ED&#8217;s note: Health Labs is no longer a feature within 23andMe&#8217;s current product.
In 2009, we added six tools to 23andMe Labs, our technology sandbox, where we showcase experimental features. In case you haven&#8217;t played around with them yet, here&#8217;s a brief review:
<h6>Health Labs </h6>
Reynolds Risk Score 
This tool calculates a 10-year risk for heart-attack using information including cholesterol and blood pressure.
ABO Blood Type 
There actually are more than 25 different blood groups that go into determining your particular &#8220;type,&#8221; but you&#8217;re probably most familiar with the blood group defined by the ABO gene. This gene determines whether you will be type O, A, B, or AB.
Genetic Weight Calculator 
See how much of your weight you can blame on your genes (not your jeans)!
<h6>Ancestry Labs</h6>
<a href="https://blog.23andme.com/articles/23andme-labs-kicks-off-with-haplogroup-tree-mutation-mapper/" target="_blank" rel="noopener noreferrer">Haplogroup Tree Mutation Mapper</a>This feature shows you which particular mutations in a person&#8217;s mitochondrial DNA (maternal ancestry) or Y chromosome (paternal ancestry) were used to determine their haplogroup assignment.
Family Inheritance: Advanced 
Bit by bit, compare your DNA to see what segments you share with close and distant family.
Native American Ancestry Finder 
Search for evidence of Native American ancestry in a person&#8217;s genome.
Customers who have purchased the Complete Edition of our service have access to both Health and Ancestry Labs. Customers with either the Health or Ancestry Editions of 23andMe have access only to the Labs relevant to their received data.
The point of Labs is to let you, our customers, play around with cutting-edge tools while our scientists are still developing them.   What can we say?   We&#8217;re super excited about genetics, and we love to share!   Each Lab has its own community, so you can compare notes, ask questions, and share ideas.   We love to hear your ideas and comments!
But please remember that labs are a free feature and are not part of our regular service.   Some labs require specialized knowledge or may be of interest only to a subset of our customers. Because they&#8217;re still in development, you can expect labs to be a little less refined than our regular product and somewhat fluid. All of them are still in beta.   A feature could be discontinued at any time or elevated to full integration with our Personal Genome Service.

23andMe Blog

23andMe Blog Team

23andMe Labs

In our last post we highlighted a few of the coolest (in our opinion!) health-related developments of 2009.   But human genetics isn&#8217;t all about disease.   Here are a few more favorites:
The Romanovs
2009 saw the identification of the remains of the missing members of this Russian royal family, as well as identification of the mutation that caused the hemophilia that plagued their youngest son.
<a href="https://blog.23andme.com/articles/leaving-no-stone-unturned-dna-analysis-confirms-identities-of-missing-romanovs" target="_blank" rel="bookmark noopener">Leaving No Stone Unturned: DNA Analysis Confirms Identities of Missing Romanovs</a>
<a href="https://blog.23andme.com/articles/researchers-discover-the-true-identity-of-the-royal-disease" target="_blank" rel="bookmark noopener">Researchers Discover the True Identity of the “Royal Disease”</a>
The Celtic Fringe
The genetics of adorable little critters helped scientists understand the prehistory of the British Isles.
<a href="https://blog.23andme.com/articles/life-on-the-fringe-shrews-and-voles-reveal-clues-to-british-prehistory" target="_blank" rel="bookmark noopener">Life on the Fringe: Shrews and Voles Reveal Clues to British Prehistory</a>
Link Between Australian Aborigines and India
Scientists discovered mitochondrial DNA markers shared by isolated tribes in India and native Australians&#8230;and nobody else.
<a href="https://blog.23andme.com/articles/direct-genetic-link-between-australia-and-india-provides-new-insight-into-the-origins-of-australian-aborigines" target="_blank" rel="bookmark noopener">Direct Genetic Link between Australia and India Provides New Insight into the Origins of Australian Aborigines</a>
Largest Ever Study of Modern African Genetics 
2,432 DNA samples from 113 diverse and distinct groups of people from across the African continent as well as 60 non-African groups. Everyone from the Mozabite Berbers of Morocco to the hunter-gatherer San of the Kalahari Desert, and many in between.
<a href="https://blog.23andme.com/articles/scientists-publish-largest-ever-study-on-the-genetics-of-modern-africans" target="_blank" rel="bookmark noopener">Scientists Publish Largest-Ever Study on the Genetics of Modern Africans</a>
Dogs
We can&#8217;t forget all those dog genetics studies.   Man&#8217;s best friend is certainly a friend of the Blog&#8217;s!
<a href="https://blog.23andme.com/articles/single-gene-responsible-for-stubby-legs-in-dogs" target="_blank" rel="noopener">Single Gene Responsible For Stubby Legs In Dogs</a>
<a href="https://blog.23andme.com/articles/whence-rover-genetic-study-suggests-africa-may-have-whelped-mans-best-friend" target="_blank" rel="noopener">Whence Rover? Genetic Study Suggests Africa May Have Whelped Man’s Best Friend</a>
<a href="https://blog.23andme.com/articles/study-sniffs-out-genes-behind-doggy-dos" target="_blank" rel="noopener">Study Sniffs Out Genes Behind Doggy ‘Dos</a>

