<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-16243" title="Amy_Kiefer V4" src="https://blog-api.23andme.com/wp-content/uploads/2012/10/Amy_Kiefer-V4-225x300.jpg" alt="" width="225" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/10/Amy_Kiefer-V4-225x300.jpg 225w, https://blogcms.23andme.com/wp-content/uploads/2012/10/Amy_Kiefer-V4.jpg 300w" sizes="auto, (max-width: 225px) 100vw, 225px" />Amy Kiefer is a Survey Research Manager at 23andMe. She joined the company in 2008. 
What do nearsightedness, stretch marks, and motion sickness have to do with each other? They don’t appear to be genetically related – at least not according to our in-house statistical geneticists – but all of them are relatively common and annoying. These three conditions are also making 23andMe scientists happy since all of them are hot on the research wagon!
Scientists at 23andMe are gearing up for the annual <a href="http://www.ashg.org/">American Society of Human Genetics</a> 
(ASHG) meeting and will be presenting on all of these topics. Here are some highlights:
<h6>Are My Genes Making me Myopic?</h6>
Myopia, or nearsightedness, is thought to be highly heritable – if your mother wore glasses to see the chalkboard chances are you might need them – but until now scientists have only known a little about the underlying genetics.
23andMe scientist Amy Kiefer* will present results from a genetic study carried out with data from 23,000 nearsighted customers and 16,000 controls, all with European ancestry. The analysis identified associations between 17 genetic factors and myopia and replicated the only two <a href="https://www.nature.com/ng/journal/v42/n10/full/ng.663.html">previously identified</a> <a href="https://www.nature.com/ng/journal/v42/n10/full/ng.664.html">associations</a> in Europeans. Many of the new factors are located in genes that play important roles in eye development and function. This analysis is the largest ever gene association study on this topic.
<h6>Making a Stretch for My Genes</h6>
Some of us are all too familiar with stretch marks – red or white lines that appear on the skin, often after pregnancy. The appearance of these marks has encouraged many to open their wallets (to the tune of $5-10 billion annually) and fill their cupboards with cosmetics that claim to prevent or treat stretch marks.
But despite the range of products promising to “make those lines vanish”, very little is understood about what causes them in the first place. And up until 23andMe took a stab, no genetic factors had been associated with stretch marks in the general population.
Meghan Mullins* from 23andMe will present results from a genetic study with 30,000 customers who responded to the following question on the 23andMe website: “Do you have stretch marks on your hips, thighs, or backs of your arms? Yes/No/I’m not sure”. The analysis identified an association between stretch marks and a variant near a gene called elastin. Defects in the elastin gene are known to affect the integrity of the skin as well as cause heart defects. This study also identified an association between stretch marks and a variant in a protein called SRPX, but more work is needed to understand how this protein could play a role in this condition.
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<h6>Your Participation Makes Research Possible</h6>
 
The results presented in this post were made possible because of 23andMe customers. 23andMe offers a variety of ways for customers to contribute to research – all it takes is a little bit of spit and the willingness to answer web-based questionnaires. What you get back is the knowledge that you’ve personally helped move science forward. 

<img loading="lazy" decoding="async" class="alignleft size-full wp-image-12163" src="https://blog-api.23andme.com/wp-content/uploads/2012/04/JRBgdIBXKIeVIdETJrxYIw_ttam_logo.jpg" alt="" width="24" height="40" />Check out our latest survey on empathy. 
Not yet a customer? <a href="https://www.23andme.com/store/cart/">Visit our store!</a>
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A Motion for the Genetics of Motion Sickness
Roughly one in three individuals is highly susceptible to motion sickness; the remaining two-thirds of the population may experience motion sickness if the conditions are extreme. We understand what provokes motion sickness – traveling in cars, boats, planes, and also more unusual modes of transportation like skiing or riding a camel. Partaking in simulator experiments, for instance those carried out by the US Air Force and NASA, and escaping into virtual reality environments (aka playing video games) can also provoke motion sickness.
It’s estimated that up to 70% of a person’s risk for motion sickness is due to genetics, but the genetics of motion sickness has been very poorly understood &#8230; until now.
23andMe scientist Bethann Hromatka* will present results from a genetic study of nearly 37,000 customers who were surveyed about motion sickness. The analysis identified 14 genetic associations with motion sickness that fall into a few different biological categories. Three genetic variants are involved in development, including development of the eye and ear. Other variants are involved neurological processes and glucose/insulin regulation.
*Numerous 23andMe employees contributed to these studies. Statistical geneticist Nicholas Eriksson carried out the genetic analyses and others on the 23andMe Research Team contributed to survey design, data analysis, and scientific review.
<h6>Related posts:</h6>
&#8211;<a href="https://blog.23andme.com/23andme-research/cilantro-love-hate-genetic-trait/" rel="bookmark"> Cilantro Love and Hate: Is it a Genetic Trait?</a> 
&#8211;<a href="https://blog.23andme.com/23andme-research/highlighting-23andme-research/" rel="bookmark"> Highlighting 23andMe Research</a> 
&#8211;<a href="https://blog.23andme.com/news/announcements/23andme-scientists-head-to-montreal-for-ichgashg-eh/" rel="bookmark"> 23andMe Scientists Head to Montreal for ICHG/ASHG, Eh</a>

