<img loading="lazy" decoding="async" class="alignright size-medium wp-image-13375" title="macPC" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/macPC-300x239.png" alt="" width="300" height="239" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/macPC-300x239.png 300w, https://blogcms.23andme.com/wp-content/uploads/2012/05/macPC.png 541w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Last week we quizzed our readers on traits that differed between 23andMe customers who use Macs versus those who use Windows. Congratulations to Brenda, the winner of the quiz! She got all three answers correct and will receive a $25 Amazon gift card. So what were the correct answers? Read on…
Which of these personality traits is most strongly linked with being a Mac user? Openness.
If you had a tough time choosing which of these traits was most associated with being a Mac user, that’s totally understandable. All of them were. Yep, that’s right. Mac users were significantly more extraverted, assertive, full of ideas, and aesthetically-oriented, but where they most differed was on openness. Openness is a one of the so-called <a href="https://en.wikipedia.org/wiki/Big_Five_personality_traits">“Big Five” personality traits</a> (five aspects of personality thought to be found across all human cultures), and it’s linked with being curious, adventurous, unconventional, intellectual, and artistic. Does this confirm the stereotype, or just underscore the value of targeted marketing campaigns? We’ll let you decide.
Which is NOT true of Mac versus Windows users? About 40% of men are Mac users, but only 29% of women.
Actually, 39% of men are Mac users, and 38% percent of women. Definitely not a big difference! Of course, this means that all the other answers are true: Mac users were more likely to report being atheist or agnostic, more likely to drink alcohol, less likely to say they were exclusively attracted to the opposite sex, and more likely to have had braces. We thought the braces finding might be related to income, but Mac users were still significantly more likely to have had braces when we controlled for household income and childhood socioeconomic status.
Which of these is true? All of the above are true.
Mac users had significantly higher incomes, were more likely to have had mono (the so-called kissing disease), more likely to have taken medication to prevent malaria (perhaps a sign of adventurousness), and less likely to be politically conservative.
Do these differences jive with the <a href="http://flowingdata.com/2011/04/26/mac-vs-pc-people/">stereotypes of Mac and Windows users</a>? Leave a comment below and let us know!

23andMe Blog

23andMe Blog Team

Quiz Answers: Mac vs. Windows — Was Your Intuition Right?

