By Bethann Hromatka
<img loading="lazy" decoding="async" class="alignright size-full wp-image-9756" title="diversity(iStockBlog)" src="https://blog-api.23andme.com/wp-content/uploads/2011/09/diversityiStockBlog.jpg" alt="" width="300" height="199">
The saying “men are from Mars, women are from Venus,” may have originated from personality differences between the sexes, but it also rings true for complex diseases that affect one sex more than the other. For instance, the prevalence of autoimmune diseases such as rheumatoid arthritis, multiple sclerosis and type 1 diabetes is higher in women than men. In addition, some diseases progress faster in one sex, and men and women can have different responses to certain therapies.
A <a href="https://www.ncbi.nlm.nih.gov/pubmed/21858542" target="_blank" rel="noopener noreferrer">recent study</a> by Linda Liu and colleagues at Stanford University attempted to identify some of the genetics underlying these differences. They analyzed data from one of the first genome-wide association studies (GWAS)–carried out by the Wellcome Trust Case Control Consortium (WTCCC), which looked at seven common diseases–in order to find gene variants that influence disease risk in only one sex. Most studies look for genetic variants associated with disease without performing in-depth analyses to identify sex-specific effects.
Although this is standard practice in GWAS, Liu and authors point out that some studies may have failed to find SNPs that influence disease risk in only one gender because they grouped men and women together. A combined sex GWAS is unlikely to detect a SNP that is simultaneously risky for women, but protective for men, because the effects will cancel each other out. Alternatively, if a SNP only influences risk in one sex, the association might not be observed unless the data from men and women are analyzed separately.
After applying novel statistical methods, the authors identified two female-specific SNPs linked to Crohn’s disease and a male-specific SNP associated with coronary artery disease. Although these associations were also found in the combined sex analysis by the WTCCC, the new findings provide evidence that the overall effects are driven by one sex and may not be applicable to both. Liu and her colleagues argue that GWAS should recruit larger cohorts and most importantly, equal numbers of women and men in order to systematically study sex-specific effects of genetic variants on disease.
This study suggests that most of the genetic associations identified to date are either those that impact the population as a whole, or those that are strong enough in one sex to produce an effect in a combined analysis. This implies that many more associations could be found that are specific to one sex. Says Liu and authors, “studying sex differences can help provide a missing link in terms of different gene-endocrine and gene-environment interactions in males and females.”
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.