23andMe Blog

23andMe Blog Team

The Genetics of Nearsightedness, Stretch Marks, and Motion Sickness

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-16184" title="broccoli like chocolate" src="https://blog-api.23andme.com/wp-content/uploads/2012/10/broccoli-like-chocolate-200x300.jpeg" alt="" width="200" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/10/broccoli-like-chocolate-200x300.jpeg 200w, https://blogcms.23andme.com/wp-content/uploads/2012/10/broccoli-like-chocolate.jpeg 250w" sizes="auto, (max-width: 200px) 100vw, 200px" />
Ever since my kids were wee tykes in diapers, I’ve gone through the same bedtime routine of reading them a story. We went from picture books to the simple joys of Seuss, to following the wizardly adventures of <a href="http://www.jkrowling.com/en_US/#/timeline/harry-potter-and-the-deathly-hallows/i" target="_blank" rel="noopener">Harry, Hermione, and Ron.</a>
Our nightly page-turners don’t usually delve into the world of science or genetics but that all changed recently thanks to the book, <a href="http://genetics.thetech.org/book-titles" target="_blank" rel="noopener">“When Will Broccoli Taste Like Chocolate?”</a>
<h6>Ask a Geneticist</h6>
Sent along by some scientists at San Jose’s Tech Museum, the book is a great compilation of questions submitted by people to the website “Ask a Geneticist” and answered by Stanford University scientists. The website is part of a hands-on exhibit at the <a href="http://genetics.thetech.org/" target="_blank" rel="noopener">Tech Museum</a>. The questions – from both kids and adults – are sometimes cheeky, sometimes straight, and always interesting. The title comes from one of those questions, from an adult who likes all the good stuff that comes with eating broccoli, just not the taste.
I brought the book home to look at how someone smarter than me talks to people about the complicated world of genetics. So the book was meant for me, but then my son picked it up.
It suddenly became our reading material for the night when my son randomly turned the page to “What would it take to develop a superpower?”
<h6>Super Strength</h6>
This is a critical question for young boys everywhere and it has been the topic of several conversations with my son. He favors super strength, understanding flight just isn’t possible. For my daughter, who is two years older and a little more sophisticated, it was the the section on eye color that drew her in. The Tech has also created a<a href="http://genetics.thetech.org/online-exhibits/what-color-eyes-will-your-children-have" target="_blank" rel="noopener"> great tool</a> to calculate the probability of blue, or green, or brown eyes.
The answers in the book offer a chance to draw in not just kids, but anybody interested in the science. In the case of superpowers, the book explores the genetics behind strength and intelligence, as well as the peculiar ability to be oblivious to pain. They illustrate the answers with examples such as a family in Pakistan that can&#8217;t feel pain. This family has a genetic mutation that interrupts the the process by which nerves to sense pain. Turns out <a href="https://abcnews.go.com/GMA/OnCall/story?id=1386322#.UG8-cPl26PI">it’s not such a super superpower</a>, as my son learned.
<h6>Learning</h6>
23andMe does a pretty good job of making the journey into your DNA both fun and fascinating, but there are always more questions to be answered. &#8220;When Will Broccoli Taste Like Chocolate?&#8221; gives a broad sampling of those queries – some big, some small, some silly and some serious – we all have around this topic. The book, as well as the “Ask a Geneticist” website, offers a very approachable way for people to explore genetics.
And what about making broccoli taste like chocolate?
My kids learned it’s not as easy as putting cocoa and broccoli plants alone in a room together. Genetics is complicated, and genetically modifying foods can still be controversial and expensive. At least for my kids they’ll continue to hold their noses when eating their broccoli, while the book is making the rounds on both their nightstands for their own exploration into science.

