Over the summer 23andMe launched a new research initiative in collaboration with Pfizer to study Inflammatory Bowel Disease.
<div style="float: right; text-align: justified; width: 300px; background-color: #eee; padding: 15px; margin-left: 10px;">Eligible Individuals 
1. You have been diagnosed with Crohn’s disease or ulcerative colitis by a qualified physician. 
2. Your willingness to submit a saliva sample for DNA testing and complete online surveys related to your condition. 
3. You have access to the internet. 
4. You are at least 6 years old (those under 18 require a parental consent to enroll). 
5. You are not a current 23andMe customer.* 
6. You reside in the United States.*If you are a current 23andMe customer, learn how you can participate here.<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-21220" src="https://blog-api.23andme.com/wp-content/uploads/2014/07/Learn-More-300x99.jpg" alt="Learn More" width="300" height="99" srcset="https://blogcms.23andme.com/wp-content/uploads/2014/07/Learn-More-300x99.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2014/07/Learn-More.jpg 744w" sizes="auto, (max-width: 300px) 100vw, 300px" /></div>
We’ve been encouraged by the numbers of people with IBD, who’ve already enrolled in the study, which will look more deeply at the role genetics and environment play in the condition.
It’s those individuals who are living with IBD – an umbrella diagnosis that includes both Crohn’s disease and ulcerative colitis – who have already taught us a lot about resilience.
We recently wrote about some of <a href="https://blog.23andme.com/articles/gut-check-a-short-list-of-ibd-blogs/" target="_blank" rel="noopener noreferrer">our favorite bloggers</a> on the topic writing about the condition with both flair and humor.
Over at <a href="https://thegreatbowelmovement.org/">The Great Bowel Movement</a>, guest blogger Christy Stone, a health advocate who runs Crohnie Bologna IBD, and also has IBD.

23andMe Blog

23andMe Blog Team

People Powered IBD Research

Since announcing our new study on Inflammatory Bowel Disease, we’ve received questions not just about the study, but about the disease itself.
<div style="float: right; text-align: justified; width: 240px; background-color: #eee; padding: 15px; margin-left: 10px;">Eligible Individuals 
1. You have been diagnosed with Crohn’s disease or ulcerative colitis by a qualified physician. 
2. Your willingness to submit a saliva sample for DNA testing and complete online surveys related to your condition. 
3. You have access to the internet. 
4. You are at least 6 years old (those under 18 require a parental consent to enroll). 
5. You are not a current 23andMe customer.* 
6. You reside in the United States.*If you are a current 23andMe customer, learn how you can participate here.<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-21220" src="https://blog-api.23andme.com/wp-content/uploads/2014/07/Learn-More-300x99.jpg" alt="Learn More" width="300" height="99" srcset="https://blogcms.23andme.com/wp-content/uploads/2014/07/Learn-More-300x99.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2014/07/Learn-More.jpg 744w" sizes="auto, (max-width: 300px) 100vw, 300px" /></div>
IBD – which includes both Crohn’s disease and ulcerative colitis – is often difficult to diagnose. The symptoms can sometimes be confused with other conditions.
The symptoms can also come and go making arriving at an accurate diagnosis very difficult.
Recently, Dr. Jennifer Choi, the Associate Director of UCLA’s Center for IBD, gave a detailed talk on the condition. Neither Dr. Choi nor the UCLA Center is involved with 23andMe’s study, but they are a great resource for information about the condition.
While the video of that presentation is long, and is sometimes graphic, Dr. Choi very clearly explains everything from the anatomy involved to the differences between Crohn’s and ulcerative colitis.
It’s a helpful primer both for those who have the condition and people who care about them, who are trying to understand what they are going through.
We’ve included the video below, but be forewarned that there are some graphic photos in the presentation that may be disturbing for some.
 
<iframe loading="lazy" width="300" height="169" src="//www.youtube.com/embed/vJ-nLpAFHd8" frameborder="0" allowfullscreen="allowfullscreen"></iframe>

More On Inflammatory Bowel Disease

Last week, 23andMe launched a new research initiative to study <img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2014/08/l_smarr_2x-221x300.jpg" alt="l_smarr_2x" class="alignright size-medium wp-image-21362" width="221" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2014/08/l_smarr_2x-221x300.jpg 221w, https://blogcms.23andme.com/wp-content/uploads/2014/08/l_smarr_2x.jpg 314w" sizes="auto, (max-width: 221px) 100vw, 221px" />
Along with collaborating with Pfizer on the study, 23andMe has also enlisted the help of five scientific advisors, who each bring deep expertise that will assist our scientists in analyzing data and developing surveys for the study.