By Meghan Mullins
Before joining 23andMe, I worked at a more traditional genetic research lab. Like virtually all research centers, we didn’t return genetic results to our research participants.
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-13288" title="CancerInfographic" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/CancerInfographic-300x254.jpg" width="300" height="254" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/CancerInfographic-300x254.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/05/CancerInfographic-768x650.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/05/CancerInfographic.jpg 849w" sizes="auto, (max-width: 300px) 100vw, 300px" />
I occasionally thought about what that meant, that I knew more about an anonymous stranger’s DNA than he or she ever would. &nbsp;These people had variants that scientists had never seen before, but the research participants would never learn of this.
Last fall I moved back to the Bay Area and joined the research team at 23andMe. I suddenly found myself in a completely different environment — not only do we return data to research participants, but they play an active role in the research process. &nbsp;23andMe partners with patients who work side-by-side with us to dramatically accelerate genetic discovery.
We recently launched a 23andMe Research Ambassador program, where research participants have volunteered to help more formally spread awareness of and expand our <a href="https://www.23andme.com/sarcoma/" target="_blank" rel="noopener">Sarcoma</a>,<a title="Myeloproliferative Neoplasms (MPN)." href="https://www.23andme.com/mpn/" target="_blank" rel="noopener"> Myeloproliferative Neoplasms (MPN)</a>, and <a href="https://www.23andme.com/pd/" target="_blank" rel="noopener">Parkinson’s &nbsp;</a> research initiatives. In honor of National Cancer Research Awareness month, we asked some of our newly minted Sarcoma and MPN Ambassadors to share their cancer stories.
Each of these ambassadors – Tracy, Ruth Ann, Natalie, Greg, and Cheryl-Anne – describe the uncertainty he or she faced when being diagnosed with a rare cancer. &nbsp;Tracy says her doctors at first did not know if her tumor “was a chondrosarcoma or a chordoma. &nbsp;Apparently [it was] one in a million.” &nbsp;For many, the simple lack of information available feels like hitting a wall. &nbsp;Ruth Ann joined our Sarcoma Community because “having been so discouraged in my own journey with the lack of information about sarcomas, I was more than willing to sign up to start a project that might provide some real answers.”
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<img loading="lazy" decoding="async" class="alignright size-medium wp-image-11373" title="researchrevolution-fist" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2012/02/researchrevolution-fist-173x300.jpg" width="173" height="300">
&#8211; Do you have sarcoma, or know someone who does? Learn how to join our <a href="https://www.23andme.com/sarcoma/">Sarcoma research community today</a>.
&#8211; Do you have an MPN, or know someone who does? Learn how to join our <a href="https://www.23andme.com/mpn/">MPN research initiative today</a>.
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Cheryl-Anne agrees, saying that “the more we know, the more we will be able to make sure the right patient gets the right drug at the right dose at the right time.” A sense of community and support also drew many to our research initiatives. &nbsp;Greg says that “connecting with others who have a similar interest in fighting sarcoma was my initial motivator in joining 23andMe.” &nbsp;When asked what advice he would give to someone who was just diagnosed, he said to “connect with others who have been in similar situations. &nbsp;Learn from their successes and mind their shortcomings.”
Our research Ambassadors also desire to look at the big picture when studying cancer risk. Greg notes that it’s currently unknown how different risk factors, like “radiation or chemical exposure, a virus or genetic factors,” interact to cause sarcomas. He wants “to help the scientists come closer to solving these questions.” &nbsp;Ruth Ann adds that “since it is so rare, there have to be many more factors than genetics alone that affect the occurrence of sarcoma. &nbsp;But, that doesn’t mean there isn’t a genetic component.” &nbsp;23andMe wants to learn more about those different factors, too, so we combine our genetic data with survey responses to study all aspects of cancer risk.
Cheryl-Anne has enjoyed exploring her own 23andMe data, saying that “it is fascinating to learn about myself, my own biology. &nbsp;This is me, my chromosomes, my DNA, and it helps me to make better choices for myself.” &nbsp;Natalie’s advice to someone else with an MPN is to “get a 23andMe spit kit. &nbsp;Find out your risks, and go back to your doctor and share that information. &nbsp;You learn a lot about yourself. . . I am very glad that I went through with that decision.”
Tracy was able “to provide the raw data to a genetic counselor for hereditary cancer testing for a condition called Ollie&#8217;s disease, where tumors mutate into sarcomas.” &nbsp;Ruth Ann has “enjoyed filling out the surveys, and getting the results about ordinary things. &nbsp;Who knew there was an asparagus pee gene?” &nbsp;We also make sure to share new discoveries with our research participants who helped us find them. &nbsp;Greg is grateful for 23andMe’s “sincere partnership in making strides to identifying the root cause of this life threatening disease.”
Scientists may have the best in technology and theory at their disposal, but they cannot move forward without research participants who are willing to give their time and energy to scientific pursuit. &nbsp;Natalie hopes that scientists and those with rare disease can “help each other, hand in hand.” &nbsp;I feel so incredibly lucky to interact with these generous individuals on a daily basis, to see their desire to give back so that others do not have to face the fear and uncertainty that they felt.
23andMe is intended for research and educational purposes only. &nbsp;23andMe’s services are not a substitute for professional medical or diagnostic advice.
Meghan Mullins is a research assistant at 23andMe and works with our Research Communities. Meghan studied Human Biology at Stanford University. She spent a few years studying the genetics of obesity and diabetes in the Pima Indians as part of a NIH Postbaccalureate Intramural Research Training program, and played a key role in a large sequencing project that discovered several variants of interest in the MC4R gene.