2009 Blog Highlights – Part 2

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3440" title="Abstract DNA" src="https://blog-api.23andme.com/wp-content/uploads/2009/04/istock_000002166527xsmall.jpg" alt="Abstract DNA" width="334" height="243" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/04/istock_000002166527xsmall.jpg 406w, https://blogcms.23andme.com/wp-content/uploads/2009/04/istock_000002166527xsmall-300x219.jpg 300w" sizes="auto, (max-width: 334px) 100vw, 334px" />
A new study has identified more common genetic variants associated with increased risk for cleft lip and palate.   Combined with two previous studies, there are now four variations that have been associated with this birth defect that affects about one out of every 700 children born.
Clefting results from improper fusing during fetal development of the different elements that will make up the lower part of the face.   For some children only the lip is affected, while others have clefting of both the lip and palate.   Cleft palate alone is much more rare.
An international team led by German researchers analyzed the DNA of 399 people born with cleft lip with or without cleft palate and 1,318 controls.   Many of these people had been included in one of the previous studies that found a genetic association with clefting.   The researchers then examined the most promising variants in 665 families with an affected child.   All of the study subjects had European ancestry.
Two SNPs with significant associations were identified.   The results were published online yesterday in the journal <a href="https://dx.doi.org/10.1038/ng.506" target="_blank" rel="noopener noreferrer">Nature Genetics</a>. Both and are located in regions of the genome previously associated with cleft lip and/or palate in animal models and in humans.
There is some evidence that cleft lip with and without cleft palate are two separate conditions, possibly with different genetic risk factors.
The researchers believe that together the previously described variants and these two newly identified SNPs account for a substantial proportion of the risk for sporadic cleft lip with or without cleft palate.   However, they think there are probably still additional genetic variants associated with this condition left to be found.

