<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.

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LRRK2 Implications for Parkinson’s Disease

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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

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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.

Help Us Discover the Keys to Living a Long, Healthy Life

<img decoding="async" class="alignright size-full wp-image-4645" title="Lou Gehrig" src="https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1.jpg" alt="Lou Gehrig" width="275" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/09/Gehrig1.jpg 443w, https://blogcms.23andme.com/wp-content/uploads/2009/09/Gehrig1-222x300.jpg 222w" sizes="(max-width: 443px) 100vw, 443px" />
Amyotrophic Lateral Sclerosis (ALS) is a rare and deadly neurological disorder affecting voluntary muscle movement. It typically claims victims&#8217; lives about three years after symptoms begin. In the United States,  the condition is more commonly known as Lou Gehrig&#8217;s disease, after the Yankees slugger who died of ALS in 1941. About 20,000 people in the U.S. have ALS and one in 100,000 people develop the disease per year.
Despite years of research, relatively little is known about the causes and risk factors of ALS. This week, understanding of the disease moved a step forward with a <a href="https://www.pnas.org/content/early/2009/12/08/0902174106.abstract">study published in </a><a href="https://www.pnas.org/content/early/2009/12/08/0902174106.abstract">PNAS</a> that identified several new genetic variants associated with ALS risk.
A team of scientists led by Francois Gros-Louis and Jean-Pierre Julien of UniversitÃ© Laval in Canada analyzed genetic variants in the CHGB gene in more than 700 French and Swedish people with ALS and 750 people without the disease. Although most of the variants found in the CHGB gene were rare, one of the more common variants was markedly more frequent in those with ALS than in those without. The rarer T version of this SNP was associated with about 2.4 times increased odds of ALS, compared to the more prevalent C version. The SNP also seemed to affect age-of-onset: individuals with the T version of tended to develop ALS about 10 years earlier than individuals with two copies of the C version.
One of the hallmarks of ALS and some other neurodegenerative diseases is the abnormal aggregation of proteins within cells. Many of these aggregations appear in organelles known as the endoplasmic reticulum (ER) and the Golgi network, which are tasked with processing proteins into their mature forms and readying certain ones to be secreted, or released outside the cell.
Gros-Louis and his team focused on the CHGB gene because of its “guilt-by-association” relationship with SOD1, one of the few established genetic factors linked to ALS. Abnormal SOD1 proteins tend to aggregate in motor neurons of people with ALS, and recent reports have found chromogranin B, the protein encoded by CHGB, near these aggregates.
Chromogranin B is typically secreted from cells like a hormone, and so the researchers hypothesized that genetic variants in CHGB associated with increased risk for ALS might impair secretion of chromogranin B. Sure enough, in cells with CHGB containing the T version of , almost all of the protein remained sequestered inside the ER/Golgi network.   In cells with normal CHGB, only 40% of the chromogranin B protein was found there.
Previous studies in this area have indicated that stress and damage to the ER and Golgi are a defining characteristic of ALS-affected motor neurons. Gros-Louis and his colleagues suggest that further research be done to investigate whether CHGB variants like stress the ER-Golgi system and hasten the deterioration of motor neurons.