One of those advisors, <a href="http://lsmarr.calit2.net/" target="_blank" rel="noopener noreferrer">Larry Smarr</a>, PhD, who is the founding director of the California Institute of Telecommunications and Information Technolgy (Cali2), said this study could illustrate the power of the 23andMe research model.


“I believe that a more accurate stratification of IBD disease states will result from classifying based on combinations of (genetic markers) than on symptoms,” said Larry. “23andme is the best way to quickly get a large number of people classified to test this hypothesis.” 
<div style="float: right; text-align: justified; width: 300px; background-color: #eee; padding: 15px; margin-left: 10px;">Eligible Individuals 
1. You have been diagnosed with Crohn’s disease or ulcerative colitis by a qualified physician. 
2. Your willingness to submit a saliva sample for DNA testing and complete online surveys related to your condition. 
3. You have access to the internet. 
4. You are at least 6 years old (those under 18 require a parental consent to enroll). 
5. You are not a current 23andMe customer.* 
6. You reside in the United States.*If you are a current 23andMe customer, learn how you can participate here.<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-21220" src="https://blog-api.23andme.com/wp-content/uploads/2014/07/Learn-More-300x99.jpg" alt="Learn More" width="300" height="99" srcset="https://blogcms.23andme.com/wp-content/uploads/2014/07/Learn-More-300x99.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2014/07/Learn-More.jpg 744w" sizes="auto, (max-width: 300px) 100vw, 300px" /></div>
<h6>
 Self Tracking</h6>

Larry, who also holds the Harry E. Gruber professorship in the Department of Computer Science and Engineering at UC San Diego’s Jacobs School of Engineering, has over the last decade tracked everything from his weight to his sleep patterns to his caloric intake. He even tracked the microbes in his stool to learn about his own health.
But what had started as a simple effort to track weight loss soon became a focused effort to apply all his scientific skills to manage his own health and his own struggle with what he later learned was IBD.
Larry said he sees huge potential in gathering together many people with IBD.
“The study will be successful if it results in a large number of people classified with both (genetic markers) and phenotypes,” he said. “This will immediately yield a first cut at the emerging IBD stratification landscape.”

He knows why he is so interested in participating as a scientific advisor, but he also knows what might motivate someone with IBD to enroll.


“By participating in this study you will help accelerate research toward a new approach to understanding IBD,” he said. “And hopefully to creating more personalized therapy approaches.”

