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23andMe is passionate about making discoveries that will benefit you.
We give individuals access to their DNA data while in turn translating information they’ve volunteered into meaningful genetic discoveries.
Today we’re announcing the <a href="https://www.23andme.com/about/press/curetogether/" target="_blank" rel="noopener noreferrer">acquisition of CureTogether, Inc. 
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a company that we’ve admired for creating communities of people who can share information about their health conditions, support each other and together discover new insights in managing their health.
The acquisition – as well as the addition to our team of its two co-founders, Daniel Reda and Alexandra Carmichael &nbsp;– will improve our own ability to gather data for research and give customers more tools to explore and participate in online communities.
CureTogether’s core mission of enabling people to share their health information as a way to collectively gain new insight into various diseases is aligned with 23andMe’s own crowd-sourced research model. CureTogether, with more than 25,000 members, has gathered nearly four million data points on 576 different medical conditions. Welcoming in those users and the data they’ve contributed to research will improve the important work we are already doing.
At 23andMe, we’ve learned that the quality of our research communities – how engaged and active they are – is vital for quality research. 
Our research model has already made <a href="https://www.23andme.com/about/press/sgk1/">significant breakthroughs</a> in the study of Parkinson’s disease, and we are heartened by the progress we’re making in<a href="https://www.23andme.com/sarcoma/"> Sarcoma</a> and in <a href="https://www.23andme.com/mpn/">Myeloproliferative Neoplasms.</a>
23andMe puts power in the hands of patients to participate in research and accelerate new discoveries. The more people who participate, and the more engaged they are, the more powerful the research.
In this, the CureTogether community is a model for our own 23andMe research community. We’re all trying to find cures. Together, we can make even more of a difference.

23andMe Blog

23andMe Blog Team

CureTogether with 23andMe

<img loading="lazy" decoding="async" class="alignright wp-image-14230 size-medium" title="Rory and Daddy on the beach" src="http://35.88.189.111/wp-content/uploads/2012/07/Rory-and-Daddy-on-the-beach-300x300.jpg" alt="" width="300" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/07/Rory-and-Daddy-on-the-beach-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/07/Rory-and-Daddy-on-the-beach-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2012/07/Rory-and-Daddy-on-the-beach-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2012/07/Rory-and-Daddy-on-the-beach-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2012/07/Rory-and-Daddy-on-the-beach-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2012/07/Rory-and-Daddy-on-the-beach.jpg 696w" sizes="auto, (max-width: 300px) 100vw, 300px" />
It’s the most common genetic disorder in the United States, but Milo Sharp had never heard of it before.
The disorder, hemochromatosis, causes iron overload. Undiagnosed it can lead to a build up of iron in the body, particularly in the liver. This, in turn, can lead to serious health problems.
In the United States about 1 of every 300 people has <a href="https://www.23andme.com/topics/health-predispositions/hereditary-hemochromatosis">hereditary hemochromatosis</a>, but people remain largely unaware of the condition, which often has few symptoms and is hard to diagnose.
“Honestly I’d never heard of it which is kind of surprising, (because) my father is a doctor who specializes in blood,” said Milo, a 37 year-old computer programmer in Raleigh North Carolina.
Milo would have remained unaware of the lurking threat but for his wife’s interest in genetics.
“My wife decided to sign up with 23andMe, just to satisfy her curiosity,” he said.
After a little prodding from her, he also got a kit.
“Once we got our data, we found out some interesting details about our ancestry, but I found myself drawn to the health information,” Milo said.
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Read more 23andMe customer stories <a href="https://www.23andme.com/stories/" target="_blank" rel="noopener noreferrer">here</a>.
If you have one of your own that you want to share email stories@23andme.com.
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Still relatively young, Milo was dealing with a few health problems – sleep apnea, type 2 diabetes and high cholesterol – that taken together concerned him. Already a father of three boys, Milo’s wife was pregnant with a boy. Suddenly Milo’s long-term health became that much more important.
“I wanted to be there for my sons,” he said.
Milo saw that he was at increased risk for diabetes, which is something he already knew he had, but it was when he looked at his carrier status report that he learned something new.
“When I drilled down it was kind of surprising – I found not just one (variant) but two that put me at higher risk for hemochromatosis,” Milo said.
As he read more about the disease and how it can impact the body if untreated, Milo became concerned.
“I was worried that if I had it, it could exacerbate some of the other conditions I already had,” he said.
So he printed out a copy of his 23andMe results and took them with him the next time he saw his doctor.
“None of the doctors had ever heard of (23andMe) so not surprisingly they were pretty skeptical,” Milo said.
Hemochromatosis is typically hard to diagnose until it gets to more acute stages. But Milo explained that he carried two genetic variants that put him at a higher risk for the disease. Because of his existing conditions, Milo said he didn’t want to wait for symptoms to appear. He had additional blood tests done and one showed significantly elevated serum ferritin levels, essentially an indication of how much iron is stored in his organs.
“My (doctor) said, ‘this is something we’re going to want to look at,’” Milo said.
After working with other doctors and having a liver biopsy, Milo learned that he indeed had hemochromatosis.
“I had significant iron overload in my liver,” he said.
His liver was under stress and had internal scarring, but the condition was found early enough that there were specific treatments he could undergo to manage it.
“I can do other things like change my diet and lifestyle to improve my health and I’m working on that,” he said. “I think 23andMe may have saved my life or at least prolonged it and I want to let others know that.”
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View your results for genetic factors linked to Hereditary Hemochromatosis in your account. 
Not yet a customer? <a href="https://www.23andme.com/store/cart/">Visit our store!</a>
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Battling Against A Common Genetic Disease

