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

The opioid crisis presents a public health emergency without clear solutions. One key to unraveling the problem is understanding not just the causes of addiction, but understanding the steps taken leading people toward addiction.
A new genetic study by a team of scientists at UC San Diego School of Medicine proposed a cost-effective approach for studying the genetic basis of opioid addiction — termed “opioid use disorder” in the study — in large population-based cohorts instead of clinical cohorts.
Published in the journal<a href="https://t.umblr.com/redirect?z=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41380-021-01335-3&amp;t=OTRiN2RkZjZkNzY4MmI1NTliNDE0N2JmZDRiOTUxOTE0YTNhNTZhYSwwUFJVaEliQw%3D%3D&amp;b=t%3AP0Uz1DUMutRMdlhoe0mDtg&amp;p=https%3A%2F%2Fucsdhealthsciences.tumblr.com%2Fpost%2F666758608951934976%2Fgenetic-signals-linked-to-problematic-opioid-use&amp;m=0&amp;ts=1635872583"> Molecular Psychiatry</a>, the study was led by Sandra Sanchez Roige, Ph.D., and Abraham Palmer, Ph.D.
Using data from more than 132,000 23andMe customers who consented to participate in research, the study is important because it focused on the opioid misuse that can lead to opioid use disorder. In past decades opioid addiction started with heroin, but in this new era more than 80 percent of opioid addiction begins with the use of a prescription pain reliever, according to the study.
So, for this study, the researchers performed a genome-wide association study looking simply at participants reporting that&nbsp; they had ‘ever taken prescription painkillers not as prescribed.’ Essentially the researchers identified those in the first step toward from use to misuse of opioids, as a way to study the genetic underpinnings of the condition.
“Our results show that this single question captured a genetic signal that is correlated with signals from well-characterized cohorts that have been clinically diagnosed with (opioid use disorder.)”
The UC San Diego team discovered novel genomic regions that influenced using opiate drugs not as prescribed. They also identified strong genetic correlations with other substance use traits, including opioid use disorder.
Read the full study in<a href="https://t.umblr.com/redirect?z=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41380-021-01335-3&amp;t=OTRiN2RkZjZkNzY4MmI1NTliNDE0N2JmZDRiOTUxOTE0YTNhNTZhYSwwUFJVaEliQw%3D%3D&amp;b=t%3AP0Uz1DUMutRMdlhoe0mDtg&amp;p=https%3A%2F%2Fucsdhealthsciences.tumblr.com%2Fpost%2F666758608951934976%2Fgenetic-signals-linked-to-problematic-opioid-use&amp;m=0&amp;ts=1635872583"> Molecular Psychiatry</a>.