Meghan Mullins

23andMe Partnering with Patients

<img loading="lazy" decoding="async" class="alignright size-full wp-image-10815" title="Anne black and white" src="https://blog-api.23andme.com/wp-content/uploads/2012/01/Anne-black-and-white.jpg" alt="" width="110" height="166" />
[Ed: A clarifying addendum has been added to the end of this post. &#8211; 6/01/12]
23andMe has a substantial research arm with more than 20 scientists dedicated to making meaningful discoveries that will improve the lives of all of us.  We’ve made a number of discoveries that we’ve <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000993" target="_blank" rel="noopener noreferrer">published</a> in <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002141" target="_blank" rel="noopener noreferrer">peer reviewed journals</a> and on our website.
As we make these discoveries, we have often debated: what is the best way to make sure that genetic breakthroughs translate into real-world benefits?  We want to make discoveries that will impact your life and the lives of everyone on the planet.  We do not want our discoveries to just be an academic pursuit &#8212; we want to meaningfully improve lives.
Our patent, “<a href="http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&amp;Sect2=HITOFF&amp;d=PALL&amp;p=1&amp;u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&amp;r=1&amp;f=G&amp;l=50&amp;s1=8,187,811.PN.&amp;OS=PN/8,187,811&amp;RS=PN/8,187,811">Polymorphisms Associated With Parkinson’s Disease</a>” is expected to issue on Tuesday, May 29, 2012. This relates to our discovery of a variant in the SGK1 gene that may be protective against Parkinson’s disease in individuals who carry the rare risk-associated LRRK2 G2019S mutation.  Our patent is an important step in ensuring that we’ve done all we can towards successful translation of this discovery.  If the follow up work we are now doing with the Scripps Research Institute and the Michael J. Fox Foundation looks promising and moves towards drug development, the patent will be important for a biotech or pharmaceutical company to pursue drug development.
We believe patents should not be used to obstruct research or prevent individuals from knowing what&#8217;s in their genome. We believe that everyone has a right to know their genomes &#8212; their sequence of As, Ts, Cs, and Gs &#8212; and should be able to access them should they want to.  This has been our guiding principle since day one, and 23andMe has pioneered the ability for individuals to have unfettered access to their genomes.
We recognize that patents are complicated and can be controversial. Patents were created to protect innovation. Is discovering the function of a gene an innovation?
The question of whether innovations related to genetics can be patented is in hot debate as evidenced by recent rulings related to <a href="http://www.supremecourt.gov/opinions/11pdf/10-1150.pdf" target="_blank" rel="noopener noreferrer">Prometheus</a> and Myriad patents.
We want to emphasize that we are firm in our belief that individuals should have access to their own genetic data. We will continue to pursue patents that we believe will eventually benefit us all. The majority of our customers have opted to participate in research. Thanks to that community, we have been able to make an incredible number of novel discoveries. We want those discoveries to move from the realm of academic publishing to the world of impacting lives by preventing, treating or curing disease.
Addendum &#8212; June 1, 2012:
The patent announcement has generated a lot of discussion. In addition to reiterating our core beliefs I&#8217;d like to clarify a few points about our perspective:
23andMe will not prevent others from accessing their genetic data or its interpretation specific to our patents.
Other entities can present information about the genetic associations covered in our patents without licensing fees. As has always been the case, 23andMe customers can freely apply their raw genetic data to other interpretation tools whenever they wish.
23andMe is a business with a mission to improve lives.  
We sell a service to our customers and we conduct research, on our own and with partners, that we believe will lead to better treatments, diagnostics, and prevention of disease. We aim for these discoveries to benefit everyone.
Patents give organizations researching and developing new drugs confidence that their significant investments will be commercially viable.  
Developing new drugs and treatments costs time and money. A lot of time and money. Often the only way a company will even think about pursuing a drug lead is if they have assurance that they can recoup their investment. Having patent protection over the entire line of discovery gives a company confidence to invest in this resource-intensive process.
Many of you, <a href="http://blog.michaeljfox.org/2012/05/patent-23andme-step-meaningfully-improving-lives/">especially in the Parkinson&#8217;s community</a>, saw this as a major milestone and the first step in potentially having a meaningful impact on the lives of Parkinson&#8217;s patients. Our ultimate goal is to make discoveries that will benefit everyone.