<img loading="lazy" decoding="async" class="aligncenter wp-image-14184 size-full" title="three-bras" src="http://35.88.189.111/wp-content/uploads/2012/07/three-bras.jpg" alt="" width="416" height="288" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/07/three-bras.jpg 416w, https://blogcms.23andme.com/wp-content/uploads/2012/07/three-bras-300x208.jpg 300w" sizes="auto, (max-width: 416px) 100vw, 416px" />
Social norms and preferences aside, it turns out that breast size matters &#8212; but not quite in the way you think.
<a href="http://www.biomedcentral.com/1471-2350/13/53/abstract">23andMe’s latest research paper</a>, published in the journal BMC Medical Genetics, shows that genetic factors influence whether women have double As or double Ds. This might sound a bit frivolous at first but our research uncovered surprising connections between the genetics of breast size and the genetics of breast cancer. 

Analyzing data from more than 16,000 women of European ancestry, we compared their answers to survey questions with their genetic data at millions of SNPs. We found a total of seven genetic factors significantly associated with breast size, three of which are strongly correlated with SNPs already linked to breast cancer.
How do you study breast size anyway? 
In our case, no one’s personal space was violated &#8212; all of our data was self-reported by female 23andMe customers of European descent who have opted into research and filled out an online survey. We specifically asked about bra cup size as an approximation for breast size using a 10-point scale ranging from “Smaller than AAA” to “Larger than DDD”. We also took into account age, breast-related surgeries (augmentation, reduction, or mastectomy), pregnancy and breastfeeding status, and bra band size (which is correlated with body mass index (BMI)).
Most of the genetic factors we identified for breast size lie in regions of great importance for breast cancer. One of the SNPs, rs12173570, is known to regulate the expression of the estrogen receptor gene, which plays a vital role in breast growth and in the majority of breast cancer cases (known as “ER+” or “hormone positive” types).
Another one of these SNPs, rs7816345, is located in a region of the genome (8p21) that often shows abnormalities in people with a certain subtype of breast cancer. Scientists also recently reported <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076615/">genetic factors influencing breast density</a> &#8212; a <a href="http://www.nejm.org/doi/full/10.1056/NEJMoa062790">risk factor</a> for breast cancer &#8212; and our research suggests that one of those factors may also be associated with breast size.
These findings show that some of the same biological pathways underlie both normal breast growth and breast cancer. This isn’t a huge surprise if you think of cancer as unrestrained growth. But the relationship between breast size and breast cancer is complicated. <a href="https://www.ncbi.nlm.nih.gov/pubmed/10231159">Some</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/16284954">studies</a> have found that larger breast size as a young woman is associated with a slight increase in breast cancer risk, but only in women who were lean at a young age. The genetic factors we found aren’t enough to explain this association, but support the idea that breast size and breast cancer are related.
While the topic of breast size raised a few eyebrows when we first put out the survey (some thought it was too personal, or couldn’t be serious science), this paper demonstrates that important scientific insights can come from the most unlikely of places. Although the connections between these genetic factors, breast size, and breast cancer aren’t fully understood, our findings give clues to the function of some of these genes and regions that might be useful in combating breast cancer.

