictions on how people will vote.
<h6>Genetics and Politics</h6>
But do they ever consider genetics in making their predictions?  Probably not. A new study, however, suggests that such preferences may indeed be influenced by our genetic makeup.
Led by Daniel Benjamin of Cornell University and Peter Visscher of the University of Queensland a team of researchers studied 3,200 individuals for four traits believed to influence economic preferences (risk-aversion, patience, trust, and fair-mindedness), as well as five categories of political preferences (immigration/crime, economic policy, environmentalism, feminism/equality, and foreign policy). Each individual’s preferences in these areas were determined using an extensive survey. The results of the study were published in the <a href="https://www.pnas.org/content/109/21/8026.long">Proceedings of the National Academy of Sciences</a> in May.
<div style="border: 1px solid #ccc; padding: 10px; font-style: italic; font-size: 11px; margin-bottom: 15px; width: 250px; float: right; margin-left: 15px; margin-top: 5px;">
Technical note:
<a href="https://blog.23andme.com/articles/quiz-answers-heritability-demystified/">Heritability</a> is a common measure of the average influence genetics has on a trait relative to other, non-genetic influences in a population.The heritability of a trait can range from zero (variance in the trait is independent of genetics) to one (variance in the trait completely explained by genetics). Heritability is often estimated using using twin studies; if identical twins are, on average, more similar than fraternal twins in a given trait, this increase in similarity is attributed to shared genetics.
The Visscher team, however, used a newer method for estimating heritability that relies on the genetically-determined relatedness of study subjects, which is potentially more accurate. The heritability estimates generated by this method were noisy, but three of the nine traits had statistically-significant heritability estimates: trust (heritability = 24%, p-value = 0.05), foreign policy (heritability = 35%, p-value = 0.01), and economic policy (heritability = 34%, p-value = 0.01). Despite the noisiness, the heritability estimates are not inconsistent with earlier findings from twin-designed studies (after for accounting for the biases in the two estimation methods).
</div>
<h6>Trust and Economic Policy</h6>
Before asking which genes are involved, we have to ask: are genes involved in economic and political preference, or are these preferences solely determined by environmental factors, such as family and friends? Three of the nine traits Benjamin and Visscher’s team analyzed appeared to be heritable to some extent &#8212; trust, foreign policy, and economic policy &#8212; which is consistent with previous studies.
Although Visscher and his fellow researchers were able to establish that genetics likely influences some aspects of our economic and political preferences, they were not able to determine which genes or genetic variants may be involved.
<h6>Many Genes</h6>
Visscher and his co-workers conclude that economic and political preferences are, most likely, influenced by many different genes, each affecting these traits in very small ways. In order to capture such small effects, much larger sample sizes are needed. Thus, economic and political preferences, along with the canonical examples of height and schizophrenia, fall into a group of very complex traits that are heritable but for which we may never find one single gene as the “smoking gun.”
If you’re voting in today’s primaries in California, Montana, New Jersey, New Mexico, or South Dakota, it’s likely that genetic influences are with you in the voting booth. Which genes are involved in economic and political preferences, however, remains to be discovered. Perhaps by the 2016 election we’ll better understand the genetics of politics.

Elephants Are Red, Donkeys Are Blue, Genetics Can Influence Politics, Too

Last week we quizzed our readers on heritability, a genetics concept that is often misinterpreted. Congratulations to Monica P., the winner of the quiz! She got all the answers correct and will receive an Amazon gift card. Read on for the answers and to learn more about what we can say about nature vs. nurture&#8230;
by Emily Chang and Chuong Do
<img loading="lazy" decoding="async" class="size-large wp-image-12225 aligncenter" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/Wordle.jpg" alt="" width="535" height="392" /> 
 
This image shows the heritabilty of several diseases; the font size is proportional to the heritability of the disease. Celiac disease, for instance, is highly heritable, whereas lung cancer is much less heritable.  Click on the chart to see a larger version. (Source: Chuong Do, unpublished manuscript)
What can you blame for those extra pounds, your great grandma Bertha’s obesity or that extra bowl of ice cream? “Nature” and “nurture” are commonly pitted against each other in discussions on genetics, but for most disease, both play a contributing role. In any population, individuals vary in their propensity for developing a given disease.  The proportion of this variation in the population that can be explained by genetics is known as “heritability.”