Understanding Opioid Use Disorder

Some of the same genes that influence a person’s propensity toward impulsiveness also affect whether or not he or she will use drugs, according to a new study led by researchers at the University of California, San Diego School of Medicine.
&nbsp;
Published today in the <a href="https://www.jneurosci.org/lookup/doi/10.1523/JNEUROSCI.2662-18.2019">Journal of Neuroscience</a>, the study is another in a series of studies done by researchers looking at the genetic underpinnings of behavior, addiction, and psychological disorders. For this work the scientists used data from more than 20,000 23andMe customers who consented to participate in research, making it the largest genetic study of impulsive behavior to date.
<h6>Behavior</h6>
“By studying the genetic basis of normal variation in behavior, we can learn about the role of genetics in complex psychiatric disorders like drug abuse,” said lead author of the study <a href="http://profiles.ucsd.edu/abraham.palmer">Abraham Palmer, Ph.D</a>., a professor of psychiatry and vice chair for basic research at the University of California, San Diego School of Medicine. “Additional studies of younger and more diverse populations could provide additional insights into the genetics and consequences of impulsiveness.”
<div id="attachment_25919" style="width: 209px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-25919" src="https://blog-api.23andme.com/wp-content/uploads/2017/12/Abraham-Palmer-photo-199x300.jpg" alt="" class="size-medium wp-image-25919" width="199" height="300" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/12/Abraham-Palmer-photo-199x300.jpg 199w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/12/Abraham-Palmer-photo-768x1156.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/12/Abraham-Palmer-photo-680x1024.jpg 680w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/12/Abraham-Palmer-photo-585x880.jpg 585w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/12/Abraham-Palmer-photo-784x1180.jpg 784w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2017/12/Abraham-Palmer-photo.jpg 1063w" sizes="auto, (max-width: 199px) 100vw, 199px" />Prof. Abraham Palmer</div>
For this work, and a study Palmer and his team did last year that also looked at another measure of impulsivity called <a href="https://blog.23andme.com/23andme-research/wait-new-genetic-research-impulsivity/">“delay discounting,”</a> the researchers compared genetic data with survey responses on impulsivity and a history of drug use from 23andMe customers who consented to participate in research. The genome-wide association study found variants in the gene CADM2 — previously implicated in risk-taking, alcohol consumption, and cannabis use — associated with impulsivity and drug use. The team also identified an association with a variant in a gene previously implicated in schizophrenia risk — CACNA1I. They also saw an association with something called “negative urgency”— a tendency to act impulsively in the face of adversity.
&nbsp;
<h6>Big Data</h6>
These findings demonstrate how an individual’s genetic makeup may predispose them to engage in risky behavior, including drug use and abuse. Additional studies of younger and more diverse populations could provide further insights into the genetics and consequences of impulsive personality traits, the researchers said.
&nbsp;
The study also shows the potential of large datasets like 23andMe.
&nbsp;
&#8220;Data shared by 23andMe research participants helped make this work possible &#8212; and this is one of several recent publications we&#8217;ve worked on related to personality, behavior and psychiatric conditions,” said Sarah Elson, PhD, Senior Scientist, 23andMe.
“These findings may have potentially significant effects on how we interpret the relationships between genetics and mental health; and, in the future, predict and treat some of these hard-to-understand conditions.&#8221;

Genetic Study of Impulsiveness Reveals Associations with Drug Use

A new genetic study looking at smoking and drinking has confirmed much of what we already know about their impact on your health, but the study also found genetic associations that offer new insights into alcohol and tobacco use, as well as addiction.<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2019/01/Smoking-image-2-300x201.jpg" alt="" class="alignright size-medium wp-image-26841" width="300" height="201" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/01/Smoking-image-2-300x201.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/01/Smoking-image-2-768x514.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/01/Smoking-image-2-1024x685.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/01/Smoking-image-2-880x589.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/01/Smoking-image-2-1180x790.jpg 1180w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2019/01/Smoking-image-2.jpg 1252w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Published this week in the journal<a href="http://dx.doi.org/10.1038/s41588-018-0307-5"> Nature Genetics</a>, the study is one of the largest genome-wide association studies to date, using data from more than 1.2 million people. Researchers working on this study found more than 500 genetic variants associated with smoking and alcohol use, including newly identified genetic associations that link alcohol and tobacco use with the release of dopamine in the brain. Dopamine plays an essential role in reward-based behavior, and the finding may help researchers better understand why quitting smoking or problem drinking is more difficult for some than it is for others.
<h6>Smoking, Drinking and Disease</h6>
The study also showed that tobacco use was closely associated with a range of diseases — not just lung cancer. While that was not unexpected, the researchers were surprised that social drinkers — those who drank a moderate amount of alcohol each week — had fewer illnesses. This adds more fodder to the debate around whether moderate drinking may be beneficial to one’s health. Of course, there may be other explanations for this; for example, individuals who are more open and extraverted may be more likely to be social drinkers, and individuals with outgoing personalities may have better outcomes than those who are more anxious and less social, who in turn may be less likely to drink.
Much of the data for this study came from 23andMe customers who consented to participate in research and answered survey questions about smoking and drinking. The remaining data came from more than two-dozen other study cohorts. Led by researchers at the University of Minnesota, the work on this study also involved contributions from dozens of other scientists from institutions that are part of<a href="https://gscan.sph.umich.edu/"> GWAS &amp; Sequencing Consortium of Alcohol and Nicotine Us (GSCAN)</a>.
<h6>Other Studies</h6>
This is one of several genetic studies published in the last few months to look at addictive behavior, including alcohol and nicotine use. In November, a team of researchers<a href="https://blog.23andme.com/23andme-research/new-research-shows-shared-genetic-link-between-alcohol-dependence-and-psychiatric-disorders/"> found shared genetic influences</a> between alcohol dependence and depression, ADHD, and schizophrenia. They also looked at genetic correlations between alcohol dependence and individual traits, like nicotine addiction, depression, and BMI. That study also found a distinct difference between casual alcohol consumption and heavier alcohol use, suggesting that social drinking is not associated with depression, but problem drinking and alcoholism are.
Another study on<a href="https://blog.23andme.com/23andme-research/the-genetics-of-alcoholism/"> alcohol dependence</a> published last fall also found genetic associations that overlapped with increased genetic risk for major depression, schizophrenia, and attention-deficit/hyperactivity disorder.
The GSCAN study published this week adds to these previous findings, offering more information to better understand the genetics of substance use and addiction.
You can find the paper in<a href="http://dx.doi.org/10.1038/s41588-018-0307-5"> Nature Genetics</a>.