Genetics linked to breast size and breast cancer risk

<img loading="lazy" decoding="async" class="aligncenter wp-image-4273 size-full" title="blooddonation" src="http://35.88.189.111/wp-content/uploads/2009/08/blooddonation.jpg" alt="A photo of a woman giving blood." width="350" height="232" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/blooddonation.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/08/blooddonation-300x199.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />Simply giving blood is one of the best ways to treat iron overload.
It’s the most common genetic disease you never heard of.  <a href="https://www.23andme.com/topics/health-predispositions/hereditary-hemochromatosis/">Hemochromatosis</a>, sometimes called the “Celtic Curse,” affects an estimated one in every 300 Americans, but many who have it have no idea they do.
<h2>Serious Medical Condition</h2>
July is National Hemochromatosis Month, and 23andMe will highlight stories and research related to this genetic disease, which can quietly lead to iron overload – a serious medical condition – over time. Some people may never know they have the problem because the symptoms often appear later in life – between the ages of 40 and 60 in men and after menopause in women.
However, iron overload can cause severe damage to the liver, kidney, heart, and other organs. When iron levels in the body become dangerous, lowering those levels can be done relatively simply by having blood drawn regularly. Changes in diet can also help maintain safe levels and avoid the problems caused by chronic high levels of iron.
<h2>Hereditary Hemochromatosis</h2>
There are several forms of hereditary hemochromatosis. 23andMe currently reports on two of the most common genetic variants in the HFE gene that can lead to the condition – C282Y and H63D. Mutations in other genes can cause other kinds of hereditary hemochromatosis.
Up to 90 percent of those with hereditary hemochromatosis have two copies of the most severe variant in the HFE gene – C282Y – and they are at the highest risk of developing iron overload. Not everyone develops symptoms, and environmental factors also affect iron levels. Individuals with one copy of the C282Y variant and a second milder variant in the HFE gene are also at some risk for iron overload, though they are less likely to end up with organ damage.
The Centers for Disease Control notes that early disease detection is important, but diagnosing it can sometimes be challenging. Knowing your family history and whether you have a genetic risk for the disease can help you and your doctor decide whether you should be more proactive in screening for the condition, which can be easily managed.

The Most Common Genetic Disease

(Editors note: Dan Vorhaus pointed out an error in an earlier version of this introduction concerning the SCOTUS blog. We&#8217;ve corrected the error. Thanks Dan.) In light of the Supreme Court’s ruling this week largely upholding the health care reform law, we’re reposting a story we did back in March. 
If you missed the news about the ruling there is plenty out there to help you make sense of it all. The <a href="http://www.scotusblog.com/" target="_blank" rel="noopener">SCOTUS blog</a> sponsored by Bloomberg Law has some <a href="http://www.scotusblog.com/">helpful summaries</a> of the decision as well as posts detailing its <a href="http://www.scotusblog.com/2012/06/dont-call-it-a-mandate-its-a-tax/">core points</a>. And almost immediately after the 5-4 ruling, most major papers had coverage including the<a href="https://www.washingtonpost.com/politics/courts-law"> Washington Post</a>,<a href="http://topics.nytimes.com/top/reference/timestopics/organizations/s/supreme_court/affordable_care_act/index.html"> New York Times</a> and the<a href="https://online.wsj.com/article/SB10001424052702303649504577494553982451864.html?mod=googlenews_wsj"> Wall Street Journal</a>. 

