<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.

23andMe Blog

23andMe Blog Team

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

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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!)

Do These Genes Make Me Look Fat? It Depends on What You Eat

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Even if you do everything right — exercise, healthy eating, no smoking&#8211; whether or not you&#8217;ll make it to the century mark depends to some extent on your genes.
<h6>FOXO3A</h6>
One of the important longevity genes seems to be FOXO3A.   It&#8217;s been linked to lifespan in several experimental animal models. In humans, studies have shown that certain variations in the FOXO3A gene increase the odds of being extremely long-lived.
It&#8217;s not exactly clear how FOXO3A affects longevity because it&#8217;s known to play a part in several important cellular functions, including cell growth, cell specialization, response to oxidative stress and   the regulation of cell death.   Two studies published last month in the journal Cell Stem Cell added to the list of the FOXO3A&#8217;s talents.
<h6>Brain Function and Repair</h6>
<a href="https://www.ncbi.nlm.nih.gov/pubmed/19896443" target="_blank" rel="noopener noreferrer">Renault et al.</a> and <a href="https://www.ncbi.nlm.nih.gov/pubmed/19896444" target="_blank" rel="noopener noreferrer">Paik et al.</a> showed that in mice FOXO3A and related FOXO genes are involved in maintaining the brain&#8217;s ability to generate new cells, a function critical for both normal brain functions and repair in response to natural degeneration or injury.
New brain cells arise from a pool of specialized self-renewing cells called neural stem cells.   The FOXO genes appear prevent the brain from burning through its supply of these important cells prematurely.
&#8220;Because [neural stem cells] have been shown to be important for learning, memory, and mood regulation, our findings could give insight into the decline in cognitive function that occurs during aging,&#8221; Renault et al. wrote in their report.
More research will be needed to fully understand the role of the FOXO genes in neural stem cells.   Experiments will also be needed to test whether these findings can be extended to humans.
Despite the work that is left to be done, Paik et al. optimistically suggest the new understanding of the importance of the FOXO genes in neural stem cells may help guide the development of drugs that could help improve central nervous system health in the elderly and people suffering from neurodegenerative disease or brain injury.

Mouse Studies Show that Longevity Gene May Play a Role In Maintaining Stem Cells in the Brain

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Looking for something to talk about between mouthfuls of green bean casserole and cranberry dressing?
Instead of discussing the big game or Friday&#8217;s shopping prospects, U.S. Surgeon General Regina Benjamin would like you to consider chatting up your relatives to learn their medical histories in honor of Family Health History Day.
“An important first step in preventing illness is learning about health conditions in our families that may put us at risk for inheriting diseases such as diabetes, heart disease, cancer, Alzheimer’s, mental illness, and many others,” said Dr. Benjamin in a press release.   “Discussing family health information with each other can often uncover things you never knew, simply because no one ever asked.”
Here are a few resources to help you get you started:
<h6>The U.S. Surgeon General’s Family History Initiative</h6>
You can use the online tool “My Family Health Portrait” to help guide you in collecting your own family’s health history. (Also available in Chinese, Polish, Spanish, French and Portuguese from the Brigham and Women’s Hospital National Family Health Initiative Website.)
<h6>The Genetic Alliance</h6>
Links to sites that can help with collecting a family health history, including resources for family reunion organizers who want to incorporate this into their next gathering.