Genetic Study of Nicotine and Alcohol Use Offers Insight into Addiction

The latest episodes of<a href="https://www.iheart.com/podcast/1119-spit-29676456/"> Spit</a>, iHeartRadio’s podcast with 23andMe, includes more intelligent and raw conversations with artists, thinkers, and scientists across a variety of topics. This next batch of episodes take a different turn looking at the influence of genetics and personal experiences around emotional wellbeing, addiction, and family.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-26715" src="https://blog-api.23andme.com/wp-content/uploads/2018/11/Spit-Podcast-300x168.jpg" alt="" width="300" height="168" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/Spit-Podcast-300x168.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/Spit-Podcast.jpg 512w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Hosted by the writer, comedian and cultural critic,<a href="http://baratunde.com/"> Baratunde Thurston</a>, the podcast continues to probe into the ways genetic science is changing how we see the world and the issues many of us wrestle with every day. And the show stays true to its fearless march into difficult territory with conversations that attempt to break the stigma around mental health and addiction.
<div id="attachment_26712" style="width: 1034px" class="wp-caption aligncenter"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-26712" class="wp-image-26712 size-large" src="https://blog-api.23andme.com/wp-content/uploads/2018/11/0022_WesandAlex_SpitPodcast_NikkiSixx-1024x682.jpg" alt="" width="1024" height="682" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/0022_WesandAlex_SpitPodcast_NikkiSixx-1024x682.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/0022_WesandAlex_SpitPodcast_NikkiSixx-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/0022_WesandAlex_SpitPodcast_NikkiSixx-768x512.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/0022_WesandAlex_SpitPodcast_NikkiSixx-880x587.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/0022_WesandAlex_SpitPodcast_NikkiSixx-1180x786.jpg 1180w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/0022_WesandAlex_SpitPodcast_NikkiSixx.jpg 2000w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />Spit podcast host Baratunde Thurston, left, with addiction specialist Dr. Adi Jaffee, Ph.D., center, and Mötley Crüe bassist Nikki Sixx.</div>
<h2>All About Addiction</h2>
Baratunde’s frank discussion<a href="https://itunes.apple.com/us/podcast/id1422827494"> about addiction</a> with former Mötley Crüe bassist Nikki Sixx, and Adi Jaffe, Ph.D., an addiction specialist, and author, gets personal fast. Both men share their own stories of troubled childhoods, and falling into addiction, and they hash out the many ways both nature and nurture contribute to addictions. Sixx kicked a punishing addiction to heroin while Jaffe, who also lectures at UCLA, once had drug problems of his own.
While the first part of the conversation touches on the science, Baratunde takes things deeper into the biology of addiction during the second part of this podcast by engaging with two academics from UC San Diego, School of Medicine’s Department of Psychiatry —<a href="https://profiles.ucsd.edu/Abraham.Palmer"> Abraham Palmer</a>, Ph.D., and Sandra Roige, Ph.D. Palmer and Roige have recently published papers using data from 23andMe that offered insight into addiction, most recently on<a href="https://blog.23andme.com/23andme-research/the-genetics-of-alcoholism/"> alcoholism</a>, and before that on something called<a href="https://blog.23andme.com/23andme-research/wait-new-genetic-research-impulsivity/"> “delay discounting”</a> — a tendency to overvalue immediate rewards over future ones, which is also associated with impulsivity and addiction. The researchers emphasize that genetics is not deterministic and environment plays a critical role in addiction, but genetics matters too. It matters not just in one’s tendency toward addiction, but also in how someone’s body reacts to alcohol or drugs, or a person’s tolerance or their inability to quit.
<h2>Mental Health Awareness</h2>
For the podcast on mental health, Baratunde sits down with<a href="https://drgailsaltz.com/"> Gail Saltz, Ph.D</a>., a professor of psychiatry and a psychoanalyst, and singer and songwriter<a href="http://www.mikeshinoda.com/"> Mike Shinoda</a> of the band<a href="https://linkinpark.com/"> Linkin Park</a>. Shinoda has become an advocate for mental health awareness after the death of his close friend and Linkin Park bandmate Chester Bennington, who died last year of an apparent suicide. Shinoda poignantly asks Dr. Saltz:
“Is there more we can do? And if so, how?”
<div id="attachment_26710" style="width: 1034px" class="wp-caption aligncenter"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-26710" class="wp-image-26710 size-large" src="https://blog-api.23andme.com/wp-content/uploads/2018/11/5A5A8705-1024x688.jpg" alt="" width="1024" height="688" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/5A5A8705-1024x688.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/5A5A8705-300x202.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/5A5A8705-768x516.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/5A5A8705-880x591.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/5A5A8705-1180x793.jpg 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />On the left, Professor Gail Saltz, PhD, with Baratunde Thurston, center, and Mike Shinoda of the band Linkin Park.</div>
During their conversation with Baratunde, Saltz and Shinoda talk about combating the stigma of mental illness, and resources for those battling depression or helping others in a mental health crisis. Together they explore some of the genetic and environmental factors that influence anxiety, depression and other behavioral issues. 23andMe has been working on a study on the genetics of<a href="https://www.23andme.com/depression-bipolar/"> major depression and bipolar disorder</a>. In August of 2016, researchers from 23andMe, Massachusetts General Hospital, and Pfizer, published<a href="https://www.washingtonpost.com/news/to-your-health/wp/2016/08/01/large-dna-study-using-23andme-data-finds-15-sites-linked-to-depression/"> a landmark study</a> on the genetic connection between genetics and depression. The study, the largest of its kind to date, identified 15 genetic regions that were linked to depression, but the work is ongoing.
<h2>We Are Family</h2>
In the podcast on family, the conversation takes a lighter turn as Baratunde poses the question of whether people would be more unified if they understood we are all “related.”
<div id="attachment_26711" style="width: 1034px" class="wp-caption aligncenter"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-26711" class="wp-image-26711 size-large" src="https://blog-api.23andme.com/wp-content/uploads/2018/11/KatherineTyler_DarrenCriss_SpitPodcast_2018-8831-1024x683.jpg" alt="" width="1024" height="683" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/KatherineTyler_DarrenCriss_SpitPodcast_2018-8831-1024x683.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/KatherineTyler_DarrenCriss_SpitPodcast_2018-8831-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/KatherineTyler_DarrenCriss_SpitPodcast_2018-8831-768x512.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/KatherineTyler_DarrenCriss_SpitPodcast_2018-8831-880x587.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/KatherineTyler_DarrenCriss_SpitPodcast_2018-8831-1180x787.jpg 1180w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/11/KatherineTyler_DarrenCriss_SpitPodcast_2018-8831.jpg 1200w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />From left to right Darren Criss, his brother Chuck, writer AJ Jacobs and Spit podcast host Baratunde Thurston. Photo: Katherine Tyler for iHeartRadio</div>
For this discussion he sat down with<a href="https://ajjacobs.com/"> AJ Jacobs</a>, a humorist and the author of the book “It’s All Relative,” along with the brothers Darren and Chuck Criss of the band Computer Games. Jacobs, who is a friend of 23andMe, talked about trying to create a global family tree to illustrate how we are all related. A few years ago he helped organize a “global family reunion,” and he talked about what he saw as the talked about one moment during the event when everyone at the event and those tuning in online started singing the song, “We Are Family.”
“It was quite moving,” he said.
The Criss brothers talked about their own family, and not really connecting with their distant relatives until they were older. But they also talk about how they feel family-like connections to many of those with whom they work, connections that have nothing to do with genetics.
“We are surrounded by people in our lives we consider cousins,” said Darren. “They feel closer to us than blood family.”
You can find these or any of the<a href="https://www.iheart.com/podcast/1119-spit-29676456/"> Spit</a>, podcasts at <a href="https://www.iheart.com/podcast/1119-spit-29676456/">iHeart</a>, or on <a href="https://itunes.apple.com/us/podcast/spit/id1422827494?mt=2">iTunes</a>.