Announcing 23andMe’s First Patent

<img loading="lazy" decoding="async" class="aligncenter wp-image-13198 size-full" title="whitebloodcell" src="http://35.88.189.111/wp-content/uploads/2012/05/whitebloodcell.jpg" alt="" width="350" height="260" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/whitebloodcell.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2012/05/whitebloodcell-300x223.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />Crohn’s disease develops when the immune system mistakenly attacks the body’s own gut cells.
Although most people with European ancestry are pretty genetically similar, some sub-groups like Ashkenazi Jews have distinct genetic characteristics that carry important implications for health. For instance, people with <a href="https://blog.23andme.com/articles/detail-for-ashkenazi-ancestry">Ashkenazi ancestry</a> have higher rates of numerous rare genetic disorders like <a href="https://www.23andme.com/topics/carrier/tay-sachs-disease">Tay-Sachs disease</a> and are at increased risk for certain multi-gene conditions like Crohn’s disease.
The exact cause of Crohn’s disease isn’t known, but this inflammatory bowel disease may result from a case of mistaken identity – the immune system mounts a reaction to an invader and ends up attacking the body’s own cells, too. At least 12 genetic factors have been associated with Crohn’s disease in Europeans. Although researchers don’t know why people with Ashkenazi ancestry are two to four times more likely to develop Crohn’s disease, they suspect that the genetic “uniqueness” of this group may have something to do with it. 
 
To investigate this intriguing idea, a research team led by scientists at Columbia University and Mount Sinai carried out a study looking at nearly 2,000 people with Crohn’s disease and roughly 4,500 people without it, all of <a href="https://blog.23andme.com/articles/ashkenazi-ancestry-and-health">Ashkenazi descent</a>. The results, published in <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002559">PLoS Genetics</a> earlier this year, replicate previously reported associations for people of European descent and also identify novel factors specific to those with Ashkenazi ancestry.
In the new study by lead author Eimear Kenny, individuals with the C version of and the G version of had slightly higher odds of developing Crohn’s disease. Two other factors seemed to be protective. People with the T version of and the G version of had slightly lower odds of developing Crohn’s disease. More research is needed to understand how these genetic variants influence the biology of the disease.
These new findings confirm that genetics likely has something to do with the higher rates of Crohn’s disease in people with <a href="https://blog.23andme.com/articles/detail-for-ashkenazi-ancestry">Ashkenazi ancestry</a>. All of the newly discovered factors appeared to be specific to Ashkenazi ancestry as they weren’t found in previous studies carried out with broader European study groups.
May is Jewish American Heritage Month. Read about <a href="https://blog.23andme.com/?p=13178">the “uniqueness” of Ashkenazi Jewish ancestry</a> and how it’s important for health. Read more about Jewish ancestry in guest posts by 23andMe&#8217;s Ancestry Ambassadors, Tim Janzen,  CeCe Moore, and  Andrea Badger.

Genetic Factors for Crohn’s Identified for Ashkenazi Jewish Ancestry

<img decoding="async" class="alignright size-full wp-image-13288" title="CancerInfographic" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/CancerInfographic.jpg" alt="" width="625" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/CancerInfographic.jpg 849w, https://blogcms.23andme.com/wp-content/uploads/2012/05/CancerInfographic-300x254.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/05/CancerInfographic-768x650.jpg 768w" sizes="(max-width: 849px) 100vw, 849px" />
23andMe is passionate about fighting cancer. We’re researching specific forms of cancer and treatments (see sidebar) and also learning more generally about cancer through our Cancer Family History survey (men’s version and women’s version). Personal experiences have the potential to fuel important research discoveries and by taking this survey customers can tell us how cancer has touched their lives.
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May is National Cancer Research Awareness Month
You can contribute to research on cancer by taking the Cancer Family History survey (men’s version and women’s version) and if eligible, participating in the following studies:
&#8211; Do you have sarcoma, or know someone who does? Learn how to join our <a href="https://www.23andme.com/sarcoma/">Sarcoma research community today</a>.
&#8211; Do you have an MPN, or know someone who does? Learn how to join our <a href="https://www.23andme.com/mpn/">MPN research initiative today</a>.
&#8211; If you or someone you know has been diagnosed with metastatic breast cancer, check out our <a href="https://www.23andme.com/invite-study/">innovative online study with Genentech</a>.
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Within just 2 months of launching the survey over 20,000 customers (9,700 women and 11,000 men) have completed it! Although we’ll likely need more data to be able to find interesting genetic and non-genetic associations for different types of cancer, what people are already telling us is very interesting:
<ul>
<li>Cancer is relatively common in the 23andMe database</li>
</ul>
About 20% of women and 16% of men had a diagnosis of some form of cancer (this included relatively common non-melanoma skin cancers). These numbers are higher than the <a href="https://www.cdc.gov/nchs/fastats/cancer.htm" target="_blank" rel="noopener noreferrer">national adult average of 8.5%</a>, which may reflect the fact that 23andMe customers include individuals enrolled in our <a href="https://www.23andme.com/sarcoma/" target="_blank" rel="noopener noreferrer">Sarcoma</a>, <a href="https://www.23andme.com/mpn/" target="_blank" rel="noopener noreferrer">MPN</a> and <a href="https://www.23andme.com/invite-study/" target="_blank" rel="noopener noreferrer">Metastatic breast Cancer</a> research communities. People with a strong family history of cancer might also be more interested in undergoing genetic testing and taking this survey.
<ul>
<li>Approximately 50% have a 1st degree relative with cancer</li>
</ul>
Just over half of respondents have a mother, father, child or sibling who had been diagnosed with cancer.
<ul>
<li>Many have parents who suffered from breast or prostate cancer</li>
</ul>
Nearly 10% of respondents (combined male and female) have a mother with breast cancer while just over 1% had a father with prostate cancer.