Bethann Hromatka

Let’s Talk About Sex… in GWAS

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-9696" title="Immune(iStock)" src="https://blog-api.23andme.com/wp-content/uploads/2011/09/ImmuneiStock-300x225.jpg" alt="" width="300" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/09/ImmuneiStock-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2011/09/ImmuneiStock.jpg 400w" sizes="auto, (max-width: 300px) 100vw, 300px" />
By Bethann Hromatka
Autoimmune diseases are caused by an overactive immune system. In these diseases, white blood cells, which normally help your body fight infections, ramp up and attack your own cells and organs.
These disorders can be very debilitating and are relatively common, affecting roughly 1 in 20 individuals. Some well-known examples include psoriasis, Crohn’s disease, celiac disease, multiple sclerosis, systemic lupus erythematosus (or lupus), type 1 diabetes, and rheumatoid arthritis. Although most of these disorders manifest in different parts of the body, all are characterized by excess inflammation.
<h6>Understanding Autoimmune Diseases</h6>
Our understanding of the causes of immune disorders has been limited due to their complexity. These diseases are not caused by changes in a single gene, but are influenced by many genes as well as environmental and lifestyle factors. For example, mutations in at least 22 different genes have been linked to type 1 diabetes to date. At the same time, it is well known that <a href="https://blog.23andme.com/2009/05/28/environment-not-genes-key-to-increasing-disease-rates/" target="_blank" rel="noopener">non-genetic factors</a> can increase or decrease a person’s risk of developing this disease.
An interesting observation about autoimmune diseases is that they tend to run in families. For instance, a mother with type 1 diabetes might have a daughter with celiac disease. Or, someone with Crohn’s disease might also develop celiac disease or psoriasis. There also appears to be a pharmacological link–for example with the use of a drug to treat both rheumatoid arthritis and type 1 diabetes. These observations have led researchers to wonder if there could be a common genetic basis to autoimmune diseases.
<h6>Understanding Risks for Autoimmune Diseases</h6>
A recent study published in <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002254" target="_blank" rel="noopener">PLoS Genetics</a> on behalf of the FOCiS Network of Consortia tested this very hypothesis: do some mutations put an individual at risk for more than one autoimmune disease? To address this question, the researchers looked at previously published genome wide association studies (GWAS) and compiled a list of 107 SNPs that associated with at least one of seven immune diseases. Then, they applied a new statistical method to identify SNP versions that were linked to multiple autoimmune diseases.
The authors reported that nearly half of the SNPs influenced risk for at least two autoimmune diseases. In most cases, the same version of the SNP was associated with higher risk for each disease.   Interestingly, nine SNPs were simultaneously associated with higher odds for one disease and lower odds for a different disease. One SNP – in the SH2B3 gene–was associated to varying degrees with all seven diseases; the C version was risky for celiac disease and multiple sclerosis, but protective for psoriasis, rheumatoid arthritis, lupus, Crohn’s disease and type 1 diabetes.
The authors also found that certain SNPs grouped together based on their disease associations. For example, SNPs associated with both Crohn&#8217;s disease and psoriasis formed a distinct cluster and those linked to both rheumatoid arthritis and type 1 diabetes also comprised a distinct cluster. In many cases, SNPs in a particular group were located in genes involved in the same biological processes. These results suggest that shared genetic factors can point to the underlying cellular pathways that are disrupted in different classes of immune disorders.
These findings are exciting because they point to a common genetic basis to autoimmune diseases. Understanding the genetic relatedness of diseases could help researchers develop new therapies to target common cellular pathways or redirect currently available treatments to a genetically related disease. Similarly, the approach used in this paper could be applied to other classes of complex diseases, such as psychiatric disorders, to determine if they also share common genetic components.

23andMe Blog

23andMe Blog Team

Researchers Investigate Shared Genetic Factors for Autoimmune Diseases

California Governor Jerry Brown<a href="http://www.genomeweb.com/california-enacts-broad-genetic-discrimination-law" target="_blank" rel="noopener"> signed into</a> law civil rights protections to prevent discrimination against people based on their genetic information.
Authored by State Sen. Alex Padilla, the California law the use of genetic information to discriminate against a person in housing, employment, education, health insurance, life insurance, mortgage lending and elections. It takes effect January 1, 2012..
“This new law enhances the civil rights of every Californian,” Senator Padilla said in a <a href="http://dist20.casen.govoffice.com/index.asp?Type=B_PR&amp;SEC={5EACFA15-EA6B-41D8-9711-C030F9FAD5EE}&amp;DE={F9BFE373-43E6-4782-BE02-5A015BFE4341}" target="_blank" rel="noopener">press release</a> Wednesday. “Ten years from now as more and more Californians obtain their genetic information they will look back and thank Governor Brown for protecting them from discrimination.”
The new law extends California&#8217;s long standing civil rights protections and the federal protections against genetic discrimination passed by Congress in 2008. That law, the Genetic Information and Nondiscrimination Act (GINA), limits protections to   to employment and health insurance coverage.    SB 559 would ensure that the range of protections for Californians applies to all California civil rights laws and would include genetic information as a prohibited basis for discrimination.
See also: <a href="https://blog.23andme.com/articles/california-law-would-extend-genetic-non-discrimination-protections/">California Law Would Extend Genetic Non-Discrimination Protections</a>