This post from our archives looks more broadly at issues related to health care costs. 
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-11984" title="robert_pearl" src="https://blog-api.23andme.com/wp-content/uploads/2012/03/robert_pearl1-300x290.jpg" alt="" width="300" height="290" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/03/robert_pearl1-300x290.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/03/robert_pearl1.jpg 488w" sizes="auto, (max-width: 300px) 100vw, 300px" />Robert Pearl, MD
In the lead up to this week’s arguments at the Supreme Court over the health care reform law, 23andMe got the opinion of two doctors on what’s ailing the country’s medical system. 
On separate visits we heard from<a href="http://www.venrock.com/team/#/team/?item=99"> Bob Kocher</a>, an MD and partner at<a href="http://www.venrock.com/?home=1"> Venrock</a> who previously served as a special assistant to the president for Healthcare and Economic Policy and was instrumental in writing the reform law. A few weeks after hearing from Kocher we heard from<a href="http://xnet.kp.org/newscenter/aboutkp/bios/california/pearl.html"> Robert Pearl</a>, also an MD and the Executive Director and CEO of<a href="https://members.kaiserpermanente.org/kpweb/aboutus.do"> The Kaiser Permanente Medical Group</a>. Under Pearl’s leadership Kaiser has been singled out as an example of how to deliver quality affordable health.
While Kocher’s and Pearl’s opinions on the law and whether the court will uphold it diverged on some points, both men offered a pretty grim diagnosis if some sort of reform doesn’t go forward. Spending on health care continues to grow more rapidly than the economy as a whole. We now spend about 18 percent of our GDP on health care or &nbsp;– a larger share than what we spend on manufacturing or retail trade. Back in the early 1960s health care costs were only about 4 percent of GDP. According to Pearl, the rapidly growing costs are on course to cripple the economy. 
The irony about all this spending is that while we pay out far more than any other country in the world and more than twice the average for industrialized countries, our<a href="http://blogs.ngm.com/.a/6a00e00982269188330120a7a46406970b-popup"> outcomes are worse</a>. We have lower life expectancy and higher infant mortality rates than countries that spend far less. 
Under the current system there aren’t incentives for preventing diseases. All the upside is in treatment or interventions and this drives costs up. 
“People have a hard time understanding that we are able to spend less and improve quality,” said Pearl. 
“If every American got the same care (as they do at Kaiser) there would be 200,000 fewer strokes each year, 75,000 people wouldn’t die of cancer and the mortality rate of AIDS/HIV would be halved; sepsis in hospitals would diminish by 40 percent,” Pearl said. 
Some of this is done through better use of data, integrating treatment and preventative care and effectively using technology. He pointed out that in many ways medical care is still a cottage industry in America with doctors providing “piecemeal” services isolated from each other. And he said the system is largely out of touch with the economic efficiencies and technologies we see in other sectors, like banking. &nbsp;He foresees simple fixes such as the widespread use of electronic records similar to the system used by Kaiser, as well as video-links for some types of doctors visits and the use of more email exchanges between doctors and patients. All these can reduce costs and improve efficiency, he said. 
Much of this is in line with Kocher’s prescription for reform.
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-11979" title="Bob Kocher - Venrock" src="https://blog-api.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-300x300.jpg" alt="" width="300" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-768x768.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-1024x1024.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-880x880.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-1180x1180.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD-980x980.jpg 980w, https://blogcms.23andme.com/wp-content/uploads/2012/03/Bob-Kocher-MD.jpg 1395w" sizes="auto, (max-width: 300px) 100vw, 300px" />Bob Kocher, MD
Back in 2009, Kocher and several others authored a report for the Brookings Institute, called “Bending the Cost Curve,” that outlined in detail several strategies for reducing the growth of health care costs. Many of these ideas were incorporated into the health care reform bill. 
He outlined for us some of the things he felt were key components of those strategies, foremost of which was moving away from paying by treatments toward a system that bundled payments. For example instead of compensating a hospital for all the different treatments they delivered to a diabetes patient in a year, the hospital would be paid one lump sum for treating everything related to that patient’s care in a year while meeting certain quality metrics. 
Both Kocher and Pearl also talked about giving patients access to more information to involve them in their own health decisions and empower them to make choices. Kocher mentioned that giving people more information about the costs and performance of doctors and hospitals empowers them to be better consumers. They’ll know which doctors and hospitals have better outcomes and this will help them make smarter decisions when choosing where they spend their health care dollars. This is also the premise behind the company Castlight Health, where Kocher is on the board of directors. 
Both Kocher and Pearl believe that genetics tests like 23andMe’s will play a role in making health care more personal and they believe that the tests will become increasingly more commonplace. But, as Pearl said, there is a long delay in the adoption of new technology within the health care industry. There is also a lot of negative inertia within the system in which the rewards are for treatment not for prevention. 
23andMe CEO and co-founder Anne Wojcicki<a href="https://www.huffingtonpost.com/anne-wojcicki/secret-code-dna_b_1187141.html"> recently wrote</a> about this explaining: 
“If I develop type 2 diabetes, the whole healthcare system knows how to deal with it, treat and profit from it. But if I discover I am at high risk for type 2 diabetes, I change my diet and exercise patterns and successfully prevent it, no one profits but me. We believe that engaging people in their own health care by giving people access to their genetic information and informing them of how to prevent disease can help.” 
While all the attention this week is on the legal questions being argued in front of the Supreme Court, this broader question about how best to lower costs, improve quality and empower people in their own health care isn&#8217;t going to go away any time soon.