Cancer Touches Everyone

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-12716" style="border: 1px solid #ccc;" title="DNA USA.indd" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/DNA-USA-197x300.jpg" alt="" width="197" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/DNA-USA-197x300.jpg 197w, https://blogcms.23andme.com/wp-content/uploads/2012/05/DNA-USA.jpg 300w" sizes="auto, (max-width: 197px) 100vw, 197px" />
Bryan Sykes, the evolutionary geneticist at Oxford University and the author of<a href="../2008/08/14/recommended-reading-the-seven-daughters-of-eve/"> The Seven Daughters of Eve,</a> is adding to his oeuvre of popular work on genetics with his new book,<a href="https://www.amazon.com/DNA-USA-Genetic-Portrait-America/dp/0871404125%3FSubscriptionId%3DAKIAIXFKFJI6IH6DO5KQ%26tag%3Dkirkus-20%26linkCode%3Dxm2%26camp%3D2025%26creative%3D165953%26creativeASIN%3D0871404125"> DNA USA, A Genetic Portrait of America.</a>
As with his previous work, Sykes breaks down some of the complicated aspects of genetics in ways that are easily understood. This book is both travelogue and a snapshot of the genetic melting pot that is the United States of America.  As Sykes writes America is the place “where the genes of the three great continents converge.”
The book offers some intriguing, although mostly anecdotal, observations. During his journey Sykes meets people who agree to have their DNA tested anonymously. He then creates DNA portraits of these individuals, using 23andMe to create ancestry paintings of each individual. From that he drew conclusions about early America and the rich mixing of European, Asian and African people in America. The book also offers Sykes a chance to discuss the history of the earliest Americans.
Last week, our own senior director of research Joanna Mountain – who along with 23andMe scientist Mike Macpherson acted as consultants for some of the genetics in the book – introduced Sykes at a lecture he delivered at Berkeley Arts &amp; Letters.
He got a good response from the audience and his book has some buzz including a<a href="https://www.kirkusreviews.com/book-reviews/bryan-sykes/dna-usa/#review%20http://www.oxfordancestors.com/"> thumbs-up</a> from the Kirkus Review. 
We’re offering two signed copies of the book &#8212; simply submit the form below for a chance to win!

