Get ready — there’s a whole new way to do genealogy.

You may have already heard about a new feature 23andMe is offering its customers, called Relative Finder. With the launch of our new Ancestry Edition, we wanted to tell you more about it.

Don’t just settle for two branches of your family tree…

Relative Finder is a breakthrough feature that uses autosomal DNA to help you find relatives from all parts of your family tree. With Relative Finder, you can grow your family tree like never before, and discover relatives you never knew you had.

Relative Finder is available to people who buy the Ancestry or Complete Edition of the 23andMe service.

How is Relative Finder Different?

Until now, DNA genealogy tests could only tell you about a small part of your family tree, because they only used DNA from the Y chromosome and mitochondria. By using autosomal DNA, Relative Finder can trace any ancestor, no matter where they are in your family tree.

What’s so special about autosomal DNA? The autosomal chromosomes, which make up most of our DNA, have the unique property of randomly mixing in specific ways when passed down from parent to child. The result is that we are a mosaic of DNA segments that we inherited from our ancestors.

…With Relative Finder, find relatives from all branches of your family tree!

To give an example of the benefits of using autosomal DNA for learning about your ancestors, let’s consider your four grandparents. When looking at the Y chromosome (if you are male), you can trace your lineage through your paternal grandfather. When looking at the mitochondria, you can trace your lineage through your maternal grandmother. But this is only half of your grandparents! By using autosomal DNA, you can trace the lineages through all four grandparents. Extending this back 10 generations, instead of two ancestors detectable via Y and mitochondria, autosomal DNA can give you access to over 1000 ancestors and their descendants.

Relative Finder in Action

Relative Finder takes advantage of autosomal DNA by looking for shared segments with other 23andMe customers, which indicate a common ancestor. We list your closest matches first, but also let you sort and filter on other criteria you find important. Interested in relatives living abroad, or a particular Y or mitochondrial haplogroup? We can help you find them.

Take your time — users with European ancestry often have more than 100 matches, and users with Ashkenazi Jewish ancestry often have more than 1000! As the 23andMe database grows, you’re likely to get even more matches.

Once you’ve found an interesting match, you can take the next step and contact them directly. Go ahead: Introduce yourself to that fifth cousin who lives in Macedonia, or your ninth cousin who lives just down the street. With Relative Finder, you can discover more about your ancestry than you ever thought possible!

We Want You.

Up to now, we’ve been testing and tweaking Relative Finder extensively, both internally and with feedback from genealogy enthusiasts. Starting today, we are opening up that testing to all 23andMe customers who want the opportunity to experience Relative Finder. During the remainder of this beta period, participants can instantly contact any potential relatives also participating in the beta.

By participating in the Relative Finder Public Beta, you will get early access to this revolutionary new feature. In return, we hope that you will send us feedback, suggest improvements and — most importantly — share your success stories.

We hope you enjoy taking your family tree to a whole new level with Relative Finder. After all, you never know who you might find.

The following is a joint letter addressing the Opinion piece by Pauline C. Ng, Sarah S. Murray, Samuel Levy and J. Craig Venter that appeared in the October 8, 2009 issue of Nature (coverage here, here, here, and here).  Unfortunately, Nature could not publish the letter because of space restrictions, so 23andMe and Navigenics decided to publish the letter to our respective sites.

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Dear Editor:

We read with interest the Opinion piece entitled “An agenda for personalized medicine” in the October 8, 2009 edition of Nature. Our two companies, though commercially distinct with differentiated products, would like to respond to this piece jointly to show our commitment to working together in an open, transparent fashion.

Our companies agree with most of the recommendations Ng and colleagues made.  Without doubt, genotype-based risk prediction for common, multifactorial diseases is still in its infancy.  More work must be done to standardize markers used; to better explain the contribution of genetics to common, complex diseases; and to incorporate common genetic variants into clinical practice.  Each company, however, has a few points of disagreement and/or explanation it feels important to articulate.  These points from each company follow.

Continue Reading »

PET scans showing dopamine activity in a normal brain and a Parkinson’s patient’s before and after treatment with a therapeutic implant.

More than a million Americans have Parkinson’s disease, and another 50,000 are diagnosed each year. Scientists know that many of the characteristic symptoms of Parkinson’s — tremors, rigid muscles and movement problems — can be traced back to the loss of dopamine-producing brain cells.  But what researchers don’t fully understand is why these cells are damaged in the first place.