California Governor Signs Law to Protect Against Genetic Discrimination

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-9657" title="nerves(iStock)" src="https://blog-api.23andme.com/wp-content/uploads/2011/09/nervesiStock-300x225.jpg" alt="" width="300" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/09/nervesiStock-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2011/09/nervesiStock.jpg 400w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Scientists know that there isn’t one cause for multiple sclerosis (MS), but understanding this complex autoimmune disease has vexed medical researchers for years.
In the <a href="https://www.nature.com/nature/journal/v476/n7359/full/nature10251.html" target="_blank" rel="noopener">largest MS study</a> to date, researchers recently identified 29 new genetic variants associated with the disease in people of European descent, bringing the list of MS-related genetic factors to more than 50.
The work, led by scientists at the Universities of Cambridge and Oxford and funded by the Wellcome Trust, also sheds more light on the molecular biology of the disease. Most of the variants discovered are in or near genes that drive the body’s immune responses, specifically those involved in the production of T-cells.
<a href="http://www.nationalmssociety.org/about-multiple-sclerosis/what-we-know-about-ms/what-is-ms/index.aspx" target="_blank" rel="noopener">Multiple sclerosis</a> is an autoimmune disease in which a person’s immune system attacks the myelin sheath that insulates nerve fibers in the brain and spinal cord. The damage to the sheaths impairs the signals traveling along the nerves, which in turn causes a range of symptoms including weakness, sensory disturbance, fatigue, visual impairments and loss of coordination. About 2.5 million people suffer worldwide from MS with about 400,000 of those in the United States.
“Our research settles a longstanding debate on what happens first in the complex sequence of events that leads to disability in multiple sclerosis,” said Alastair Compston, of the University of Cambridge, who led the study with Peter Donnelly from the Wellcome Trust Center for Human Genetics on behalf of the International Multiple Sclerosis Genetics Consortium.
“It is now clear that multiple sclerosis is primarily an immunological disease,” Compston said in a press release in early August.
What is also interesting about this latest research is that many of the genetic factors involved in MS are shared with other <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002254" target="_blank" rel="noopener">autoimmune diseases</a>, like Crohn’s disease, lupus and type 1 diabetes.
One of the authors of the study, Dr. David Hafler, a professor of neurology and immunobiology at Yale University, said the breakthrough goes beyond just research into MS, but may help researchers in finding new ways to fight both MS and other diseases.
While researchers know that genetic plays an important role – people of European ancestry are more susceptible and a family history of MS also increases the odds of developing the disease – it’s only one of a large combination of factors that include environmental factors such as vitamin D intake, smoking, exposure to toxic chemicals and things like whether someone has had certain viruses like Epstein-Barr. In short multiple sclerosis is unpredictable and complex.
The new study involved nearly 10,000 people with MS from 15 different countries and a group of more than 17,000 people without the disease. In all, 23 research groups collaborated on the research.