Health Care Costs and Reform

<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-12994" title="egg+sperm" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/egg+sperm-300x225.jpg" alt="" width="300" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/egg+sperm-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/05/egg+sperm.jpg 400w" sizes="auto, (max-width: 300px) 100vw, 300px" />
As a woman ages her fertility naturally declines such that by the time she reaches menopause her “ovarian reserve” is depleted, meaning that she has few to no eggs – oocytes – remaining in her ovaries.
Some women, however, have problems with fertility relatively early in life and this may be due to premature ovarian decline (reduced number and quality of eggs). Although it’s not clear why this occurs, it’s likely that both genetic and environmental factors play a role.
In the first genome-wide association <a href="https://www.ncbi.nlm.nih.gov/pubmed/22116950">study on this topic</a>, researchers from Stanford, UCSF, and Kaiser Permanente have attempted to identify genetic and environmental factors associated with markers of ovarian reserve. The study enrolled around 230 women with European ancestry and 200 with African-American ancestry, aged 25-45. The women were recruited from the general population and were of normal reproductive health.
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How is Ovarian Reserve Measured? 
There are a number of clinical tests for <a href="http://humrep.oxfordjournals.org/content/23/3/699.long">measuring a woman’s remaining egg pool</a>, though no single one is a perfect proxy for ovarian reserve. Blood levels of hormones involved in follicle development – follicular stimulating hormone (FSH) and anti-Mullerian hormone (AMH) – are typically measured. Physicians also use ultrasound to count the number of antral follicles, the structures in the ovaries that release an egg when a woman ovulates. Like ovarian reserve, AMH levels and antral follicle count both decline with age. Conversely, levels of FSH go up as a woman ages and higher levels are typically found in women with reduced ovarian reserve. 
<img loading="lazy" decoding="async" class="aligncenter wp-image-14095 size-thumbnail" title="ovarian reserve" src="http://35.88.189.111/wp-content/uploads/2012/06/ovarian-reserve3-150x150.png" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/ovarian-reserve3-150x150.png 150w, https://blogcms.23andme.com/wp-content/uploads/2012/06/ovarian-reserve3-271x271.png 271w, https://blogcms.23andme.com/wp-content/uploads/2012/06/ovarian-reserve3-372x372.png 372w" sizes="auto, (max-width: 150px) 100vw, 150px" />
This figure shows that AMH and antral follicle count parallel declining ovarian reserve, while FSH levels increase as a woman&#8217;s egg pool declines. The relative levels are arbitrary in this graph as it is just meant to show the general relationship between different markers of ovarian reserve. 
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The researchers first confirmed that levels of two fertility-related hormones – FSH and AMH (see sidebar) – correlated with maternal age and antral follicle number, though they found more variability in the African-American women than in the European women. They also found several genetic factors that may correlate with antral follicle count in the African-American group but did not find any factors for this trait in the European cohort.
These findings are very preliminary and larger studies are needed to confirm and expand upon these results.
Of course, the environment can also play an important role in fertility. Although the findings were not definitive, the researchers found some indication that women who smoked had a higher rate of antral follicle decline as they got older.
The data also suggested that oral contraceptive use might lead to reduced follicle count, though for the most part this only seemed to be the case in African-American women.
Overall, these findings provide preliminary results for a very complex biological phenomenon.
If the identified genetic markers are confirmed in future studies, they could be used to identify women at risk for premature ovarian decline and possible fertility problems. More research on environmental factors influencing fertility may also help in preventing, delaying, or treating ovarian decline.