SNPwatch: Two More Genetic Variants Linked to Cleft Lip and Palate

<img loading="lazy" decoding="async" class="alignright size-full wp-image-5677" title="alzheimers" src="https://blog-api.23andme.com/wp-content/uploads/2009/12/alzheimers.jpg" alt="alzheimers" width="357" height="254" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/12/alzheimers.jpg 435w, https://blogcms.23andme.com/wp-content/uploads/2009/12/alzheimers-300x214.jpg 300w" sizes="auto, (max-width: 357px) 100vw, 357px" />
More than a million Americans have Parkinson’s disease, and another 50,000 are diagnosed each year. There is active research to try to understand this devastating condition, but scientists still don&#8217;t really know what causes it.   There are no clear environmental triggers for the disease, and genetics doesn’t seem to play a large role either — it is estimated to be involved in fewer than 10% of cases.
Of the <a href="https://blog.23andme.com/2009/03/19/understanding-the-genetics-of-parkinsons-disease-a-work-in-progress/" target="_blank" rel="noopener">few known genetic causes of Parkinson&#8217;s</a>, one of the most common is the LRRK2 G2019S mutation. While the average person has a 1-2% chance of developing Parkinson’s, the risk for someone with the G2019S mutation is much higher and increases with age. One recent study found that a person who inherits this mutation from either parent has a 28% chance of developing Parkinson’s by the age of 59, 51% by the age of 69 and 74% by the age of 79.
Previous research had suggested that the LRRK2 G2019S mutation is associated with a form of Parkinson&#8217;s where the predominant symptom is tremor.   But a new study, published this week in the <a href="http://archneur.ama-assn.org/cgi/content/abstract/66/12/1517?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;fulltext=motor+phenotype&amp;searchid=1&amp;FIRSTINDEX=0&amp;resourcetype=HWCIT" target="_blank" rel="noopener">Archives of Neurology</a>, suggests that carriers of this mutation are in fact more likely to manifest a different form of Parkinson&#8217;s called the postural instability and gait difficulty (PIGD) phenotype.    Though this result must be borne out by further studies, it could have important implications for what mutation carriers can expect from their disease: the <a href="http://www.pdonlineresearch.org/responses/3614/289/clinical-pd-subtypes-tremor-dominant-and-postural-instability-gait-difficulty-pig" target="_blank" rel="noopener">PIGD phenotype</a> of Parkinson&#8217;s is associated with a less favorable prognosis.
Dr. Roy Alcalay and colleagues analyzed the DNA of 691 people with early-onset Parkinson&#8217;s disease (symptoms starting before age 51) from13 movement disorder centers throughout the United States, 26 of whom carried the LRRK2 G2019S mutation.   Patients were scored for various measures of tremor and the PIGD phenotype using the Unified Parkinson&#8217;s Disease Rating Scale (UPDRS).   A ratio of the two scores was then used to assign a designation as tremor dominant, PIGD, or intermediate.   Earlier studies of LRRK2 G2019S carriers did not employ this careful scoring system.
After adjusting for Ashkenazi Jewish ancestry (the G2019S mutation is especially common in this group) and disease duration, Alcalay et al. found that mutation carriers were more likely than non-carriers to have the PIGD phenotype.   Due to the small sample size it&#8217;s hard to say precisely how large the effect was, but the researchers estimate an increase in odds of 17.7 times, although the true increase may fall anywhere between 3.8 and 83.1 times.
In general, studies have indicated that the people with Parkinson&#8217;s who have the PIGD phenotype have more severe disease and faster cognitive decline than patients with tremor dominant disease.   Whether this prognosis applies to LRRK2 G2019S carriers with the PIGD phenotype remains to be tested.
More work with larger and more ethnically diverse study samples that are followed for a longer period of time will be needed to confirm these findings.
Even though it is the most common known genetic cause of Parkinson’s disease, the G2019S mutation is responsible for only a small fraction of all cases worldwide – about one or two in a hundred. But in some ethnic groups it is a much more frequent cause of the condition. According to published research, up to 40% of people of North African Arab ancestry and 20% of Ashkenazi Jewish people with Parkinson’s have this mutation.

LRRK2 Implications for Parkinson’s Disease

<img loading="lazy" decoding="async" class="alignright size-full wp-image-5653" title="H1N1-blog-post-pic" src="https://blog-api.23andme.com/wp-content/uploads/2009/12/H1N1-blog-post-pic.gif" alt="H1N1-blog-post-pic" width="350" height="245" />
By now, you&#8217;re probably sick of hearing about the 2009 H1N1 flu, also known as the swine flu.
But if you believe you&#8217;ve had it, and you&#8217;ve already recovered from your symptoms, please take a few minutes to complete our new survey.
<h6>H1N1 Flu Symptoms</h6>
There have been heard reports of people holding &#8220;swine flu parties&#8221; in hopes of getting the &#8220;mild form&#8221; of the H1N1 virus.   But there&#8217;s really only one H1N1 virus out there.   Any variability has to do with how people&#8217;s bodies are reacting to it. (BTW: The <a href="https://www.cdc.gov/H1N1FLU/" target="_blank" rel="noopener">CDC</a> says this is one kind of party you <a href="https://www.npr.org/templates/story/story.php?storyId=114144189" target="_blank" rel="noopener">definitely want to skip</a>!)
Some who&#8217;ve been infected with H1N1 have suffered from nothing more than a few miserable days stuck in bed.   For others, the virus has caused severe illness resulting in hospitalization and even death.   Some of these differences have to do with age, gender and pre-existing disease burden.
<h6>But there are probably genetic factors at work too.Genetics of Susceptibility</h6>
A <a href="http://www.sciencedaily.com/releases/2009/12/091217122528.htm" target="_blank" rel="noopener">study</a> published just today shows that human cells have proteins that seem to be natural flu fighters.   The researchers who made this discovery suggest that genetic changes that affect the levels of these proteins could determine different levels of vulnerability to the H1N1 virus.
By asking our large and diverse group of customers about their experiences with the flu, and then correlating this information with their genetics, 23andMe hopes to help scientists continue to unravel the mysteries of H1N1.
Genetic markers indicating a propensity for an especially severe reaction to the flu could someday be used to identify people in need of extra attention during outbreaks.   And learning more about the flu in general might lead to new management strategies that could benefit us all.   So please, take a few minutes to answer our H1N1 Survey.
P.S. If you don&#8217;t think you&#8217;ve had the swine flu this year, don&#8217;t worry — there are <a href="https://www.23andme.com/you/23andwe/surveys/" target="_blank" rel="noopener">plenty of other surveys</a> for you to take.   You can always participate in this new survey if you do happen to get sick (though we hope you don&#8217;t!).