New Associations Found for Multiple Sclerosis

UPDATE (9/7/2011) California Governor Jerry Brown signed into law civil rights protections in the state to prevent discrimination against people based on their genetic information.
A new California law, awaiting Gov. Jerry Brown’s signature, would apply California’s broad anti-discriminatory protections to genetic information.
Authored by California State Senator Alex Padilla (D — Pacoima) the law, SB 559, extends the protections in the federal Genetic Information and Nondiscrimination Act (GINA). GINA currently prohibits the use of genetic information to discriminate against people in employment and insurance.
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-8732" title="DNA-chains" src="https://blog-api.23andme.com/wp-content/uploads/2011/03/DNA-chains-300x225.jpg" alt="" width="279" height="210" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/03/DNA-chains-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2011/03/DNA-chains.jpg 400w" sizes="auto, (max-width: 279px) 100vw, 279px" />
Gov. Brown hasn’t indicated whether he will sign the bill. He has until next week to decide.
Beyond the new California protections, the law and its history offer a lesson in the difficulty of drafting legislation for genetic testing.
<a href="http://www.leginfo.ca.gov/pub/11-12/bill/sen/sb_0551-0600/sb_559_bill_20110824_enrolled.pdf">Padilla’s legislation</a> prohibits using genetic information to discriminate against people in housing, education, lending, elections, and other areas.
The proposed law essentially extends California’s existing civil rights legislation.
“Discrimination on the basis of genetic information is no less offensive than discrimination based on race, gender, or sexual orientation,” Padilla said. “California has a compelling interest in promoting and fostering the medical promise of genomics while relieving the fear of discrimination by strengthening laws to prevent it.”
Jeremy Gruber, the executive director of the Council for Responsible Genetics, applauded the law saying it would help both consumers and the industry. People will be more willing to use genetic testing knowing that the results of their tests can’t somehow be used against them.
But the legislation won’t change the regulatory framework under which direct-to-consumers genetic testing companies are currently operating.
Padilla, with the help of 23andMe, tried to do that two years ago, but that effort failed. Attorney Dan Vorhaus discussed those efforts and the nature of the new bill in a Genomics Law Report <a href="http://www.genomicslawreport.com/index.php/2011/03/23/ca-proposal-for-genetic-legislation/#more-5464">blog post</a> in March.
But when Padilla’s previous bill failed, he attempted to bring all sides together for a meaningful policy discussion. 23andMe sponsored  a daylong forum with Padilla, “Genomics and the Consumer: The Present and Future of Personalized Medicine,” last summer in San Francisco.
As 23andMe president and co-founder Anne Wojcicki said last summer, the forum was an attempt to shed light on an issue that had, up to that point, only seemed good at generating  “a lot of heat.” The forum was also an attempt to find some common ground.
Padilla noted that part of the friction surrounding the debate had to do with the speed at which genomic science has progressed. An MIT graduate, Padilla said his concern was that the inability to reach a consensus on proper oversight could hurt the development of an industry with great potential for scientific and therapeutic breakthroughs.
In many ways Padilla anticipated the current federal debate over how best to regulate the industry. In the year since that policy forum 23andMe has been in discussions with the FDA  regarding its own regulatory path, which it hopes will aid in the evolution of a rational regulatory framework for genetic testing services generally.
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California Law Would Extend Genetic Non-Discrimination Protections

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In March earlier this year, <a href="https://blog.23andme.com/articles/23andme-presents-at-fda-advisory-panel-meeting-on-direct-to-consumer-genetic-tests/" target="_blank" rel="noopener">23andMe presented its views</a> on possible federal regulation of the direct-to-consumer (DTC) genetic testing industry at an Advisory Committee meeting convened by the FDA. We reiterated our belief that individuals have a right to access their own genetic information without physician involvement, and suggested components of a regulatory framework that would ensure the high quality of that genetic information while maintaining direct-to-consumer access to personal genetic testing and enabling innovation.
Despite compelling arguments for DTC genetic testing the panel concluded that access to most types of health-related genetic tests should require a physician’s approval. At 23andMe, we encourage individuals to discuss their genetic test results with their health care providers and involve them fully in decision-making about their health. But we also contend that individuals should be allowed direct access to this information. We continue to work with FDA to develop a reasonable path forward.
In the months before and following the meeting, many of you responded to our call and submitted public comments to the FDA supporting as well as arguing against direct-to-consumer genetic testing. More open and honest debate about this issue can only be beneficial for the industry over the long run.
On September 22, 2011, Bay area citizens will have another chance to make their voices heard. FDA’s Center for Devices and Radiological Health (CDRH) will be holding the third of its 2011 public town hall discussions where individuals can present their views directly to senior CDRH officials, including the Center Director, the Deputy Director for Science, and the head of the Office of In Vitro Diagnostics, which regulates DTC genetic testing. The September town hall will be held at the Embassy Suites Hotel near the San Francisco international airport.
For more information about the town hall, see the official FDA announcement. Note that while anyone in attendance can ask questions during the Q&amp;A session, individuals must register and specifically request to speak if they would like to make comments during the public presentation period.
If you have strong opinions on whether individuals should have direct access to their genetic information, we encourage you to continue making your views known to FDA, whether through in-person meetings such as the town hall in September, or through letters and other correspondence. After all, we believe that having more information is a good thing!