Remember: Turkey Day is Also National Family Health History Day

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Type 2 diabetes is a common disease characterized by high blood glucose levels and unresponsiveness to insulin. Individuals with type 2 diabetes may produce insulin at normal levels but do not respond to it sufficiently, either because the insulin receptors in their cells have become less sensitive or because the insulin produced in the pancreas isn’t being delivered to other cells. One reason that insulin might not make it where it’s supposed to go is that insulin secretion from pancreatic Î²  cells is impaired.
In an article published in <a href="https://dx.doi.org/10.1126/science.1176827">Science</a> last week, Anders Rosengren, Erik Renstrom and their team from the <a href="http://www.ludc.med.lu.se/">Lund University Diabetes Centre</a> in Sweden used newly created rat strains — called N1I5 and N1I11, both derived from a well-studied type 2 diabetes strain — to identify the Adra2a gene as one of the genetic culprits behind defective insulin secretion. They then tied a variation in this gene to type 2 diabetes in humans.
When Rosengren and his colleagues stimulated Î²  cells from each strain with glucose, they found that N1I5 cells secreted less insulin than both N1I11 and normal cells. Other experiments verified that whatever was causing impaired insulin secretion was unique to N1I5.
Of the handful of possible gene candidates, only Adra2a showed different expression between the two strains, causing N1I5 cells to produce almost twice as much of the encoded Î±(2A)AR   protein as N1I11 cells. Additional experiments confirmed that Î±(2A)AR was indeed responsible for impaired insulin secretion. Î±(2A)AR is known to be involved in suppressing insulin secretion but variations in the gene had not previously been associated with the development of type 2 diabetes.
Based on the strong evidence from their rat experiments, Rosengren’s group hypothesized that variations in the human version of Adra2a, helpfully called ADRA2A, would contribute to type 2 diabetes risk in humans. Using two independent populations totaling about 5500 people, they first found that the less common A version of was associated with impaired insulin secretion.
To see whether the results extended to actual diabetes risk, Rosengren and his team then compared a group of 2830 type 2 diabetics to 3740 non-diabetics. They found that was also significantly associated with type 2 diabetes, with each copy of the A version increasing the odds of having the disease by about 1.4 times. The final piece of evidence came from laboratory experiments. Pancreatic cells from people carrying the riskier A version of behaved just like the cells from the insulin-secretion impaired N1I5 rats.

New Study Rats Out A Genetic Variant Associated with Type 2 Diabetes

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More than 30 million people worldwide are living with HIV, and about three million more are infected each year. Although people infected with the virus are living longer and healthier lives thanks to intense research, there is still no cure.
<h6>Fighting HIV and AIDS</h6>
One way to identify new strategies for fighting HIV is to look to those people whose bodies are naturally able to keep the virus as bay, at least for a time.
In <a href="https://www.ncbi.nlm.nih.gov/pubmed/17641165?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_MultiItemSupl.PMC_FreeArticle_ad&amp;linkpos=1&amp;log$=pmcad6_article" target="_blank" rel="noopener">2007</a> researchers identified a variation near the HLA-C gene that was shown to affect the amount of virus present in the body after acute infection but before onset of AIDS symptoms.   This so-called &#8220;viral set point&#8221; correlates with rate of disease progression, infectiousness and response to treatment.
Now another set of researchers has yet again shown that this variant affects viral set point.
Their results, published online this week in the journal <a href="https://dx.doi.org/10.1038/ng.486" target="_blank" rel="noopener">Nature Genetics</a>, further show that this variant influences the time it takes to progress to AIDS.
<h6>Viral Loads</h6>
Rasmi Thomas and colleagues analyzed the DNA from 828 people infected with HIV, all of European ancestry.   Patients were divided into groups with low, medium and high viral loads (&lt;2,000 copies of viral RNA per milliliter of blood, 2,000-10,000 copies, and &gt;10,000 copies). About 62% of people with two Cs at had a viral load below 2,000, while only about 15% of people with two Ts controlled the HIV virus to this extent.   About 33% of people with CT at fell into the &#8220;controller&#8221; group.   These results agree with what was found by previous researchers.
In a separate group of 763 people infected with HIV (also all of European descent), the researchers found that the C version of was somewhat protective against progression from HIV infection to extremely low CD4 cell count, a measure of immune system strength.   The C version of this SNP also conferred some protection against progression to an AIDS-defining complications and death.
As noted above, low viral set point is known to correlate with slower progression to AIDS, but the analysis by Thomas et al. indicates that the effects of on viral set point and progression are at least somewhat independent.
The researchers examined blood from 50 health donors to investigate the function of .     They found that the C version was associated with increased HLA-C protein on the surface of immune cells.   They conclude that this increased protein expression must be what helps the body fight off HIV, although the details of how increased HLA-C is beneficial are still unknown.   Further research will be needed in order to translate these findings into new strategies for treatment or prevention of HIV infection.
<ul>
<li>When was initially identified as a variant that could affect HIV viral set point, researchers <a href="http://www.dukehealth.org/HealthLibrary/News/10080" target="_blank" rel="noopener">suggested that vaccines</a> designed to elicit an immune response mediated by HLA-C might be a good idea.   Perhaps this new research, which further solidifies the importance of HLA-C variation in virus control, will rekindle that idea, especially in light of recent HIV vaccine disappointments (more <a href="http://latimesblogs.latimes.com/booster_shots/2009/10/aids-vaccine-results-questioned.html" target="_blank" rel="noopener">here</a> and <a href="http://latimesblogs.latimes.com/booster_shots/2009/11/cold-virus-may-have-caused-2007-aids-vaccine-trial-failure.html" target="_blank" rel="noopener">here</a>).</li>
</ul>