23andMe H1N1 Flu Survey: Share Your Experience

<img decoding="async" class="alignright size-full wp-image-5641" title="Mycobacterium_leprae" src="https://blog-api.23andme.com/wp-content/uploads/2009/12/Mycobacterium_leprae.jpg" alt="Mycobacterium_leprae" width="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/12/Mycobacterium_leprae.jpg 489w, https://blogcms.23andme.com/wp-content/uploads/2009/12/Mycobacterium_leprae-293x300.jpg 293w" sizes="(max-width: 489px) 100vw, 489px" />
Leprosy is a chronic, disabling disease caused by a bacterium (Mycobacterium leprae) that infects only humans and armadillos.
The disease affects the skin and peripheral nerves, leading to sores, numbness in the limbs, muscle weakness, and, in severe cases, disfiguring nodules on the skin. Known since biblical times, leprosy was highly stigmatized until the latter part of the 19th century when Norwegian doctor Gerhard Hansen discovered that it was caused by a microorganism.
<h2>Treatment and Prevention</h2>
Although multi-drug therapy has cured millions of people of leprosy in recent decades, hundreds of thousands of new cases still occur per year, mostly in developing countries. Finding a way to eradicate the disease is therefore considered essential for reducing the number of preventable disabilities worldwide.
Because Mycobacterium leprae is specific to humans and cannot be grown in lab dishes, research into factors influencing disease susceptibility and clinical outcomes has been limited. But the host environment, as well as the bacterium itself, can affect the course of the disease; in other words, human genetic factors may play an essential role in determining who is more susceptible to infection.
Since leprosy has been shown to cluster in families, scientists suspect that much of the variability in disease susceptibility and symptoms stems from diversity in individual human immune systems rather than differences between and within strains of the bacteria.
<h2>New Research</h2>
In a new study published today in <a href="http://content.nejm.org/cgi/content/full/NEJMoa0903753">New England Journal of Medicine</a>, researchers report new human genetic factors associated with susceptibility to leprosy in Asians. Led by Fu-Ren Zhang of the Shangdong Academy of Medical Sciences in China and Jian-Jun Liu of the Genome Institute of Singapore, the scientists tested 93 variants across an estimated 50 genes in 3254 Chinese individuals with leprosy and 5955 Chinese individuals without the condition. Their analysis identified seven gene variants to be significantly associated with leprosy.
&#8220;The discovery of these genes is a major breakthrough for research in leprosy and infectious diseases in general and will be significant in the early diagnosis and development of new treatments,&#8221; said Dr. Liu in a <a href="http://www.eurekalert.org/pub_releases/2009-12/afst-lsg121409.php">press release</a>.
The strongest associations were in HLA-DR-DQ, C13orf31, and NOD2. In addition, some of the genetic variants were more strongly associated with a form of leprosy that results in more severe symptoms, known as the multibacillary form. These included NOD2 and the variant in LRRK2.
<h2>Association with Crohn&#8217;s</h2>
Altogether, five of the seven genes identified in the study could be shown to interact biologically in the context of immune response to infection. Two of these five genes, NOD2 and TNFSF15, harbor genetic variants associated with Crohn’s disease. Crohn’s manifests some common features with leprosy at the cellular level, and other researchers have suggested that mycobacterial infection may be a risk factor for Crohn’s. The findings reported by Zhang and Liu and their colleagues provide additional evidence for shared disease mechanisms between Crohn’s disease and leprosy. They may increase the range of treatment options for both conditions.
** This effect is only applicable to the multibacillary form of leprosy. LRRK2 is better known as a susceptibility gene for Parkinson&#8217;s disease (see 23andMe&#8217;s <a href="https://www.23andme.com/health/Parkinsons-Disease/">report</a> on this condition). Interestingly, PARK2, another gene linked to Parkinson&#8217;s, was associated with leprosy in earlier studies. The reason for the connection between Parkinson&#8217;s and leprosy is unclear, though researchers have speculated that some of the same treatments may be effective for both conditions.