A New Genetic Variant Associated with ALS Risk and Age-of-Onset

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Esther Dyson is a Director of 23andMe and an investor in numerous Internet, private aviation, space and health care ventures.   She has also shared her genetic data, medical records and other personal information with the research community and the general public as a research subject for the <a href="http://www.personalgenomes.org/" target="_blank" rel="noopener">Personal Genome Project</a>, an initiative led by Harvard&#8217;s George Church that aims to make personal genome sequencing more affordable, accessible and useful for humankind.
The Blog talked with Esther to get some of her thoughts on the value and future of personal genomics.
<h6>You&#8217;ve received information about your genetics from both 23andMe and the Personal Genome Project.   How do these two experiences compare?</h6>
There was no &#8220;news&#8221; from either service.   Based on current knowledge, there&#8217;s nothing in my genes that I need to be particularly worried about.
There was a difference in how I got my genetic information from PGP versus 23andMe.   PGP gives you a single report, and you sit down with a scientist who explains anything out of the ordinary, but that’s it.
But with 23andMe, the website lets me go back again and again to learn–both about myself and about genomics in general.   Also, I can look at the data for my close relatives [who have also joined] and see what&#8217;s in their genomes and how they compare to me.   If something new comes out, chances are that I can go to 23andMe and see if there is something relevant in my own DNA or my family’s.   The value isn’t just in the genome; it’s in the explanation of the genome.
<h6>So 23andMe gives you the tools to really get to know your genes.   Why is that important?</h6>
I&#8217;m a big fan of knowledge, in particular and in general.   The more you know about your body and your genome, and about how what you do interacts with your genome, the better off you are.   Of course, the same applies to knowing more about the people you care about–with their consent!   It&#8217;s always better to understand more about yourself and how you work.
As for the meaning–the value–there&#8217;s still a lot of research to be done by scientists.   Yet at first, those research results aren&#8217;t accessible. The real value to individuals is going to be in applying research findings to their own genomes in order to get something meaningful.
Like a bank filled with money, your genome is full of value. But without a way to get at that value, it&#8217;s worthless to the individual.   23andMe fits into the picture in two ways.   It&#8217;s like the ATM that gives you access to the wealth locked within your genes.   But it&#8217;s also like a financial tool that helps you analyze that wealth:   What is fixed and what is risky, for example?
<h6>Do you think there is a broader role for 23andMe than just telling people about their genetics?</h6>
23andMe&#8217;s website also has information about diseases and risk factors.   Even if I&#8217;m not at increased risk for something, I&#8217;m still at some risk for almost every condition.   23andMe helps you get more educated about your body.   It helps you understand that a lot of what happens is due to your genes and also to what you do with them through your behavior.   Once you know how genes work, you realize you need to consider other factors as well.
I&#8217;m a big believer in the “<a href="http://www.kk.org/quantifiedself/" target="_blank" rel="noopener">quantified self</a>” movement, in which people quantify or measure themselves–genes, weight, pulse, blood sugar, blood pressure and more.   You can now monitor your physical activity and your sleeping patterns.   All these metrics both reflect and interact with your genes.
The more you pay attention to your body, the better you’re likely to treat it.   Exploring 23andMe implicitly encourages you to consider other things, like how you should be exercising, or not smoking, or what drug interactions might be an issue for you.   Once you understand your genes you realize how much there is to understand about everything else as well.
You alluded to the ability to share and compare genomes.   What have you found?
<img loading="lazy" decoding="async" class="alignleft size-full wp-image-5529" title="dyson" src="https://blog-api.23andme.com/wp-content/uploads/2009/12/dyson.jpg" alt="dyson" width="470" height="277" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/12/dyson.jpg 1212w, https://blogcms.23andme.com/wp-content/uploads/2009/12/dyson-300x177.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/12/dyson-768x454.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2009/12/dyson-1024x606.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2009/12/dyson-880x521.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2009/12/dyson-1180x698.jpg 1180w" sizes="auto, (max-width: 470px) 100vw, 470px" />
I’m one of those lucky people with a large family, most of whom have gotten their 23andMe data: 26 people so far–including a pair of identical twins, half-siblings and whole siblings, and other neat combinations.   It’s endlessly fascinating to see which sisters are most alike, which grandchildren take after which grandparents–and to see that reflected in the data.   You can also see which relatives match on particular traits, such as circadian rhythm or pigmentation.
<h6>23andMe just released Relative Finder, a tool that allows you to find relatives you never knew you had.   What do you think so far?</h6>
I think <a href="https://blog.23andme.com/articles/introducing-relative-finder-the-newest-feature-from-23andme" target="_blank" rel="noopener">Relative Finder</a> is way cool and will be really interesting.     The science behind it is similar to techniques used to detect plagiarism.   Everyone&#8217;s genome is made up of the same basic ”letters”–A, C, T and G.   Small sequences of these letters are common between lots of people.     Likewise, in literature, phrases such as   “and then she said” occur again and again and are useless in distinguishing one novel from another.   But when you find whole paragraphs that match, then you figure the two segments must have a common source.   Same thing with SNPs:   When you find a big enough block that is the same between two people, you figure they must have a common ancestor.
<h6>What do you see happening as Relative Finder takes off?</h6>
I think it is going to start with individuals and families, but eventually it will affect how people think about their place in the world.   Their sense of nationalism will erode.   People will find out that they share a lot of genetic material with people they considered their enemies.
<h6>Why did you get involved with 23andMe?</h6>
I invested in 23andMe and joined the board because I knew I would learn a lot…and I knew we would face interesting problems!   This market is full of them.   There are legal, ethical, scientific and business questions to answer.   We have to figure out how to explain the value of our service without overselling it; we have to overcome privacy fears that are unfounded, while acknowledging those that are valid.   I&#8217;ve learned a ton.
Beyond the quantified self, another trend that excites me is the broader notion of user-generated science.   It starts with self-quantification, but those people who are measuring themselves can contribute their own data–genetic, medical, behavioral and environmental–to science.   You can’t just do research in a lab anymore; you need to analyze statistics about thousands and ultimately millions of people out in the real world.  It excites me that people can analyze themselves and contribute for themselves, rather than simply be the subjects of research carried out by professionals.   23andMe and its partnerships with research organizations will give them that opportunity.