Spit, The Next Installment

By Amick B.
<img loading="lazy" decoding="async" class="aligncenter wp-image-18399 size-full" src="http://35.88.189.111/wp-content/uploads/2013/06/mug_drinking.png" alt="" width="507" height="407" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2013/06/mug_drinking.png 507w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2013/06/mug_drinking-300x241.png 300w" sizes="auto, (max-width: 507px) 100vw, 507px" />
There are many studies that look at the health impacts of drinking coffee, but you’d be forgiven if you weren’t clear about whether it’s good for you.
Research has found consuming coffee could potentially prevent heart disease, type-2 diabetes, Parkinson’s disease and liver cancer, but the results are often conflicting. Beyond that, other variables can potentially negate any benefits from drinking a cup of Joe.
<h6>Variables</h6>
Whether you like your coffee black or with a bit of cream and sugar, for example, makes a difference for your health.
How much you drink and even the kinds of filters you use to make coffee could also have an impact.
All the conflicting information is enough to keep non-coffee drinkers from lining up at Starbucks, while those who indulge are left scratching their heads about whether they need to cut back or keep on imbibing.
<h6>Love Coffee</h6>
But there’s one area where the science seems certain:   Some of us are just more genetically wired to like coffee. A number of studies have identified certain genetic variants associated with <a href="http://www.23andme.com/topics/wellness/caffeine-consumption/">caffeine consumption</a> and metabolism, which helps us know why some of us choose coffee, and others don’t.
Recently, a <a href="https://www.ncbi.nlm.nih.gov/pubmed/21876539" target="_blank" rel="noopener noreferrer">new study</a> found some additional genetic variants associated with a tendency toward java enjoyment, including one near NRCAM, a gene implicated in vulnerability to addiction.   The study looked at nearly 8,000 Caucasian coffee drinkers and found significant evidence of gene association at the single nucleotide polymorphism (SNP) near NRCAM.
Using coffee consumption as a model, this new research may help scientists better understand genetic problems with addiction and how to treat them.
<h6>Metabolizing Caffeine</h6>
The recent study also looked at two SNPs that lie in the region between CYP1A1 and CYP1A2 genes — CYP1A1 is known to metabolize polycyclic aromatic hydrocarbons, which are important constituents of coffee, whereas caffeine is primarily metabolized by CYP1A2. The study confirmed previous studies and added a new SNP, to the list of those associated with consumption of coffee and metabolism of caffeine.
23andMe looks at a variant that affects how quickly a person  metabolizes caffeine based on preliminary research of the SNP. People with and the slower version of the CYP1A2 enzyme who also drank at least two to three cups of coffee per day had a significantly increased risk of a non-fatal heart attack, according to the research, while, according to the study, fast metabolizers could actually reduce their heart attack risk by drinking coffee.
<h6>A Look Back</h6>
Additionally, in a 2011 blog post, 23andMe discussed <a href="https://blog.23andme.com/23andme-research/snpwatch/coffee-i-must-have-coffee/">two studies</a> that found an association between coffee and caffeine consumption and SNP variants near the CYP1A1 and AHR genes, helping us know which genes influence the amount of coffee people consume.   One study found the SNP near CYP1A1 had a fairly consistent effect – people with the T version were prone to drink about a quarter cup more of coffee a day — and the other showed that people with two copies of a T at near the AHR gene drank  about a third of a cup of coffee more each day than those without any copies.
To find out whether genetic variants influence their caffeine consumption, 23andMe customers can look up their data for and using the Browse Raw Data feature.
Amick Boone is a freelance writer who&#8217;s written about health and life sciences for nearly 10 years.  When she&#8217;s not at her computer, she&#8217;s usually in motion &#8211; doing yoga, riding her bike or traveling.