FDA to Hold Public Town Hall Discussion in San Francisco

Not all the discoveries made on 23andMe are quite as profound as <a href="https://blog.23andme.com/articles/stories-from-23andme-neil-schwartzman" target="_blank" rel="noopener noreferrer">Neil Schwartzman</a> finding his half-sister and mother, but even when 23andMe’s Relative Finder links distant cousins together those connections can still be electric.
Gerald Lopez, a customer who found a fourth or fifth cousin and information about his mixed ancestry, said it was like discovering “history that’s not written in history books.”
23andMe’s <a title="Relative Finder" href="https://www.23andme.com/ancestry/relfinder/" target="_blank" rel="noopener noreferrer">Relative Finder</a> &nbsp;uses genetic data instead of archived records to identify family relationships. Where written paper records fail, genetic information can sometimes fill in the gaps. Pieces of DNA are passed down from generation-to-generation, so that our genetic data is our own repository of information about our ancestry. Comparing any two people’s DNA can also determine whether they are related.
<img loading="lazy" decoding="async" class="alignright wp-image-9549 size-medium" title="RF Results Sample" src="http://35.88.189.111/wp-content/uploads/2011/08/RF-Results-Sample-300x65.jpg" alt="" width="300" height="65" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/08/RF-Results-Sample-300x65.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2011/08/RF-Results-Sample.jpg 569w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Customers have identified more than 700 previously unknown family relationships discovered through Relative Finder. They’ve found fifth and fourth cousins like Gerald and a few, like Neil, have even found parents and siblings.
Among our more than <a href="https://blog.23andme.com/articles/state-of-the-database-2011" target="_blank" rel="noopener noreferrer">100,000 customers</a>, Relative Finder has identified 82,000 relationships that are either 4th cousins or closer.
Recently we updated Relative Finder to make it easier to use and search. Now users can show genealogical information &#8212; surnames, family locations, etc. This makes it easier for users to sort through potential matches. We also updated Relative Finder so that users can record notes about their matches, and confirm relationships. And the information available is rapidly increasing.
Even if you don’t consider yourself a genealogist, you might be surprised how fulfilling it can be to discover a common connection. You can remain anonymous if you choose, and only information in your profile that you designate as “visible to all 23andMe members” will be shown to your Relative Finder matches, so you can share as little or as much as you like.
And if you need help tracing a connection, many experienced Relative Finder “sleuths” are available in the community to offer tips and encouragement.
If there’s something that binds all 23andMe users together, it is a healthy curiosity about themselves and their DNA. So let Relative Finder broaden your horizons and let your DNA give you more to relate to!
If you’ve already discovered something interesting about your family through Relative Finder, do tell. We’re interested in hearing your stories &#8212; simply send them along to <a href="mailto:stories@23andme.com" target="_blank" rel="noopener noreferrer">stories@23andme.com</a>.
<a href="https://blog.23andme.com/category/23andme-customer-stories/">Read more 23andMe customer stories &gt;&gt;</a>