Genetic Association Study of Leprosy Yields New Insights into an Ancient Disease

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Multiple sclerosis (MS) afflicts the central nervous system, causing unpredictable and varying symptoms that differ from person to person. About one in 700 people in the United States is affected by the disease. Although there is currently no cure for MS, there are treatments that can slow the progression of the disease and enhance the quality of life for people who have this condition.
Researchers have identified several genetic variants in the HLA region of the genome —an area containing many genes involved in immune system function — that seem to affect MS symptoms, disease severity, and response to treatment. One of these variants is in the HLA-DRB1 gene. Known as HLA-DRB1*1501, this variant is associated with increased risk for MS, though exactly how it is involved in development of the disease is unclear.
In a report published online today in the journal &nbsp;<a href="http://archneur.ama-assn.org/cgi/content/abstract/66/12/1531">Archives of Neurology</a>, a team of researchers led by Drs. Madeleine Sombekke and Chris Polman of Vrije University in Amsterdam uncovered a clue which may elucidate the connection between the HLA-DRB1*1501 variant and multiple sclerosis. They analyzed *1501 and other genetic variants in 150 Dutch individuals with multiple sclerosis to see if any of the SNPs were associated with variation in brain and spinal cord lesions.
One SNP in particular, (used as a proxy for HLA-DRB1*1501), was associated with spinal cord lesions. People carrying at least one copy of the A version of had significantly more spinal lesions and had more segments of the spinal cord affected than people with two copies of the G version.
MS is believed to be an autoimmune disorder — wherein the immune system attacks the body’s own cells rather than foreign invaders — and so it makes sense that genetic variants in immune system genes would influence the course of the disease and its clinical features. HLA genes, in particular, encode proteins that contribute to self vs. non-self immune recognition. Previous studies have proposed a link between HLA-DRB1*1501 and disease severity. Since lesions on the spinal cord are often used to diagnose MS and the degree of disability, Sombekke’s team suggests that the association of HLA-DRB1*1501 with spinal cord lesions might help explain its relationship with severity of the disease.

Genetic Link between MS and Spinal Cord Lesions

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Nobody likes that sick feeling you get in your stomach when you watch a young college athlete hit the ground in pain and you wonder if his or her career is over before it even started.
And who can forget how Bo Jackson, Steve Young and Dikembe Mutombo, all superstar professionals, saw their illustrious careers end as a result of sports-related injuries.   Even for us amateurs who have a lot less riding on our performance, missing a game or workout because the old knee is acting up again is a total bummer.
<h2>The Genetics of Sports Injuries</h2>
23andMe would like to learn more about how genetic factors might predispose athletes of all skill levels to certain sports injuries and you can help.
Injuries can have a huge impact on a person’s life.  For example, more than half of professional American football players retire because of an <a href="https://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2002/09/01/IN183821.DTL" target="_blank" rel="noopener noreferrer">injury</a>.   One fifth of National Football League wide receivers and running backs who suffered anterior cruciate ligament injuries (ACL, a knee ligament that joins the upper leg bone to one of the lower leg bones) <a href="http://ajs.sagepub.com/content/34/12/1911.abstract" target="_blank" rel="noopener noreferrer">never played another NFL game</a>.
<h2>Let&#8217;s Look at Some Numbers</h2>
While getting injured is a fact of life in professional sports, it&#8217;s no less of an issue for the non-professional weekend warrior.
About 40% of people over the age of 50 have rotator cuff tears, which can cause shoulder pain.   Every year, there are 200,000 ACL injuries, and 100,000 surgeries to try to repair those ACL tears and ruptures.
To add insult to injury, having an ACL tear puts you at higher risk for eventually developing knee osteoarthritis.   This type of problem isn&#8217;t restricted to athletes either.   Playing sports like golf or tennis can cause tendinitis, but so can everyday repetitive activities like raking or painting.
The types of activities you&#8217;re involved in are obviously a huge factor in your risk for a sports-related injury, but there is evidence that genes play a role as well.   People with a parent, sibling, or child who had an ACL tear are <a href="https://www.ncbi.nlm.nih.gov/pubmed/15610995" target="_blank" rel="noopener noreferrer">much more likely to suffer a tear themselves</a>.
<h2>Some Injuries Run in Families</h2>
There&#8217;s also likely to be a <a href="https://www.ncbi.nlm.nih.gov/pubmed/19411462" target="_blank" rel="noopener noreferrer">familial predisposition</a> towards rotator cuff tears.
Knowing ahead of time what injuries you are prone to, either based on the activities you do, or what you&#8217;re genetically predisposed to, could be a key to prevention.   Those who are at risk for ACL tears can follow an ACL conditioning program, while strengthening and maintaining the flexibility of the <a href="https://www.23andme.com/topics/wellness/muscle-composition">muscles</a> in your shoulders can help prevent rotator cuff injuries. For those who are at risk of tendinitis, taking things slowly and limiting repetitive activities may help prevent inflammation or irritation of the tendon.
There&#8217;s some tantalizing data to suggest that our genes can tell us something about our risk for sports injuries, but frankly, very little is known.   23andMe wants to change that, and it&#8217;s easy for you to get involved &#8212; all you have to do is take our Sports Injuries survey.   By making new discoveries, we can help everyone stay in the game.