Craving Coffee Might be Genetic

<img loading="lazy" decoding="async" class="alignright size-full wp-image-4551" title="iStock_000005457151XSmall" src="https://blog-api.23andme.com/wp-content/uploads/2009/09/iStock_000005457151XSmall.jpg" alt="iStock_000005457151XSmall" width="346" height="229" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2009/09/iStock_000005457151XSmall.jpg 425w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2009/09/iStock_000005457151XSmall-300x199.jpg 300w" sizes="auto, (max-width: 346px) 100vw, 346px" />
Although environment plays a major part in addiction – you can&#8217;t get hooked on something you&#8217;ve never tried – genetics plays a substantial role in determining whether a person who does use a drug will become addicted to it.
A few DNA variations have been identified that seem to increase the odds a person will become addicted to a specific drug. But <a href="https://www.ncbi.nlm.nih.gov/pubmed/10401514" target="_blank" rel="noopener noreferrer">twin studies suggest</a> that there might be genes influencing addiction in general.
Xiang Chen and colleagues at Yale and Princeton set out to find some of these genes by analyzing the genetic data from several cohorts of people previously studied for addictions. &nbsp; The researchers&#8217; approach was to look for variations found more frequently in people addicted to at least two out of six categories of substances: nicotine, alcohol, marijuana, cocaine, opiates and other drugs. &nbsp; Their results, published online this week in the Proceedings of the National Academy of Sciences, reveal a significant association between addiction and variations in a gene, PKNOX2, previously associated with alcohol dependence in mice.
The strongest signal was seen with in white women was found at a SNP inthe PKNOX2 gene and was associated with a higher risk for addition. The association of with addiction did not hold when the researchers looked at individual substances separately.
&#8220;This suggests that substance dependence or addiction as a whole has different risk genes compared to any single addiction outcome,&#8221; the authors write.
The authors admit that there are weaknesses in their study. &nbsp; For example, people addicted to two or more substances might just have more access to drugs – not a biological predisposition to addiction. &nbsp; Moe research in this area will definitely be needed.
SNPwatch gives you the latest news about research linking various traits and conditions to individual genetic variations. These studies are exciting because they offer a glimpse into how genetics may affect our bodies and health; but in most cases, more work is needed before this research can provide information of value to individuals. For that reason it is important to remember that like all information we provide, the studies we describe in SNPwatch are for research and educational purposes only. SNPwatch is not intended to be a substitute for professional medical advice; you should always seek the advice of your physician or other appropriate healthcare professional with any questions you may have regarding diagnosis, cure, treatment or prevention of any disease or other medical condition.
&nbsp;