Making Connections with Relative Finder

It started innocently enough with a simple question from his daughter.
“Where did our family come from?”
<img loading="lazy" decoding="async" class="alignright size-full wp-image-9594" title="Vicksburg 014 Jan 08" src="https://blog-api.23andme.com/wp-content/uploads/2011/08/Vicksburg-014-Jan-08.jpg" alt="" width="226" height="170" />(Image from Larry Vick&#8217;s <a href="http://vickfamilyhistory.blogpost.com/" target="_blank" rel="noopener">blog</a>)
For 20 years Larry Vick has been trying to answer that question. His first source was a chart drawn up by an uncle, but since then Vick has turned to old Census files, birth certificates and historical documents to piece together his family tree. It’s grown to 40 pages that trace ancestors back to the early 1600s in colonial America and another branch of the family back to Germany.
He traced the origin of his family name, and created a whole website on the study of the <a href="http://vickfamilyhistory.blogspot.com/" target="_blank" rel="noopener">name Vick</a>.
Retired from the Air Force, Vick is fascinated by genealogy, so when he learned about “genetic genealogy” and the ability to trace ancestry through DNA, he decided to give it a try.
He first used 23andMe in 2009.
“My most distant (that I can identify) paternal line ancestor (Y-DNA) was Joseph Vick of Lower Parish, Isle of Wight Co., VA, born about 1640-1650,” Vick said. “My most distant maternal line ancestor (mtDNA) was Elizabeth, born about 1792 in NC.”
The test also revealed some surprises.
He noticed on his maternal line African ancestry. “I thought, ‘that’s an artifact,’” he said.
But what he found was that his mother’s 2nd great grandmother, Elizabeth Collins, probably did indeed have some mixed ancestry. She’d come from an area in Tennessee called Newman’s Ridge, where people often referred to themselves as “Black Dutch.” The population there – and in the Cumberland Gap area of Appalachia – was also referred to as “<a href="https://en.wikipedia.org/wiki/Melungeon" target="_blank" rel="noopener">Melungeon</a>,” tri-racial with a mix European, African and Native American ancestry.
Vick’s use of 23andMe’s ancestry finder also helped him track down a distant cousin – who also happened to share his interest in genealogy. They traced back their connection to a common ancestor in pre-revolutionary America. That story was picked up by CNN three years ago.
While Vick’s interest is primarily in the ancestry functions of 23andMe, he said the service offers more.
“At first I had no interest in the health side,” Vick said.
That has since changed he learned his granddaughter, who has also been tested by 23andMe, had a high risk for deep vein thrombosis. He immediately talked to his daughter. Since neither he nor his daughter had an elevated risk for deep vein thrombosis, it appeared his granddaughter had inherited this risk from his son-in-law’s side of the family. Because his son-in-law was adopted and did not know anything about his biological parents’ health history, the insight about this risk told them something they otherwise would not have known. This risk can be heightened for women who are also taking an oral contraception, hormone replacement or who are pregnant.
Vick said that because the number of people who use 23andMe, its power grows.
“It’s kind of like panning for gold, when you find a relative it can be golden,” he said.
23andMe provides genetic testing services for informational purposes; your results may or may not help you to search for or identify relatives or family members.
What&#8217;s your story? If you&#8217;re willing to share, we want to hear. Drop us a line at <a href="mailto:stories@23andme.com">stories@23andme.com</a>.