Chocolate Broccoli

<img loading="lazy" decoding="async" class="alignright wp-image-6586 size-medium" title="23andMe_Logo_blog" src="http://35.88.189.111/wp-content/uploads/2010/05/23andMe_Logo_blog-300x300.jpg" alt="An image of 23andMe's logo" width="300" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog.jpg 350w" sizes="auto, (max-width: 300px) 100vw, 300px" />
We would like to give a little shout-out to Holly Dunsworth, an assistant professor of anthropology at the University of Rhode Island and a blogger, for her thoughtful post<a href="http://ecodevoevo.blogspot.com/2012/10/be-afraid-of-fear-not-personal-genomics.html"> “Be Afraid of Fear, Not Personal Genomics.”</a>
<h6>Fear</h6>
While there are legitimate topics for debate about genetic testing, some coverage veers far from those real issues, and seemingly serves only to scare people.
Dunsworth cites a few paragraphs from a recent<a href="http://m.npr.org/news/Health/160958948"> NPR piece</a> that includes a quote from Mark Rothstein, a bioethicist at the University of Louisville.
“We&#8217;re basically not ready for a society in which very exquisite, detailed genomic information about every individual, potentially, is out there,” Rothstein said.
Why that might be is not explained by Rothstein, and this is Dunsworth’s point. It just hangs out there playing on people’s fear.
<h6>Access</h6>
It’s a disservice to play up those fears. In this case, the statement by Rothstein supposes that because a person knows his or her own genomic information, somehow anyone else can learn about it. But that’s not true. There are strong privacy protections for that data. At the same time, if a person is comfortable sharing their information with others, they have the right to do that. This goes back to some of the bedrock  principles of ethics that include the autonomy and respect for individuals. Those  principles should make clear that a person both has a right to access to their own DNA data, and the right to use it as they see fit.

<img loading="lazy" decoding="async" class="alignright wp-image-16032 size-medium" title="mermaid's tale blog" src="http://35.88.189.111/wp-content/uploads/2012/10/mermaids-tale-blog-300x45.jpg" alt="An image of the Mermaid's Tale website logo" width="300" height="45" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/10/mermaids-tale-blog-300x45.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/10/mermaids-tale-blog.jpg 654w" sizes="auto, (max-width: 300px) 100vw, 300px" />
<h6>Understanding</h6>
In a comment to her own post, Dunsworth points out that in the NPR piece in early September there is more space dedicated to the 1997 fictional dystopian movie Gattaca than to real topics for discussion. For Dunsworth, this feeds into people’s own fears and ignorance about the science rather than informing them.
“Even if you don&#8217;t get an ounce of joy from the experience, when you&#8217;re informed you don&#8217;t fall uncritically for claims that (genetic testing is) … dangerous or venomous,” she writes.
One of the missions of 23andMe is to <a href="https://www.23andme.com/gen101/genes/" target="_blank" rel="noopener noreferrer">introduce people to their DNA</a> and help them navigate what all the As, Gs, Ts and Cs mean. Our hope is that the more you know about yourself the more you will take charge of your own health. It is also fascinating and fun to explore your genetics and learn about how it may impact your health, or how it makes you unique, or what it says about your ancestry. In the process, we learn that science is dynamic and our knowledge constantly evolving as we find out more about ourselves and what our DNA means.
The journey you take can be both awe-inspiring and fascinating. And as Dunsworth says:
“There&#8217;s not a whole lot on the planet that&#8217;s cooler than that.”