Genetic Variant Affects HIV Viral Set Point and Disease Progression

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Inflammatory bowel disease (IBD) is a chronic autoimmune disorder encompassing Crohn’s disease and ulcerative colitis that affects more than a million people in the United States.
Our immune system usually works to fight off harmful pathogens that might pass through our digestive tract. In IBD, however, the immune system stays in overdrive and attacks normal intestinal cells. Chronic inflammation causes abdominal cramps, diarrhea, pain and fever, and weight loss.
<h2>New Research</h2>
Most studies of IBD have investigated genetic factors for Crohn’s disease, but a set of articles published this week in Nature Genetics on IBD address two less-explored angles.
Two studies identify new genetic associations with ulcerative colitis in European and Asian populations. The third study focuses on early-onset IBD (diagnosed before age 19), which is typically more severe than adult-onset IBD and is believed to have a more robust genetic component.
In a joint effort, the UK IBD Genetics Consortium and the <a href="https://www.wtccc.org.uk/ccc2/">Wellcome Trust Case Control Consortium 2</a> identified <a href="https://dx.doi.org/10.1038/ng.483">three genetic variants associated with ulcerative colitis</a> in 4,682 people with the condition and over 10,000 healthy individuals, all of European ancestry. These variants are located in regions of the genome that had not previously been associated with ulcerative colitis.
<h2>Intestinal Lining and Cell Interaction</h2>
Each of the three SNPs was associated with slightly increased odds of ulcerative colitis. The researchers highlight several proteins encoded by genes near these variants that help maintain the lining of the intestine and regulate cell-cell interactions, including HNF4a, E-cadherin, and laminin. However, their exact roles in ulcerative colitis are unclear.
The <a href="https://dx.doi.org/10.1038/ng.482">second study</a>, led by Kouichi Asano and Michiaki Kubo of the RIKEN Center for Genomic Medicine in Japan, looked for genetic variants associated with ulcerative colitis in a group of about 1,380 Japanese individuals with the disease and 3,050 individuals without it. Their two strongest associations were SNPs near genes involved in the immune response.
<h2>More on Immune Response</h2>
One of these SNPs is in a genome region that encodes antigen-presenting proteins, which are important for the immune system&#8217;s recognition of “self” vs. foreign substances. Antigen-presenting proteins display bits and pieces of proteins or sugars (antigens) from cells and other microorganisms to immune cells that generally ignore “self” antigens but destroy foreign ones. In autoimmune diseases like IBD, the immune system loses the ability to distinguish between the two types of antigens and mistakenly reacts to the body’s own cells.
The other strongly associated SNP is located in the FCGR2A gene and causes a change to the encoded protein, which is expressed on the surface of several types of immune cells. Previous studies by other groups have shown that this SNP can play a significant role in the development of other autoimmune disorders. The version of the SNP that increased risk for those other disorders is the opposite version compared to the version associated with increased risk for ulcerative colitis in the current Japanese study.
<h2>Early Onset</h2>
In the <a href="https://dx.doi.org/10.1038/ng.489">third study</a>, a team led by Marcin Imielinski and Hakon Hakonarson of the Children’s Hospital in Philadelphia identified genetic variants associated with early-onset IBD. Almost 3,500 individuals of European ancestry who had been diagnosed with IBD — either Crohn’s disease or ulcerative colitis — before their nineteenth birthday were compared to close to 12,000 individuals free of IBD.
Imielinski’s team identified three SNPs significantly associated with early-onset Crohn’s disease. For two of the SNPs, and , the less common version was associated with slightly increased odds of early-onset Crohn’s disease, while the less common version of was associated with slightly decreased odds. They also observed an association between and early-onset ulcerative colitis.
When they conducted a combined analysis of all early-onset IBD cases (Crohn&#8217;s and ulcerative colitis), the researchers found that the three genetic variants associated with early-onset Crohn’s disease were also associated with early-onset IBD in general. The effect sizes were similar to those seen when they looked at just Crohn&#8217;s disease. In addition, they identified another SNP associated with early-onset IBD.
<h2>Early Onset and Immune Response</h2>
Of the four genetic variants associated generally with early-onset IBD, Imielinski and his colleagues consider it to be especially important given its proximity to IL27, a gene involved in the immune system. The researchers showed in a small sample that individuals with early-onset Crohn’s disease express the gene at much lower levels than healthy people. IL27 encodes a protein that suppresses inflammatory immune cells in the intestine, so lower expression of IL27 may contribute to a hyperactive inflammatory response.
Although the biology of IBD is complex, these three studies contribute to a more comprehensive picture of the genetic factors underlying the condition and suggest potential directions for the development of therapeutics.
&#8220;This is an evolving story of discovering what genes tell us about the disease,&#8221; said Dr. Baldassano from the Children’s Hospital team in a <a href="http://www.eurekalert.org/pub_releases/2009-11/chop-lgs111209.php">press release</a>. &#8220;Pinpointing how specific genes act on biological pathways provides a basis for ultimately personalizing medicine to an individual&#8217;s genetic profile.&#8221;