Stories From 23andMe: James Larry Vick and the “Black Dutch” of Newman’s Ridge

In May, Neil Schwartzman opened an email message from a complete stranger.
“Hey,” it said. “I think you’re my brother.”
Neil is one of now thousands of 23andMe users who’ve discovered family relationships they never knew they had.
In June, we updated <a href="https://www.23andme.com/ancestry/relfinder/" target="_blank" rel="noopener noreferrer">Relative Finder</a> to make it easier to search for family connections. In just a few weeks 23andMe users have told us they’ve discovered more than 500 previously unknown relationships. People have linked up mostly with distant cousins, but a handful, like Neil, have found sisters, brothers, and even parents.
Neil, a 50 year-old Canadian activist who works to stop the spread of junk email, has seen his fair share of fake come-ons. But the email he got in May was different. It was a message from another 23andMe user showing that they were related through DNA.
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-9522" title="Neil Schwartzman" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2011/08/neil-s.-200x300.jpg" width="200" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/08/neil-s.-200x300.jpg 200w, https://blogcms.23andme.com/wp-content/uploads/2011/08/neil-s.-768x1152.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2011/08/neil-s.-683x1024.jpg 683w, https://blogcms.23andme.com/wp-content/uploads/2011/08/neil-s.-587x880.jpg 587w, https://blogcms.23andme.com/wp-content/uploads/2011/08/neil-s.-787x1180.jpg 787w, https://blogcms.23andme.com/wp-content/uploads/2011/08/neil-s..jpg 900w" sizes="auto, (max-width: 200px) 100vw, 200px" />Neil Schwartzman found his sister, Jolie Pearl, on 23andMe
Stunned by the message he began corresponding with the woman. He had always wondered about his background and if he had relatives out there still living, because Neil was adopted when he was just 10 days old. He never knew his biological mother. Although he loved his adoptive parents, he always yearned to know more about his background. He made a few attempts to find his biological mother in the 1990s, but after getting nowhere, he gave up.
“Fast-forward to three years ago when I became a 23andMe member,” said Neil, executive director of the <a href="http://www.cauce.org/" target="_blank" rel="noopener noreferrer">Coalition Against Unsolicited Commercial Email</a>. “I’d some hope to find family somewhere, but really I had just turned 50 and I thought it’d be nice to know if I had any medical condition I should be concerned about.”
In early May of 2011 in California Jolie Pearl, a 53 year-old union organizer and mother of a 13 year-old daughter, had begun to play around with 23andMe’s Relative Finder for the first time.
“I hit the button to find your closest relative and this thing popped up, ‘a predicted sibling,’” Jolie said. “I thought maybe it was a mistake or that it was my half-brother.”
The next morning, Jolie went to her mother’s house and before going in she spoke briefly with her mom’s best friend.
“She matter-of-fact said to me, ‘yeah, you’re going to want to know about him,’” Jolie said.
Her mother’s best friend was one of only three other people who’d ever knew that Jolie had another brother who’d been given up for adoption.
At first Jolie felt anger, but then was overwhelmed by the thought that she had another younger brother. She said she instinctively felt protective toward him. When she talked to her mom, Jolie’s mother explained that indeed she’d given birth to a baby boy in 1960 and just 10 days after his birth she handed him over to another couple.
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-9530" title="Jolie and Sheila" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2011/08/Jolie-and-Sheila-300x225.jpg" width="300" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/08/Jolie-and-Sheila-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2011/08/Jolie-and-Sheila.jpg 720w" sizes="auto, (max-width: 300px) 100vw, 300px" />Jolie Pearl with their mother
“It was the most difficult thing she’d done in her life,” Jolie said. “But she felt she didn’t have a choice. She couldn’t raise both of us.”
After talking to her mom Jolie sent the email to Neil.
After the initial exchange of emails, Neil, who had a scheduled business trip to California, arranged to meet his new found sister.
The two had dinner together, talking so long that they closed the restaurant down. The next day they went together to visit Neil and Jolie’s mother. Neil stopped to buy some flowers, asking his sister what kind their mother liked. They settled on a potted orchid because it was more lasting than cut flowers.
For Neil, who had anxiously anticipated the moment, meeting his mother and sister wasn’t what he’d expected. He’d anticipated a “massive emotional event.”
What he got instead was something more “nuanced, subtle, deep.”
It was the start of a relationship, he said.
At the end of the conversation, Neil’s mother grabbed his hand and held it for a long time.
“He told me that physical connection meant so much to him,” Jolie said. “He said it was like electric shocks going through his system.”
Finding her raised so many emotions, and Neil was struck by weighty questions about what makes you who you are. His niece noticed how both he and his sister had similar nervous hand gestures. Both are union activists.
“So this caused me to reflect on what the components of a person are,” Neil said. “There are morals and values imparted on me partially by my circumstances, by my adopted parents, my experience, all the things that life brings us. Then there’s this genetic thing.”
His mother is an artistic person and so is he. They’re both highly intelligent and opinionated.
“It’s fascinating to think that for all the free will we pride ourselves in having so many things may be predetermined,” he said. “It’s something to think about.”
The family has arranged to gather again.
“Obviously I never expected any of this when I signed up,” Jolie said. “It’s been the best thing. I want to thank 23andMe.”
Neil, too, expressed his gratitude, even citing 23andMe as an example of the miracle of modern science and the promise of the internet after receiving an award recently for the work he’s done to curb junk email.
“It’s beyond awesome,” said Neil. “I couldn’t be happier. I mean I’d really given up all hope. I can’t say how absolutely grateful I am to 23andMe for facilitating this.”
23andMe provides genetic testing services for informational purposes; your results may or may not help you to search for or identify relatives or family members.
What&#8217;s your story? If you&#8217;re willing to share, we want to hear. Drop us a line at <a href="mailto:stories@23andme.com">stories@23andme.com</a>.
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