Egg Hunt: New Research on Female Fertility

<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-14021" title="Quebec flag 2" src="https://blog-api.23andme.com/wp-content/uploads/2012/06/Quebec-flag-2-300x218.png" alt="" width="300" height="218" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/Quebec-flag-2-300x218.png 300w, https://blogcms.23andme.com/wp-content/uploads/2012/06/Quebec-flag-2.png 549w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Editor&#8217;s note: This post has been edited from its original.
“<a href="https://en.wikipedia.org/wiki/Qu%C3%A9b%C3%A9cois">Quebecois</a>” will likely be celebrating <a href="https://en.wikipedia.org/wiki/National_Holiday_%28Quebec%29">John the Baptist</a> and French-Canadian heritage on June 24th with lively parties, parades and bonfires.
<h6>French Canadians</h6>
At 23andMe we’re paying tribute to French-Canadian ancestry with the release of two new health reports on rare genetic disorders (Leigh Syndrome, French Canadian Type; and Tyrosinemia Type I) that affect French Canadians more than the general European population.
You’re more likely to encounter these and a few other rare conditions in Quebec because of the interesting history of this region. When French immigrants arrived in “New France” (modern day Quebec) in the 17th century, they likely brought a few “genetic stowaways” with them – mutations that don’t cause any problems on their own but when paired up can result in serious diseases. (Many of the genetic conditions that affect French Canadians today are so-called “recessive” conditions and are caused by having two bad copies of a gene – one from mom and one from dad.)
<img loading="lazy" decoding="async" class="alignnone size-medium wp-image-8068" src="https://blog-api.23andme.com/wp-content/uploads/2010/12/carrier-chances-255x300.png" alt="" width="255" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/12/carrier-chances-255x300.png 255w, https://blogcms.23andme.com/wp-content/uploads/2010/12/carrier-chances.png 614w" sizes="auto, (max-width: 255px) 100vw, 255px" />Mendelian Recessive Disorders 
For a recessive disorder like most of those described here, a child whose parents are both carriers will have a 25% chance of developing the disease, a 50% chance of being a carrier, and a 25% chance of being neither.
<h6>Founder Effect</h6>
They also encountered remote lands that hadn’t been settled yet, so they didn’t have many choices when it came to finding a mate! Through generations of marrying within their own community, the founders’ stowaway mutations got passed down and became more common, thus raising the chances that two people carrying a mutation would have a child that inherits both copies of the mutation.
This <a href="https://www.pbs.org/wgbh/evolution/library/06/3/l_063_03.html">“founder effect”</a> phenomenon is most obvious today in the Saguenay-Lac-Saint-Jean region of Quebec where roughly one person in 20 carries a mutation for a rare recessive disorder and about one in 2000 is born with the condition.
<h6>Founding Immigrants</h6>
Although some of these disorders affect more than just French Canadians, all of them are found at relatively high rates in Quebec and especially in Saguenay-Lac-Saint-Jean. (See table below for more information about these conditions).
French Canadians aren’t the <a href="https://blog.23andme.com/articles/ashkenazi-ancestry-and-health">only group with higher rates</a> of certain diseases, but they are unique in that they can trace their ancestry both genetically and through genealogical records generated by the Roman Catholic Church.
Some researchers have even begun to pinpoint which <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1224533/">founding immigrants</a> first introduced the stowaway mutations into their new home of Quebec.