DNA USA

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-12933" title="Jennie Cole" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/Jennie-Cole-169x300.jpg" alt="" width="169" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/Jennie-Cole-169x300.jpg 169w, https://blogcms.23andme.com/wp-content/uploads/2012/05/Jennie-Cole.jpg 270w" sizes="auto, (max-width: 169px) 100vw, 169px" />Jennie Cole, c.1895
As the series <a href="https://www.pbs.org/wnet/finding-your-roots/">Finding Your Roots with Henry Louis Gates, Jr.</a> begins its 10-week run on PBS, The Blog will feature posts from 23andMe’s Ancestry Ambassadors featuring their own stories about using DNA to dig into ancestry.
By CeCe Moore
I have always felt a special affinity for Jewish people and their heritage. Throughout my life I have had many Jewish friends.
I have even been mistaken for a Jewish person despite having no known Jewish ancestors.
As a result, I was especially intrigued when, after 23andMe&#8217;s Ancestry Finder launched in 2010, I found that a number of people with segments of DNA that matched mine were self-identified as <a href="https://blog.23andme.com/articles/detail-for-ashkenazi-ancestry">Ashkenazi Jews</a>. The Ancestry Finder lab seeks to graphically illustrate the country of origin for specific segments of your DNA by locating stretches that match those of people from specific geographic regions. Ancestry Finder also identifies matching segments for <a href="https://blog.23andme.com/articles/ashkenazi-ancestry-and-health">Ashkenazi Jewish ancestry</a>.
<img loading="lazy" decoding="async" class="aligncenter wp-image-13008 size-full" title="CeCe's Uncle's matches with one gparent" src="http://35.88.189.111/wp-content/uploads/2012/05/CeCes-Uncles-matches-with-one-gparent.jpg" alt="" width="419" height="227" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/CeCes-Uncles-matches-with-one-gparent.jpg 419w, https://blogcms.23andme.com/wp-content/uploads/2012/05/CeCes-Uncles-matches-with-one-gparent-300x163.jpg 300w" sizes="auto, (max-width: 419px) 100vw, 419px" />My Ancestry Finder chart shows matches with people who have three Ashkenazi grandparents
In particular, in my Ancestry Finder results I noticed a cluster on my seventh chromosome that appeared to contain many matches with self-declared Ashkenazi ancestry. When I examined the downloaded spreadsheet of Ancestry Finder matches, I discovered that on Chromosome 7, between the positions 51,500,000 and 146,700,000, I had no less than 47 matches with people who self-identify as at least partially Jewish. These matches all appeared to be rather small and concentrated on that one spot, but it did cause me to ponder the possibility that I could have distant Jewish ancestors.
In further investigation, I found that my mother had no matches associated with Ashkenazi Jewish ancestry in her Ancestry Finder lab. Since my father is deceased, I asked my paternal uncle to test in his place. When I received his results, it was clear as day that the same Ashkenazi cluster on his seventh chromosome!
In fact, his Jewish connection appeared to be even more substantial than mine, with 69 self-described “Ashkenazi” matches on Chromosome 7 between positions 39,400,000 and 103,400,000 found in the Ancestry Finder match download.
<img loading="lazy" decoding="async" class="aligncenter wp-image-13042 size-full" title="CeCe's Uncle's matches" src="http://35.88.189.111/wp-content/uploads/2012/05/CeCes-Uncles-matches1.jpg" alt="" width="434" height="218" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/CeCes-Uncles-matches1.jpg 434w, https://blogcms.23andme.com/wp-content/uploads/2012/05/CeCes-Uncles-matches1-300x151.jpg 300w" sizes="auto, (max-width: 434px) 100vw, 434px" />Paternal Uncle&#8217;s matches with people who have three Ashkenazi grandparents.
Notably, my paternal uncle’s results also included several Public Matches in 23andMe’s <a href="https://www.23andme.com/you/relfinder/">Relative Finder</a> who list their ancestry as Jewish. Most of these are predicted as &#8220;Distant Cousins,&#8221; which probably explains why they don&#8217;t appear in my Relative Finder. In this case, testing just one generation further back in time revealed very useful information.
While this Ashkenazi ancestry is fairly distant, it certainly appears to be authentic. With approximately 70% of my uncle’s chromosomes covered in Ancestry Finder, 3.6% &#8211; 7.8% is declared <a href="https://blog.23andme.com/articles/detail-for-ashkenazi-ancestry">Ashkenazi</a>. With this in mind, I would guess that he and my father have a 2nd great-grandparent of primarily Jewish descent or several ancestors with lesser amounts of Jewish ancestry.
<img loading="lazy" decoding="async" class="aligncenter wp-image-13008 size-full" title="CeCe's Uncle's matches with one gparent" src="http://35.88.189.111/wp-content/uploads/2012/05/CeCes-Uncles-matches-with-one-gparent.jpg" alt="" width="419" height="227" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/CeCes-Uncles-matches-with-one-gparent.jpg 419w, https://blogcms.23andme.com/wp-content/uploads/2012/05/CeCes-Uncles-matches-with-one-gparent-300x163.jpg 300w" sizes="auto, (max-width: 419px) 100vw, 419px" />Paternal Uncle&#8217;s matches with people who have one Ashkenazi grandparent. 
Since the majority of the matches cluster in the same area, the most likely conclusion is that this DNA is inherited from a single ancestor. My paternal family tree is fairly complete and so far without an obvious suspect, but since my father’s great-grandmother, Jennie Cole’s father, is unknown, this scenario is a viable possibility. To focus in on this prospect, I would need to test more of Jennie’s descendants to isolate her DNA and determine if there is evidence of Jewish ancestry in the portions of the DNA that each of them inherited from Jennie. Since the paternity of Jennie has long been an enigma to me, this is a very intriguing new avenue of exploration for my genealogy research.
Before testing at 23andMe, I never would have imagined that I had Jewish ancestry. Now that I have discovered this tantalizing fact, I am on the hunt to learn more about this elusive ancestor!
23andMe provides genetic testing services for informational purposes; your results may or may not help you find or identify relatives or family members.
<img loading="lazy" decoding="async" class="alignright size-full wp-image-12939" title="CeCephoto" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/CeCephoto.jpg" alt="" width="114" height="162" />
CeCe Moore is a genetic genealogist specializing in the use of autosomal DNA for genealogy. She writes the popular blog <a href="http://www.yourgeneticgenealogist.com/">Your Genetic Genealogist</a> and works as a television producer with StudioINTV.   CeCe is the Southern California Regional Coordinator of the International Society of Genetic Genealogy (ISOGG), serves on the Advisory Board of the Mixed Roots Foundation, and is a member of Mensa.  Her favorite genetic experiment is her seven-year-old son, Nicolas.