<div style="width: 250px; background-color: #ffc; border: 2px solid #ccc; padding: 10px; margin-left: 15px; float: right; font-size: 11px;">Q: Among Europeans, which disease is the least heritable? 
A: Bladder cancer. The heritability of bladder cancer is approximately 7%, suggesting that environmental factors contribute much more to variations in risk for this disease than genetics.</div>
Heritability estimates vary considerably across common diseases.  For instance, celiac disease is highly heritable, meaning that the variability in the disease is mostly due to genetic differences. Other diseases are less heritable, such as lung cancer; the variability in this disease may be more correlated with non-genetic risk factors (e.g., smoking habits, diet, air pollution, etc.) than with genetic differences.
<div style="width: 250px; background-color: #ffc; border: 2px solid #ccc; padding: 10px; margin-left: 15px; float: right; font-size: 11px;">Q: True or false? Schizophrenia is over 50% heritable. This means that your genes play a bigger role in whether you will develop schizophrenia than your environment. 
A: False. Heritability describes the extent to which genetics explains variations in risk across a population, but does not explain the genetic contribution towards risk for an individual, for whom specific genetic or non-genetic factors may play a bigger role.</div>
Heritability is a complex concept, and not surprisingly, is often misinterpreted. The most common misconception is that heritability describes the relative importance of genetics and environment for a specific individual. While useful at the population level, heritability actually doesn’t mean much at the individual level. For example, IQ is a highly heritable, but one can’t assume that a child born to parents of high IQ will also have a high IQ without factoring in the extremely important role played by his or her upbringing. As another example, breast cancer is estimated to have relatively low heritability (less than 33%), yet for a woman carrying a rare mutation in the BRCA1 or BRCA2 genes, knowledge of this single genetic factor will often have a substantially greater significance for her breast cancer risk than any known environmental factor.
<div style="width: 250px; background-color: #ffc; border: 2px solid #ccc; padding: 10px; margin-left: 15px; float: right; font-size: 11px;">Q: True or false? Ovarian cancer has a relatively low heritability of about 20%. This means there are no genetic mutations that greatly increase the risk of developing ovarian cancer. 
A: False. Genetic factors may play a relatively small role in ovarian cancer risk for the general population, but there may still be rare genetic factors that contribute greatly to a woman&#8217;s risk for the disease.</div>
Another misconception is the idea that a disease that is highly heritable must be determined by only a few genes that have a strong effect. Some diseases, such as cystic fibrosis, can be attributed solely to mutations in a single gene; this, however, is not always the case. The high heritability of schizophrenia, for example, is often believed to result from the contributions of many, many genes, each with small impact on disease risk.  A person could harbor lots of risk-predisposing variants for schizophrenia, yet still not have the disease.
<div style="width: 250px; background-color: #ffc; border: 2px solid #ccc; padding: 10px; margin-left: 15px; float: right; font-size: 11px;">Q: True or false? The heritability of a disease can change over time and from population to population. 
A: True. Heritability can differ depending on which population you&#8217;re looking at, and can change over time as the environment changes.</div>
Finally, many people assume that heritability for a given condition is constant across populations and over time.  In reality, heritability can be highly population dependent, and can change as the environment changes. For instance, height depends on both nutrition and genetics. In societies where nearly all children receive comparable nutrition, only genetic factors vary between individuals, so height appears highly heritable.  But in societies with greater economic disparities, height differences correlate more strongly with nutrition, resulting in lower heritability.
Although often misunderstood, heritability is a useful concept that can provide insights into the nature vs. debate.  More importantly, the low heritability of many diseases suggests that our collective disease destiny is only partially determined by our genes. You can’t change your DNA, but you can change your ice cream to frozen yogurt.
<div style="border: 1px solid #000; padding: 5px; font-style: italic; margin-bottom: 15px;">To learn more about the technical aspects of heritability, see <a href="https://www.ncbi.nlm.nih.gov/pubmed/18319743" target="_" rel="noopener">this 2008 article</a> published in Nature Reviews Genetics by Peter Visscher and colleagues. You can also learn about your personalized genetic risk for many of these conditions by visiting “My Health” in your 23andMe account. Not yet a customer? Visit our <a href="https://www.23andme.com/store/cart/" target="_" rel="noopener">store</a> or <a href="https://www.23andme.com" target="_" rel="noopener">learn more</a>.</div>
<img loading="lazy" decoding="async" class="size-large wp-image-12225 aligncenter" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/HeritabilityWithKids.jpg" alt="" width="535" height="392" /> 
 
Heritability estimates from the scientific literature are typically based on twin studies and vary widely across diseases, as illustrated in the chart above.   Click on the chart to see a larger version. 
(Source: Chuong Do, unpublished manuscript).