For most cases of Parkinson’s, the brain cell damage is probably the result of  complex interactions between multiple genetic and environmental factors.  Despite years of work, however, hardly any of these factors are known.  But now two research groups have identified several genetic variants associated with the risk of Parkinson’s in Asian and Caucasian populations.  Their results were published online this week in the journal Nature Genetics. Continue Reading »

Tags: BST1, LRRK2, MAPT, PARK16, Parkinson's Disease, SNCA

Some people want to know everything their genetics can tell them, while others are interested in only part of the story.  That’s why starting next week, on Thursday November 19^th , we will begin offering our service as two distinct products to better meet the needs of our customers:  The 23andMe Ancestry Edition and The 23andMe Health Edition.  If you are interested in both the ancestry and the health aspects of your genetics, you’ll have the option of purchasing the combined 23andMe Complete Edition.

Prices for all versions of the 23andMe Editions will be changing November 19^th, but if you act quickly you can get our Personal Genome Service, which will automatically be converted to the Complete Edition, for the lower price of $399.

Continue Reading »

Tags: ancestry, health, product, relative finder

The most common type of arthritis, osteoarthritis, occurs due to accumulated wear and tear – welcome to old age! – or from repetitive movements or injury.  Rheumatoid arthritis, on the other hand, is caused by an autoimmune attack on the lining of the joints, resulting in stiffness, muscle aches, and general fatigue. Approximately two million people in the U.S. suffer from rheumatoid arthritis, and although women are affected more often than men, men tend to have more severe symptoms.

Research has identified a number of genetic factors that contribute to one’s risk of developing rheumatoid arthritis, and new studies continue to reveal more genes that seem to be involved in this complex disease. In a report published this week in Nature Genetics, a team led by Soumya Raychaudhuri and Robert Plenge of Brigham and Women’s Hospital in Boston describe three new genetic associations with rheumatoid arthritis risk.

Continue Reading »

Tags: autoimmune, Nature Genetics, Rheumatoid Arthritis

Cisplatin, a cancer chemotherapy drug first approved by the FDA in 1978, revolutionized the treatment of many types of cancer.  Despite its effectiveness, in many cases doctors are forced to reduce the drug’s dose, or abandon it altogether, due to serious side effects on patients’ hearing.

Between 10-25% of adults and up to 60% of children being treated with cisplatin suffer from severe, permanent hearing loss in both ears. This is particularly damaging in kids, because even mild hearing loss can negatively impact learning and social development.

Researchers have suggested that genetic variants that affect the metabolism of cisplatin might explain why some people are susceptible to drug-induced hearing loss, while other patients receiving similar doses are not.  A new report, published online this week in the journal Nature Genetics, has identified variants in two genes that appear to greatly increase the risk of cisplatin-induced hearing loss.  Although the study is a small one, if replicated these findings could one day help doctors make better decisions about how to prescribe cipslatin. Continue Reading »

Tags: chemotherapy, children, cisplatin, COMT, hearing loss, TPMT

The Kaiser Permanente Research Program on Genes, Environment and Health (RPGEH) is an exceptional study that has the potential to transform medicine.  As someone who proudly spent over 25 years as a patient with Kaiser, I would be excited to see my family’s medical records used for such a worthy cause.  I was disappointed, however, to learn that Kaiser will not be giving participating individuals the option to get access to the genetic data Kaiser generates in the study, as I said in my recent TEDMED talk.  Yesterday, Cathy Schaefer, executive director of the RPGEH, commented on the Robert Wood Johnson Foundation blog that the research data will not be returned “because genetic information obtained through today’s genome-wide studies has not been designed to be useful to individuals; it is designed for use in research” (also noted by Genomics Law Report and Genetic Future).

I strongly disagree that one’s genome is currently only useful in research and not for individual use.   There are a number of highly useful genetic results that may be generated.  Individuals may learn that they are carriers for Mendelian disorders such as cystic fibrosis or sickle cell anemia.  The genetic data might reveal that an individual is at higher risk for certain diseases such as age-related macular degeneration, blood clots, Parkinson’s disease or breast cancer.  Last, the genetic data may tell an individual whether or not they are likely to respond to certain drugs, like Plavix and Coumadin.  Is it right for Kaiser to tell me what information I can or cannot have about my own body and my own genes?