CeCe Moore

Discovering Unknown Jewish Ancestry with 23andMe

There are many wonderful things about being a woman, but our increased risk of autoimmune disease is not one of them. Autoimmune diseases are essentially civil wars within the body &#8212; the body’s immune system attacks its own organs and tissues. The term “autoimmune” covers a wide variety of conditions, from rheumatoid arthritis and multiple sclerosis to the lesser-known conditions of Hashimoto’s thyroiditis and SjÃ¶gren’s syndrome.
One commonality of these conditions is that they affect women much more frequently than men. In some cases, this g<img loading="lazy" decoding="async" class="alignright wp-image-12225 size-large" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/Autoimmune1.jpg" width="535" height="392" />ender bias is quite striking; Hashimoto’s thyroiditis, a condition in which the immune system attacks the thyroid gland, affects women ten times more often than men. Some autoimmune diseases, however, are less biased; type I diabetes, for instance, affects women and men at approximately the same rate.
Why women are disproportionately affected by autoimmune disease is not fully known or understood, although the hypotheses are numerous. Some research suggests that estrogen may help antibody production and immune system response, but can also lead to an overly active immune system. Other research indicates that genes on the X chromosomes may play a role in these immune system mutinies, and women &#8212; who have two X chromosomes &#8212; may thus be at an increased risk over men who have only one X chromosome.
Still other research suggests that “fetal-maternal microchimerism” may be the root cause. In this strange-sounding phenomenon, a small number of the baby’s cells pass through the placenta into the mother and continue to live within the mother. The presence of these foreign fetal cells within the mother may result in an incorrect immune system response and autoimmune disease. More research, however, is needed to establish which of these hypotheses (if any) are correct.
Autoimmune diseases are serious medical concerns for women; indeed, when taken together, autoimmune diseases constitute one of the top ten causes of death among young and middle-aged women. The irony of these conditions is that the immune system, which should be a woman’s greatest ally in fighting disease, becomes her worst enemy. Why and how a body’s betrayal occurs needs to be better understood through further research.
<img loading="lazy" decoding="async" class="alignnone size-full wp-image-12789" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/2012-nwhw-web-banner.png" width="408" height="104" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/2012-nwhw-web-banner.png 408w, https://blogcms.23andme.com/wp-content/uploads/2012/05/2012-nwhw-web-banner-300x76.png 300w" sizes="auto, (max-width: 408px) 100vw, 408px" />

The War Waged Within: Autoimmunity in Women

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).

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