Fear Not The Genome

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-1400" title="bloodclot" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/bloodclot-300x222.jpg" width="300" height="222" />
A <a href="http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2812%2960986-6/abstract" target="_blank" rel="noopener noreferrer">study</a> in the journal Lancet regarding a new blood thinning drug brings to mind the difficulty doctors and patients have in using anticoagulants to prevent clots that could otherwise lead to heart attacks or strokes.
The mostly commonly used blood thinner, warfarin (Coumadin ®) has proven to be a godsend for millions of people at risk, but this study suggests that as many as half of those who use the drug do not benefit from it because of challenges related to finding the proper dose.
Calibrating the right prescription of warfarin is notoriously difficult because the right amount depends not just on such things as a person’s size, their diet and age, but also, importantly,their genes.
The new study isn’t about genetics. It’s by<a href="http://www.dukehealth.org/health_library/news/apixaban-superior-to-warfarin-across-wide-range-of-patient-risk-scores"> researchers at Duke Medical Center</a>, who suggest that the new blood thinner apixaban is safer than warfarin and more effective at preventing strokes in people who have atrial fibrillation, a common heart rhythm disorder.
Apixaban hasn’t<a href="https://www.forbes.com/sites/larryhusten/2012/09/27/fda-sets-new-decision-date-for-eliquis-aprixaban/"> yet received FDA approval</a>. That may soon change, but the study reminds us of all the challenges with current drugs and the tremendous amount of resources invested into finding drugs that are safe and effective for more people. Another complementary way to achieve that goal is by learning more about how individual patients may respond to specific drugs. Your genetics are a big part of that equation.
In the case of warfarin, aperson’s genetic<a href="https://www.23andme.com/health/Warfarin-Coumadin-Sensitivity/">s</a> directly impacts how sensitive they are to the drug. Although there are a number of factors that influence a person’s optimal dose of warfarin, genetic variations in the CYP2C9 and the VKORC1 genes play an important role in how the body responds to the drug. More than two years ago the FDA updated the labeling on warfarin to make note of this genetic influence but genetic testing is not required before prescribing warfarin.

Related posts: 
 &#8211;<a href="../2009/02/19/new-study-shows-that-genetic-information-can-improve-administration-of-commonly-used-blood-thinner/"> New Study Shows That Genetic Information Can Improve Administration Of Commonly Used Blood Thinner</a> 
&#8211;<a href="../big-questions/a-prescription-for-personalizing-medicine/"> A Prescription for Personalizing Medicine</a> 
&#8211; <a href="../news/announcements/23andme-launches-first-national-institutes-of-health-funded-study/">23andMe Launches Its First NIH Funded Study</a>

Blood Thinners and the Genetics Behind Drug Response

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-16009" title="23andMe-AshleyG-040" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2012/09/23andMe-AshleyG-040-210x300.jpeg" width="210" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/09/23andMe-AshleyG-040-210x300.jpeg 210w, https://blogcms.23andme.com/wp-content/uploads/2012/09/23andMe-AshleyG-040.jpeg 448w" sizes="auto, (max-width: 210px) 100vw, 210px" /> Ashley Gould, 23andMe&#8217;s Vice President Corporate Development and Chief Legal Officer 

We recently topped our goal of enrolling 1,000 people with a group of rare blood disorders known as myeloproliferative neoplasms, or MPNs. As a testament to the passion of the people who’ve enrolled in our<a href="https://www.23andme.com/mpn/" target="_blank" rel="noopener noreferrer"> MPN Research Initiative</a> and the power of our research model, this was all done in just a year. That momentum has already helped lead to some promising findings giving us more insight into the disease and offering hope for so much more. We’re excited by the possibilities for research, but more importantly we’re heartened by what it could offer for those who are battling this disease. For some of us, this is a very personal fight. Ashley Gould, 23andMe’s Vice President of Corporate Development and Our Chief Legal Officer, shares her and her father’s story of battling an MPN.
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by Ashley Gould, 
Vice President Corporate Development &amp; Chief Legal Officer, 23andMe
It all started with a phone call. My father had collapsed in his office and was in the hospital.  At first the doctors thought he had experienced a mini-stroke.  What followed was a blur of tests and months of waiting.  Finally, came the diagnosis. My father had myelofibrosis, one of the rare blood disorders known as myeloproliferative neoplasms, or MPNs.  It may sound strange, but in some ways it was a relief to know at last what he was facing.
My father’s diagnosis and the prognosis that he had just three-to-five years to live put an entirely new haze around my senses. As a newly minted lawyer working long hours to earn my stripes, I was in a continual state of exhaustion. With the news weighing on me, I seemed to move in slow motion, particularly when surrounded by people going about their lives.  In high school one of my favorite poems was WH Auden’s “<a href="http://english.emory.edu/classes/paintings&#038;poems/auden.html">Musee des Beaux Arts.”</a>  After dad’s diagnosis, every time I would see people sitting over coffee, talking and laughing or simply enjoying their life, a few lines of that poem would come back to me:
“About suffering they were never wrong, 
The old Masters: how well they understood 
Its human position: how it takes place 
While someone else is eating or opening a window or just walking dully along;”
How could people be laughing when my father had just been given a death sentence?  It was, for a period of time, unthinkable to me and incredibly incongruous. 