Quiz Answers: Heritability Demystified

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-6465" title="Tummy Time!" src="https://blog-api.23andme.com/wp-content/uploads/2010/04/iStock_000001348449XSmall-300x199.jpg" alt="" width="300" height="199" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/04/iStock_000001348449XSmall-300x199.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2010/04/iStock_000001348449XSmall.jpg 425w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Nature vs. nurture is a question scientists and non-scientists alike have grappled with since the earliest days of human history. One concept we use to describe these two complementary forces is &#8220;heritability&#8221;, or the proportion of variation in the development of a disease or trait in a population that&#8217;s due to genetics.
While this sounds simple, there are some nuances to heritability that often cause it to be misinterpreted. Show us what you know about heritability in this week&#8217;s quiz!
<a title="Quiz Answers: Heritability Demystified" href="https://blog.23andme.com/articles/quiz-answers-heritability-demystified">This quiz is now closed. See the answers here!</a>

What Do You Know About Heritability?

<img loading="lazy" decoding="async" class="alignright size-full wp-image-2610" title="friendwheel2" src="https://blog-api.23andme.com/wp-content/uploads/2009/01/friendwheel2.jpg" alt="" width="300" height="290" />
If Facebook is starting to take over your life, maybe your genes are partly to blame.
Researchers from UC San Diego and Harvard University have shown that certain aspects of a person’s social network — how many people consider that person a friend, the likelihood that two of a person’s friends are themselves friends, and how central a person is to their network of friends — have a genetic basis.
<h6>Genetics of Social Interactions</h6>
The results, published online yesterday in the <a href="https://www.pnas.org/content/early/2009/01/26/0806746106.abstract" target="_blank" rel="noopener">Proceedings of the National Academy of Sciences</a>, have led to the development of a new model of social interactions and could someday help scientists understand how diseases and traits like obesity, smoking and happiness spread through a population.
James Fowler, Christopher Dawes and Nicholas Christakis studied the social networks of 1,110 sets of twins from 142 separate school friendship networks and compared the similarity in friendship patterns between identical twins, who share 100% of their genes, and same-sex fraternal twins, who share about 50% of their genes.
<h6>Twins</h6>
The assumption of this type of study is that if genetic variation contributes to variation in a trait, then pairs of identical twins will be more similar to each another with respect to that trait compared to pairs of fraternal twins.
The researchers found that three measures of connectedness are heritable:
<ol>
<li>How many times a person is named as a friend</li>
<li>The likelihood of a person’s friends also being connected to each other directly</li>
<li>The tendency of a person to be along the shortest path between pairs of their friends</li>
</ol>
The number of friends people say they have, however, did not appear to have a genetic basis.
<h6>Attract and Introduce</h6>
The researchers then created a large number of simulations based on existing ideas about how human social networks form. When they observed that none of these simulated networks exhibited the same kind of heritability they saw in their real human networks, they invented a simple model they dubbed “Attract and Introduce.”
A model is simply a mathematical system that attempts to reproduce something seen in the real world based on a limited number of inputs. Every “person” in the Attract and Introduce model of social networks is given just two characteristics — a certain amount of attractiveness, which will determine how many friend nominations he or she will receive, and a certain a propensity for making introductions between new and existing friends, which will determine the number of friends who are friends with each other.
The heritability predictions produced by the Attract and Introduce model fit well with what was seen in the twin study. This suggests that their model may capture important features of how real human social networks form that existing models do not.
“There may be many reasons for genetic variation in the ability to attract or the desire to introduce friends. More friends may mean greater social support in some settings or greater conflict in others. Having denser social connections may improve group solidarity, but it might also insulate a group from beneficial influence or information from individuals outside the group,” the authors write.
Although more research will be needed to explore whether the findings in this study and the model developed apply to all people regardless of age, geography or other factors that could affect the interactions between people, this type of research has important implications. Understanding how people come together and interact could be used to predict or control the spread of communicable disease. The authors also note that their own previous research has shown that obesity, smoking behavior, happiness, and even political behavior spread in social networks.
“A full understanding of these traits may require a better understanding of the genetic basis of social network topology,” they suggest.

heritability