23andMe….and me: Interview with Esther Dyson

<img decoding="async" class="alignright size-full wp-image-219" title="feetscale" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/feetscale.jpg" alt="feetscale" width="350" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/05/feetscale.jpg 425w, https://blogcms.23andme.com/wp-content/uploads/2008/05/feetscale-300x199.jpg 300w" sizes="(max-width: 425px) 100vw, 425px" />
We all know people struggling with weight issues. Maybe they’re overweight and can’t seem to lose the pounds no matter what new diet or exercise regime they try. Or, maybe they’re underweight and have a hard time bulking up no matter how many donuts they consume or weights they lift. Clearly, there’s more to your weight than what you eat.
Researchers have been hot on the trail of genetic factors influencing obesity ever since the <a href="http://www.hhmi.org/genesweshare/d130.html">discovery of the gene coding for leptin</a>, a protein responsible for telling the brain “I’m full.” But just having a genetic variant linked to obesity doesn’t mean stretchy waist pants are a certainty — many factors interact with diet to affect your health.
Several years ago, a team led by Dolores Corella and Jose Ordovas discovered that the variant in the APOA2 gene is <a href="http://www.clinchem.org/cgi/content/full/53/6/1144">associated with obesity</a> as well as general food measures like total calorie and protein intake. In a new study published last month in the <a href="http://archinte.ama-assn.org/cgi/content/abstract/169/20/1897">Archives of Internal Medicine</a>, Corella and Ordovas replicated the association with obesity in three independent populations  and determined that the association depends specifically on the amount of saturated fat in the diet. More than 3400 individuals across three population groups — 2532 people of European ancestry and 930 Hispanics from Puerto Rico — participated in the study, providing data on dietary intake, physical activity, body mass index (BMI) and other variables.
In the two European populations, individuals with two copies of the C version of had significantly higher calorie intake than individuals with at least one copy of the T version  — a finding that echoed their previous work. When Corella and her colleagues looked at BMI, however, they found that was significantly associated with higher BMI, but only in individuals who consumed high amounts of saturated fat, irrespective of total calorie intake.
In all three populations, there was no association between genotype and BMI in individuals who consumed diets low in saturated fat. Furthermore, there was no significant difference in BMI for individuals who had low intake and individuals who had high intake if they had at least one copy of the T version. But people with the CC genotype who consumed diets high in saturated fat had significantly higher BMI than people with either the TC or TT genotype who also consumed high saturated fat diets. After combining data from the three groups, Corella’s team determined that individuals with the CC genotype who had high saturated fat intake also had about 1.8 times higher odds of obesity than individuals with the T version  who consumed similar amounts of saturated fat, total calorie intake being equal.
Although earlier research in animals has implicated APOA2 in obesity, its role in human health has been controversial. In this study, Corella and her team show that saturated fat intake can interact with a genetic variant in APOA2 to increase obesity risk. In fact, the variant makes more of a difference the more saturated fat one consumes. While minimizing saturated fat intake continues to be common sense, in a society characterized by rich diets and increasingly sedentary lifestyles, discoveries like this drive home the fact that genetics and environment together form an intricately interwoven picture of our health.
(Many thanks to TRK for bringing this study to our attention!)

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