23andMe Sports Injuries Survey: Staying in the Game

<img loading="lazy" decoding="async" class="alignright size-full wp-image-5593" title="longevity-blog-post-pic" src="https://blog-api.23andme.com/wp-content/uploads/2009/12/longevity-blog-post-pic.gif" alt="longevity-blog-post-pic" width="350" height="489">
From alchemists and the Philosopher&#8217;s Stone to Ponce de Leon and the Fountain of Youth, history is full of stories of people searching for a way to extend life indefinitely. &nbsp; In recent years, discoveries about the biology of aging have brought us closer to that dream than ever before. &nbsp; Now 23andMe is asking you, our customers, to help push science even further by participating in our new Longevity Survey.
Human life expectancy is now close to 78 years. Back in 1900, the average person was expected to live only about 47 years. &nbsp; The oldest person so far whose age was verified by official documents was Jeanne Calment of France, who died at the spectacular age of 122 in 1997, but one aging researcher at the University of Texas Health Science Center has bet that someone will have lived to be 150 years old by the year 2150! Our improved understanding of health and human biology, including the development of antibiotics, has helped to fuel this huge increase in how long we expect to live.
We all know that environmental factors and lifestyle factors are important when it comes to attaining a ripe old age. &nbsp; You have to eat right, exercise enough, and avoid all those vices like smoking and too much drinking. &nbsp; But it&#8217;s not all what you do and how you live that determines whether you&#8217;ll live a long life, and if you do, whether you&#8217;ll be in good shape. &nbsp; Genes are involved in aging as well.
A lot of the work on understanding the genetic factors involved in aging have been done in laboratory animal models. &nbsp; Mutations in a gene called daf-2 in soil worms can double their lifespan. &nbsp; Similar mutations can make fruit flies live up to 80% longer, and mice 30% longer than normal. &nbsp; &nbsp; Daf-2 makes a protein that&#8217;s similar to one that binds insulin, the hormone that regulates glucose intake from your blood. &nbsp; Some have speculated that daf-2 mediates the the longevity effects of dietary restriction (consuming a significantly reduced number of calories without malnutrition), which has been shown to extend the lifespan of both mice and monkeys.
That&#8217;s all well and good if you&#8217;re a worm or a fly or a mouse, but what about people? &nbsp; Well, there&#8217;s some progress in understanding aging in us too. &nbsp; Studies have shown that variants in the <a href="https://www.23andme.com/health/Longevity/" target="_blank" rel="noopener">APOC3</a> gene and the <a href="https://blog.23andme.com/2009/02/02/snpwatch-mounting-evidence-that-foxo3a-contributes-to-human-longevity/" target="_blank" rel="noopener">FOXO3A</a> gene are associated with longevity. &nbsp; On the flip side, researchers have discovered that &nbsp; mutations in the RECQL2 gene cause Werner&#8217;s syndrome, a disease that manifests as accelerated aging.
Our DNA is likely to hold many more of the secrets to living a long, healthy life. &nbsp; That&#8217;s why 23andMe wants to do research to understand more about what genes can tell us about aging and longevity. &nbsp; We&#8217;re working with experts in aging research from across the country, and you can join us! &nbsp; Start by taking our Longevity Survey, which simply asks about the ages of some of your family members. &nbsp; Hopefully together we can make discoveries that will help people enjoy even more healthy golden years.

Latest Posts — Page 180