Piecing Together The Inflammatory Bowel Disease Puzzle

Editor&#8217;s note: This no longer reflects 23andMe&#8217;s current product offering. We now offer <a href="https://www.23andme.com/dna-ancestry">DNA Relatives</a> as a way to connect with other customers with whom you share DNA.
Get ready &#8212; there&#8217;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.

<img loading="lazy" decoding="async" class="alignright size-full wp-image-5411" title="Picture 210" src="https://blog-api.23andme.com/wp-content/uploads/2009/11/Picture-210.png" alt="Picture 210" width="326" height="244" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/11/Picture-210.png 326w, https://blogcms.23andme.com/wp-content/uploads/2009/11/Picture-210-300x225.png 300w" sizes="auto, (max-width: 326px) 100vw, 326px" />Don&#8217;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.

<h6>
How is Relative Finder Different? 
</h6>

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&#8217;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.

<img loading="lazy" decoding="async" class="alignright size-full wp-image-5410" title="Picture 211" src="https://blog-api.23andme.com/wp-content/uploads/2009/11/Picture-211.png" alt="Picture 211" width="326" height="245" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/11/Picture-211.png 326w, https://blogcms.23andme.com/wp-content/uploads/2009/11/Picture-211-300x225.png 300w" sizes="auto, (max-width: 326px) 100vw, 326px" />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&#8217;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.

<h6>
Relative Finder in Action 
</h6>

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 &#8212; 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&#8217;re likely to get even more matches.
Once you&#8217;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!

<h6>
We Want You. 
</h6>

Up to now, we&#8217;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 &#8212; most importantly &#8212; 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.

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