Science Advisor, Larry Smarr

<img loading="lazy" decoding="async" class="alignright wp-image-19829 size-medium" alt="Crohn's Infographic" src="https://blog-api.23andme.com/wp-content/uploads/2013/11/Crohns-Infographic-300x201.jpg" width="300" height="201" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/11/Crohns-Infographic-300x201.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/11/Crohns-Infographic.jpg 682w" sizes="auto, (max-width: 300px) 100vw, 300px" />
By Alex Carmichael, Co-Founder of CureTogether
For Crohn’s Disease, medical interventions seem to be surprisingly effective.
This is in contrast to some of our other patient-reported treatment infographics, in which lifestyle changes are often deemed more effective than drugs or traditional medicine.
<h6>Self Report</h6>
CureTogether – a free resource owned by 23andMe that allows people to share information about their health and treatments – surveyed 275 people who self-identify as having Crohn&#8217;s Disease. They reported that interventions such as Low-Dose Naltrexone (LDN), steroids, cannabis, and dietary changes helped them feel better.
Crohn&#8217;s Disease is a kind of inflammatory bowel disease that affects the gastrointestinal tract and can involve intense abdominal pain, persistent diarrhea, and rectal bleeding.
<h6>Prescriptions</h6>
Participants in the study said they found that prescription medications like Humira and Remicade, surgery, stress reduction, and diets that avoid fiber and wheat were among the most effective treatments. The survey also found that some common treatments such as the drug Pentassa and a high-fiber diet actually made the symptoms of Crohn&#8217;s Disease worse.
<div style="float: right; text-align: justified; width: 200px; background-color: #eee; padding: 15px; margin-left: 10px;">Most Effective Rated Treatments for Patients with Crohn&#8217;s Disease 
1. Low-Dose Naltrexone 
2. Surgery 
3. Steroids 
4. Cannabis 
5. Specific Carbohydrate Diet 
6. Remicade 
7. Humira 
8. Gluten-free diet 
9. Paleo diet 
10. Stress reduction</div>
The Crohn&#8217;s and Colitis Foundation America estimates that over 700,000 Americans live with Crohn&#8217;s Disease, with genetics and environment both playing a part in the frequency of this disease. The condition can be extremely painful and is not incredibly well understood, and finding accurate recommendations on treatments that work well can be challenging, so
<h6>Top Ten Rated Treatments</h6>
CureTogether asked people who experience Crohn&#8217;s Disease to rate the effectiveness of 42 different patient-reported treatments.
Where did this data come from? This is the result of a four-year CureTogether study on <a href="http://curetogether.com/Crohns-Disease/">Crohn&#8217;s Disease</a>, in which 275 people shared information about their symptoms and what treatments worked best for them. We’d like to thank those who participated. And just as they shared their experience with treatments, we’re freely and openly sharing the results of the Crohn&#8217;s Disease study.
This is part of a regular series of CureTogether <a href="http://curetogether.com/blog/category/research-findings/">research findings</a>. CureTogether’s research findings are different than <a href="https://www.23andme.com/about/factoids/">those made by 23andMe</a>, which look at genetic associations with illness, traits and drug response. But as we continue our work with the CureTogether community, 23andMe hopes to incorporate more of this kind of self-reported information into our own research. CureTogether presents its findings just as they are – patient-reported data – to stimulate discussion and generate new insights for further research.
Please tweet, blog, or pass this along to anyone who can benefit or is interested in Crohn&#8217;s Disease. Thank you!

Alexandra Carmichael

What Patients Say Works for Crohn’s Disease

<img loading="lazy" decoding="async" class="aligncenter wp-image-13198 size-full" title="whitebloodcell" src="http://35.88.189.111/wp-content/uploads/2012/05/whitebloodcell.jpg" alt="" width="350" height="260" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/whitebloodcell.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2012/05/whitebloodcell-300x223.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />Crohn’s disease develops when the immune system mistakenly attacks the body’s own gut cells.
Although most people with European ancestry are pretty genetically similar, some sub-groups like Ashkenazi Jews have distinct genetic characteristics that carry important implications for health. For instance, people with <a href="https://blog.23andme.com/articles/detail-for-ashkenazi-ancestry">Ashkenazi ancestry</a> have higher rates of numerous rare genetic disorders like <a href="https://www.23andme.com/topics/carrier/tay-sachs-disease">Tay-Sachs disease</a> and are at increased risk for certain multi-gene conditions like Crohn’s disease.
The exact cause of Crohn’s disease isn’t known, but this inflammatory bowel disease may result from a case of mistaken identity – the immune system mounts a reaction to an invader and ends up attacking the body’s own cells, too. At least 12 genetic factors have been associated with Crohn’s disease in Europeans. Although researchers don’t know why people with Ashkenazi ancestry are two to four times more likely to develop Crohn’s disease, they suspect that the genetic “uniqueness” of this group may have something to do with it. 
 