French-Canadian Ancestry and Relevant Health Conditions

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The dance is sort of a gnome-like jig – all knees and elbows and no hint of cool – but where Matt Harding gets you is in his pure unabashed release of happiness.

As you watch, a smile creeps across your face. You can’t help yourself.

For almost a decade, Matt has cobbled together the most unlikely of careers – making a video series in which, as he says, he “travels around the world dancing badly.”

The series, called<a href="http://www.wherethehellismatt.com/" target="_blank" rel="noopener noreferrer"> “Where the Hell is Matt?”</a>, started innocently enough when he was backpacking through Vietnam in 2003 after quitting his job as a video game programmer. On a lark, his buddy suggested that Matt, “do that stupid dance you do.” His friend videotaped him doing his silly shuffle next to a busy traffic circle with people walking by. There was no intent to share it with anyone but the video wound up on YouTube and went viral.

Fast-forward nine years, and Matt’s quirky videos have attracted almost 78 million views. More than 40 million people saw his last one, and over the last two years, he’s traveled to dozens and dozens of countries shooting his next video that he released <a href="https://www.youtube.com/watch?feature=player_embedded&#038;v=Pwe-pA6TaZk" target="_blank" rel="noopener noreferrer">this week</a>. 
<iframe loading="lazy" width="560" height="315" src="https://www.youtube.com/embed/zlfKdbWwruY" frameborder="0" allow="accelerometer; autoplay; encrypted-media; gyroscope; picture-in-picture" allowfullscreen="allowfullscreen"></iframe>

As he was putting together the final touches on this latest video, Matt partnered up with 23andMe for another short little film. (Editor&#8217;s note: This video is no longer available online.)
In this one he’s meeting and dancing with strangers like in his other videos, but this time each person he’s dancing with – in Tucson, Colorado Springs, Minneapolis and San Francisco – has something in common with Matt. They each share some DNA.

Using 23andMe’s Relative Finder, Matt connected with distant cousins around the country. A few wanted to meet him in person so he crisscrossed the country in a very few days, and was introduced to relatives he never knew he had. Then, he danced with them.

“Having these people who I’ve just gotten to go around and meet, whom I’m related to, is really amazing,” said Matt. “Somewhere back on our family tree we have a common ancestor… I would’ve never known that without the DNA.”

For Matt this is where he sees the overlap with what he’s been doing over the years.

“It’s all about connectedness,” he said. “It’s all about seeing what we have in common. With 23andMe you realize that we all share the same roots, the same origin if you go back far enough. And yet we are all unique.”

Dancing with 23andMe

Editor&#8217;s note: This post has been edited to reflect changes in our product.
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Today is summer solstice, the longest day of the year in the northern hemisphere. This means that there’s a lot of light around and as a consequence, people with the “ACHOO syndrome” might be sneezing a lot.
Gesundheit! 
Two years ago 23andMe announced a <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000993">new genetic discovery</a> that at least partially explains why some people sneeze when they go from darkness to light. A certain genetic variant increases the likelihood of having this <a href="https://www.23andme.com/topics/traits/photic-sneeze-reflex/">photic sneeze reflex</a>, also called the ACHOO syndrome (short for Autosomal-dominant Compelling Helio-Ophthalmic Outburst syndrome). Each copy of the C version of is associated with 1.3 times increased odds of having the trait in people with European ancestry.
The reflex is harmless but understanding this common trait could help scientists better understand other light-triggered reactions, such as some types of epileptic seizures. This <a href="https://www.23andme.com/about/factoids/">discovery</a> was fueled by 23andMe customers who took the survey &#8220;Ten Things About You&#8221;.
We hope you aren’t sneezing today, but if you are then perhaps you can blame it on your DNA. Either way 23andMe wishes all of you a happy summer solstice!

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