Genetic Variation Associated With Addiction In Caucasian Women

<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

Some of the same genes associated with cannabis use are also associated with risk-taking personality types and psychiatric conditions like schizophrenia, according to a new large-scale genetic study.
&nbsp;
The <a href="https://www.nature.com/articles/s41593-018-0206-1">study</a>, conducted by a team of scientists who are part of the <a href="https://www.ru.nl/bsi/research/group-pages/substance-use-addiction-food-saf/vm-saf/genetics/international-cannabis-consortium-icc/">International Cannabis Consortium</a>, is the largest genome wide association study to date that looks at the use of cannabis.
&nbsp;
The researchers found that people who are at a higher genetic risk for schizophrenia are also more likely to use cannabis. The study also identified 35 different genes associated with cannabis use with the strongest associations in the gene CADM2.
&nbsp;
“CADM2 has already been associated with risky behaviour, personality and alcohol use,” said Jacqueline Vink of <a href="https://www.ru.nl/bsi/">Radboud University</a>, and the study’s lead author.
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2018/08/Cannabis-use-1024x683.jpg" alt="" class="aligncenter size-large wp-image-26491" width="1024" height="683" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/08/Cannabis-use-1024x683.jpg 1024w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/08/Cannabis-use-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/08/Cannabis-use-768x512.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/08/Cannabis-use-880x587.jpg 880w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2018/08/Cannabis-use-1180x787.jpg 1180w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />For this study, the researchers were able to look across more than a million genetic variants and found a genetic overlap between cannabis use and the use of tobacco and the use of alcohol. The researchers also saw an overlap between a higher likelihood for the use of cannabis and an increased risk for schizophrenia. There was a similar overlap between cannabis use and personality types that were prone to more <a href="https://blog.23andme.com/23andme-research/genetics-associations-personality-traits/">risky behaviour</a> or were more extraverted. This means that genetic variants impacting cannabis use partially impact other psychological or psychiatric features as well, according to the researchers.
&nbsp;
For this study, the researchers used data primarily from the UK Biobank, as well as association data from 23andMe customers who consented to participate in research. On top of that data the researchers used data from individuals in 16 other smaller study cohorts. In all the study included data from more than 180,000 people. In all the researchers found 35 genes associated with cannabis use, offering more insight into the genetic influences on personality types. The team of researchers was lead by Prof. Vink of Radboud University, and included contributions from researchers at QIMR Berghofer Medical Research Institute in Australia, as well as scientists at Virginia Commonwealth University, and 17 different research groups from Europe, North America and Australia.
The study showed that the genes increasing the risk of cannabis use partially increase the risk of schizophrenia as well. The researchers used an analysis technique called &#8220;Mendelian randomisation&#8221; to show a causal relationship between a genetic predisposition for schizophrenia and an increased risk of cannabis use. This may indicate that people with schizophrenia use cannabis as a form of self-medication. However, the researchers cannot exclude a reverse cause-and-effect relationship, meaning that a genetic predisposition for cannabis could contribute to the risk of schizophrenia.
&nbsp;
The team that worked on this study are already starting to explore which genes play a role in the frequency of cannabis use and the amount of cannabis used.
&nbsp;
.

Scientists Identify Genes associated with Cannabis Use

Up until recently, genetic research on personality has yielded few results, but that has changed with the availability of massive datasets for <img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2014/09/iStock_000015521781Small-300x199.jpg" alt="" class="alignright wp-image-21718 size-medium" width="300" height="199" />genome-wide association studies.
In a series of papers published since mid-2016, scientists have established promising new findings that rely on vast amounts of data from the likes of the the<a href="http://www.ukbiobank.ac.uk/"> UK Biobank</a>, the international<a href="http://www.med.unc.edu/pgc"> Psychiatric Genomics Consortium</a>, and 23andMe.
By conducting genome wide association studies — or meta-analyses — with data from hundreds of thousands of people, researchers have found genetic associations where they could not before. In the last year alone, they’ve found associations for such traits as <a href="https://www.nature.com/nature/journal/v533/n7604/full/nature17671.html">educational attainment,</a> depressive symptoms, <a href="https://www.nature.com/ng/journal/v48/n6/full/ng.3552.html">neuroticism</a>, and <a href="https://www.nature.com/ng/journal/v48/n6/full/ng.3551.html?foxtrotcallback=true">risk-taking behavior</a>. 
The success on these fronts has opened up the hunt for more genetic signals associated with psychological and behavioral traits. Scientists are also doubling back on the research over the last year attempting to replicate the findings — when replication was not conducted in the initial study — to ensure the associations are valid. 
<h5>The Big Five</h5>
In July, scientists from St. Louis University, the University of Cambridge and 23andMe zeroed in variants in two genes, CADM2 and MSRA, found to be associated with personality, specifically risk-taking behavior and irritability. The gene CADM2 is important in organizing the synapses in the brain, while MSRA encodes a family of enzymes in the body.
By going back and conducting a replication study, the researchers were also able to broaden the range of traits they looked at, and include additional personality traits beyond the so-called “Big Five” —neuroticism, extraversion, openness, agreeableness, and conscientiousness. 
For this <a href="https://www.sciencedirect.com/science/article/pii/S2405844017317346?_rdoc=1&#038;_fmt=high&#038;_origin=gateway&#038;_docanchor=&#038;md5=b8429449ccfc9c30159a5f9aeaa92ffb">replication study</a>, researchers included 19 additional measures to more fully describe the Big Five, adding in data for such things as anxiety, risk-taking, order, altruism, and self-discipline.
The study replicated the associations with a variant in the CADM2 gene for risk-taking, agreeableness, and extraversion. The researchers were also able to replicate the variant in the MSRA gene associated with irritability.
While both exciting and promising, the new findings are also tempered by the hurdles faced by genetic research in general. Just finding the associations is not enough — researchers are still trying to learn more about the genetic architecture and biological mechanisms underlying these complex traits. Also, these associations often have a small effect on the traits. But the findings suggest that with even larger sized studies may offer more insight.
You can read the full replication paper <a href="https://www.sciencedirect.com/science/article/pii/S2405844017317346?_rdoc=1&#038;_fmt=high&#038;_origin=gateway&#038;_docanchor=&#038;md5=b8429449ccfc9c30159a5f9aeaa92ffb">here</a>.