To investigate this intriguing idea, a research team led by scientists at Columbia University and Mount Sinai carried out a study looking at nearly 2,000 people with Crohn’s disease and roughly 4,500 people without it, all of <a href="https://blog.23andme.com/articles/ashkenazi-ancestry-and-health">Ashkenazi descent</a>. The results, published in <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002559">PLoS Genetics</a> earlier this year, replicate previously reported associations for people of European descent and also identify novel factors specific to those with Ashkenazi ancestry.
In the new study by lead author Eimear Kenny, individuals with the C version of and the G version of had slightly higher odds of developing Crohn’s disease. Two other factors seemed to be protective. People with the T version of and the G version of had slightly lower odds of developing Crohn’s disease. More research is needed to understand how these genetic variants influence the biology of the disease.
These new findings confirm that genetics likely has something to do with the higher rates of Crohn’s disease in people with <a href="https://blog.23andme.com/articles/detail-for-ashkenazi-ancestry">Ashkenazi ancestry</a>. All of the newly discovered factors appeared to be specific to Ashkenazi ancestry as they weren’t found in previous studies carried out with broader European study groups.
May is Jewish American Heritage Month. Read about <a href="https://blog.23andme.com/?p=13178">the “uniqueness” of Ashkenazi Jewish ancestry</a> and how it’s important for health. Read more about Jewish ancestry in guest posts by 23andMe&#8217;s Ancestry Ambassadors, Tim Janzen,  CeCe Moore, and  Andrea Badger.

Genetic Factors for Crohn’s Identified for Ashkenazi Jewish Ancestry

Imagine if the simple act of eating triggered your immune system to mistakenly mount an attack inside your own body.
Nearly three million people with Crohn’s or celiac disease face this distinct possibility every day in the United States, and they quickly learn that specific foods lead to a debilitating reaction.
<h6>Crohn&#8217;s and Celiac Differ</h6>
But while the two diseases share some similarities &#8212; both are autoimmune conditions localized to the digestive system &#8212; they also have many differences. For example, celiac disease is confined to the small intestine and is specifically a reaction to ingested gluten, while Crohn’s disease can occur anywhere in the digestive tract when an overactive immune system attacks “friendly” bacteria in the gut that normally help us to break down what we eat.
Despite these differences, evidence suggests that the two diseases may share some of the same risk factors and underlying causes.
<h6>Heritability</h6>
The two diseases sometimes run in families, and Crohn’s disease &#8212; which is usually quite rare &#8212; may be more common in individuals who have celiac disease. Variants near two genes, PTPN2 and IL18RAP, have already been identified as genetic factors shared between the two diseases, but researchers believe there to be more.
Recently, an international team of scientists led by Eleonora Festen of the University of Groningen in The Netherlands and Phillippe Goyette of the University of Montreal set out to uncover additional genetic risk factors contributing to both celiac disease and Crohn’s in nearly 10,000 subjects with either disease and more than 10,000 healthy individuals, all of European ancestry.
<h6>New Findings</h6>
Their results, published last month in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1001283" target="_blank" rel="noopener">PLoS Genetics</a>, confirmed the shared associations at PTPN2 and IL18RAP and identified two other shared risk variants near the PUS10 and TAGAP genes.
Variants near PUS10 have previously been shown to be associated with Crohn’s disease, as well as with celiac disease and ulcerative colitis, another bowel disorder; however, different factors seem to connect the three diseases to one another, suggesting that different variants near this gene may have different effects on disease development. The TAGAP gene was previously only associated with celiac disease, but it is thought to play a role in the immune system, making its newly identified link to Crohn’s disease more plausible. Future research may incorporate these results into elucidating the shared biological basis of these two diseases.

Researchers Identify Risk Variants Shared by Crohn’s Disease and Celiac Disease

<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

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3853" title="starry_night" src="https://blog-api.23andme.com/wp-content/uploads/2009/06/starry_night.jpg" alt="starry_night" width="350" height="260" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/06/starry_night.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/06/starry_night-300x223.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Genomewide association studies have had <a href="https://blog.23andme.com/2008/08/18/snpwatch-snps-in-ion-channel-genes-are-associated-with-type-2-diabetes-and-bipolar-disorder/" target="_blank" rel="noopener">some success</a> in finding DNA variants associated with increased risk for bipolar disorder.   But researchers from the MRC Centre for Neuropsychiatric Genetics and Genomics at Cardiff University in England have taken these studies a step further by looking for common functional themes running through the GWAS data. Their results, published online this month in the <a href="http://www.cell.com/AJHG/abstract/S0002-9297(09)00209-2" target="_blank" rel="noopener">American Journal of Human Genetics</a>, implicate some of the most basic biological pathways in the genesis of bipolar disorder.
Starting with the idea that the genetic variations increasing risk for a disorder are probably not randomly distributed throughout the genome, but instead are in one or more sets of related genes, Holmans et al. re-analyzed the SNP data from four previous studies that included a total of 4,387 cases of bipolar disorder and 6,209 controls. Researchers at the Children&#8217;s Hospital of Philadelphia recently took a similar approach (although the technical details of the analysis differ) for a study of <a href="https://blog.23andme.com/2009/02/26/researchers-make-progress-in-understanding-crohn%E2%80%99s-disease-by-looking-at-the-big-picture/" target="_blank" rel="noopener">Crohn&#8217;s disease</a>.
The bipolar disorder researchers found that biological pathways involved in broad control of cellular activity were overrepresented in the genetic variations association with bipolar disorder.   Two of the pathways, hormone activity and cellular self-digestion, are known to be impacted by lithium, the major medication used to treat bipolar disorder. As always, more research will be needed to substantiate these findings, as well as to understand how they can be used to help the more millions of people worldwide dealing with bipolar disorder.