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The “stomach flu” isn’t really the flu at all. It’s actually viral gastroenteritis, and its most common cause is a group of viruses called noroviruses. No matter what you call it, the illness is highly contagious and very unpleasant — symptoms include abdominal pain, vomiting, and diarrhea. In close quarters, a norovirus outbreak can quickly spread from person to person, earning the sickness the nickname “cruise ship disease.”

Norovirus is such a problem on cruise ships, in fact, that the Centers for Disease Control and Prevention (CDC) has a Vessel Sanitation Program in place to help control outbreaks.  But the results of a new study, published in this month’s issue of the journal Clinical Infectious Diseases, shows that even stricter criteria for cleanliness may be in order.

Analysis of data from 56 cruise liners evaluated between 2005 and 2008 shows that only 37% of 8,344 toilet area objects (toilet seat, flush handle or button, toilet stall inner handhold, stall inner door handle, restroom inner door handle and baby changing table surfaces) in 273 randomly selected public restrooms were cleaned on a daily basis.  More than half of the ships had overall “thoroughness of disinfection cleaning”  (TDC) scores less than 30%.  Several of these low-scoring ships had nearly perfect CDC sanitation scores.  TDC scores were substantially lower for the three ships that had a norovirus outbreak within four months of evaluation compared to those ships that did not.

Why bring this up in the Spittoon?  A lucky few have less to worry about when planning a seafaring vacation: variation in the FUT2 gene renders some people resistant to the most common strain of norovirus.  Check out the 23andMe Norovirus Resistance Report to learn more!

Tags: CDC, cruise ship, norovirus

New research suggests that your skills behind the wheel may be affected by your genes.

To better understand the effects of a variant in the BDNF gene on motor skills learning, Steven Cramer and colleagues at UC Irvine tested 29 subjects in a driving simulator. Their results, published in the journal Cerebral Cortex, might make you think twice about whom you go on your next road trip with.

Subjects sat in front of a screen with their hands firmly planted at “10 and 2″ on a steering wheel and guided their “car” around a track, attempting to stay centered over a black line. The steering was tuned so that subjects had to begin turning before the screen actually changed.

Over the course of 15 trials, all of the study subjects got better at the driving task. But the seven people who had a T rs6265 improved less than those with two Cs. When subjects returned to the lab four days later for a final lap, everyone had forgotten how to drive the simulator a little bit, but those with a T did worse.

“These people [with a T at rs6265] make more errors from the get-go, and they forget more of what they learned after time away,” Cramer said in a press release.

(23andMe customers can check their data for rs6265 using the Browse Raw Data feature.) Continue Reading »

Tags: BDNF, driving, Huntington's, lupus, multiple sclerosis, Parkinson's, stroke

Medco Health Solutions, Inc., announced this week that it will conduct a clinical trial to assess whether clopidogrel bisulfate (Plavix®, Bristol-Myers Squibb and Sanofi-aventis) is just as effective as the newer drug prasugrel (Effient™, Eli Lilly and Company) in people who lack a genetic variation that inhibits their metabolism of clopidogrel. This new research has important implications for both patient safety and health care costs.

Both clopidogrel and prasugrel are anti-platelet medications that reduce the ability of blood to form clots. The drugs are used to reduce the risk of a heart attack and stroke in people who have suffered from a recent cardiovascular event, and in those who have peripheral artery disease, unstable angina or a stent.

Variations in the CYP2C19 gene that prevent clopidogrel from being converted into its active form in the body have been shown to prevent patients from receiving the drug’s full benefit. People with these gene variations who are taking clopidogrel may be at a higher risk for heart attacks, strokes and death from cardiovascular causes than those whose genetics allow them to metabolize the drug.

(Prasugrel is metabolized through a different biological pathway than clopidogrel, and is not affected by CYP2C19 variants.)

23andMe customers can see their data for several important CYP2C19 variations in the ‘Clopidogrel (Plavix®) Efficacy’ Clinical Report. Continue Reading »

Tags: clopidogrel, clotting, comparative effectiveness research, CYP2C19, Effient, Francis Collins, heart, Medco, pharmacogenomics, Plavix, prasugrel