Research Confirms Genetic Associations For Personality Traits

Researchers have identified genes that influence both the risk for schizophrenia and the development of certain personality traits.<img loading="lazy" decoding="async" class="alignright wp-image-21718 size-medium" src="http://35.88.189.111/wp-content/uploads/2014/09/iStock_000015521781Small-300x200.jpg" alt="" width="300" height="200" srcset="https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2014/09/iStock_000015521781Small-300x200.jpg 300w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2014/09/iStock_000015521781Small-768x511.jpg 768w, https://blog.pub.us-west-2.prd.23andme.us/wp-content/uploads/2014/09/iStock_000015521781Small.jpg 849w" sizes="auto, (max-width: 300px) 100vw, 300px" />
The work published late last month in the journal <a href="https://www.nature.com/articles/s41598-017-02346-3">Scientific Reports</a>, a Nature Research publication, follows on a study published late last year by the same group of scientists that identified six loci associated with personality traits.
<h2>Correlations with Personality Traits</h2>
That study found correlations between those traits and psychiatric disorders. Still, the work published this week confirms that there is more than just a correlation between certain personality traits and schizophrenia. There are genetic variants that influence both.
The findings also provide new insights into the genetic processes underlying schizophrenia and personality traits, according to the researchers.
The research is consistent with what scientists have suspected all along: that certain personality traits and psychological disorders are related and share some genetic influences. Studies in recent years have shown correlations between psychiatric disorders and personality traits—measured on a spectrum known as the “Big Five” that includes neuroticism, extraversion, openness, agreeableness, and conscientiousness.
<h2>Insights from Large Amounts of Data</h2>
While scientists have long believed that genetics plays a role in personality and the risk for mental illness, pinpointing which genes are involved has been difficult. In the past, the limited size of genome-wide association studies has stymied efforts to identify specific genetic variants associated with these conditions.
The breakthrough with these most recent studies is that researchers have used a meta-analysis to combine data from numerous sources and power their research with enormous data sets.
In this case, researchers used data from about 60,000 23andMe customers who consented to participate in the research and data from more than 80,000 individuals who are part of the Psychiatric Genomics Consortium (PGC) cohort.  The PGC unites investigators from around the world to study the genetics around psychiatric conditions such as bipolar disorder, major depressive disorder, and schizophrenia. The group has also become a sort of repository for data that can be used for these studies.
<h2>Neurotocism and Schizophrenia</h2>
The researchers working on this latest study found six genetic variants shared between schizophrenia and openness to new experiences.
They found three variants that influence both schizophrenia and the personality trait of neuroticism. Although these associations were found using a meta-analysis of the combined 23andMe and PGC data, the researchers also demonstrated that these results could be replicated in the individual cohorts..
“Altogether, our study provides new insights into the genetic architecture of schizophrenia and personality traits,” the researchers said in the paper. “The findings comply with accumulating evidence from genetics and neuroscience suggesting that mental disorders are not discontinuous with normal variation in neurobiological and behavioral dimensions.”
<h2>Learn More</h2>
You can read the paper at Scientific Reports <a href="https://www.nature.com/articles/s41598-017-02346-3">here</a>.

psychiatric conditions