Researchers Look For Common Themes In Bipolar Disorder Genetics

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3045" title="skeleton" src="https://blog-api.23andme.com/wp-content/uploads/2009/03/skeleton.gif" alt="" width="300" height="219">
Throughout the course of human evolution, there have been plenty of <a href="https://blog.23andme.com/2008/09/24/what-it-means-to-be-human/" target="_blank" rel="noopener">firsts</a>. Small changes in our genetic code have laid the groundwork for our bipedal gait, our large brains, and our ability to speak complex languages.
There are countless genes throughout the human genome that distinguish us from our evolutionary relatives; now scientists have found yet another example. However, unlike novel and uniquely human mutations like <a href="https://en.wikipedia.org/wiki/FOXP2" target="_blank" rel="noopener">FOXP2</a> and <a href="https://en.wikipedia.org/wiki/MYH16" target="_blank" rel="noopener">MYH16</a>, this gene has been nestled in suspended animation within our genomes for tens of millions of years: it just needed a wake-up call. In this week&#8217;s issue of <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000403" target="_blank" rel="noopener">PLoS Genetics</a> , an international team of scientists investigates this gene&#8217;s unique history.

Their analysis centers on a family of genes known as Immunity Related GTPases (or, IRG). Most mammals have many copies of these types of genes, which play a vital role in helping the immune system resist pathogens like bacteria. But humans and our closest relatives &#8211; the Great Apes &#8211; have one IRG gene, IRGM. Yet our slightly more distant relatives, such as the monkeys, have no working copies of IRGM, or any other members of the IRG gene family.
How could it come to pass that we and the apes share more in common with mice &#8211; at least in terms of IRG &#8211; as opposed to other primates? That apparent discrepancy turned out to be central to understanding the genetic history of IRGM.
The answer, according to the geneticists, was relatively simple: When looking at the evolution of our species, going back tens of millions of years, it is clear that IRGM was never &#8216;erased&#8217; from our genomes. Instead, it simply laid dormant, and it was not until the common ancestor of apes and humans split off from monkeys that IRGM awoke from its long slumber.
The exact reason that IRGM was reborn in species such as humans and apes, but not monkeys, is not yet completely understood. We do know, however, that the fact that most humans have a working copy of IRGM is quite fortuitous. As mentioned above, the IRG genes are essential to controlling bacteria, specifically by maintaining the delicate balance of bacterial growth and immune control in our intestines. Recent research has shown that those without a working copy of IRGM have a greater risk of developing Crohn&#8217;s Disease, in which an individual&#8217;s immune system begins attacking the friendly bacteria living in our guts. The results are chronic &#8211; and painful &#8211; digestive problems. Without a doubt, IRGM is beneficial to the health and well-being of our digestive system, and its role in decreasing the risks of Crohn&#8217;s Disease cannot be underestimated.
Beyond shedding light on the practical value of IRGM, this study has revealed the first instance of a gene being &#8216;reborn&#8217; after lying dormant for millions of years. As the study&#8217;s team leader, University of Washington professor of Genomic Sciences Evan Eichler put it, &#8220;These findings tell us we shouldn&#8217;t count a gene out until it has been completely deleted.&#8221;
How many other resurrected genes are sprinkled throughout the human genome? As the field of genetics explores the hidden depths of our genomes, we can only begin to wonder how many similar discoveries await.

Crohn's disease — Page 2