<img loading="lazy" decoding="async" class="alignright size-full wp-image-9197" title="research_springboard" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2011/06/research_springboard.png" width="135" height="109" />
Once I collected myself, the first thing I did was sign up for Team in Training to raise money for the Leukemia and Lymphoma Society.  I was already a runner and I enlisted an amazing woman and friend to run the Anchorage marathon with me.  I raised as much money as I could. We ran the race, and then it was over and I was at a loss again about what else I could do to help him.
When I could I went with my dad to his doctors’ appointments. We talked often, but I felt like I wasn’t doing enough for my father – a terrible feeling when someone you love is fighting for his life.  I left my job and went to work at a biopharmaceutical company. I thought if I couldn’t do something directly to cure my father, at least I would try to lend my skills in the pursuit of making a difference for others.  After that company was sold, I was introduced to the co-founders of 23andMe. That first meeting convinced me that the company embodied not only a vision I believed in, but one that offered a way to study rare diseases, like my father’s.  I was quickly committed.
And now, just over a year after launching<a href="https://www.23andme.com/mpn/"> 23andMe’s MPN Research Initiative</a>, I am pleased to announce that we have hit our goal of enrolling 1,000 patients.  This isn’t just a number. Creating a research community of this size for such a rare disease offers great opportunities to make new discoveries. In the short time since we launched the MPN Research Initiative, we’ve already made some promising findings. Our primary aim has always been to learn if there are genetic predispositions for the development of these kinds of illnesses and through this work we’re learning more and more about MPNs.
As one Scientific Advisory Board member, Dr. Ruben Mesa, a professor of medicine and Chair of the division of Hematology &amp; Oncology and deputy director of the Mayo Clinic Cancer Center in Arizona, said:
“This is an important milestone for MPN research. We are hopeful that the opportunities to analyze genetic and molecular data, MPN disease characteristics, and symptomatic burden, all in concert will yield great benefits for the MPN patient community.”
For Scientific Advisor Board member, Dr. Jason Gotlib, an associate professor at Stanford University School of Medicine and Stanford Cancer Center, it boils down to time.
“Reaching this goal this quickly will help accelerate the search for answers,” Dr. Gotlib said.
Our MPN Research Initiative has hit its enrollment objective faster than any other 23andMe community, which is an amazing feat for such a rare group of diseases.  Those who have joined the MPN Research Initiative are outspoken and vibrant, adjectives that also describe 23andMe.  Thanks to the participation of people who are part of our MPN Research Initiative we have reported on research findings related to our replication of an MPN association.
We are learning new things about MPNs and are excited to share more of what we have learned in the coming months.  We are grateful to the MPN Community and our advisors for their support and expertise – we would not have made the amazing progress we have without them.  I am additionally grateful to the team of people at 23andMe who have dedicated themselves to this project.  We still have a lot more to do and learn about MPNs, but I’ll gladly take this encouraging beginning over doing nothing.

Ashley Gould

A Milestone in the Fight Against MPNs Marks a Moment to Reflect

<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-3613" title="Grandparent and daughter" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2009/05/istock_000004109962xsmall-300x245.jpg" width="300" height="245" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/05/istock_000004109962xsmall-300x245.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/05/istock_000004109962xsmall.jpg 383w" sizes="auto, (max-width: 300px) 100vw, 300px" />
<a href="http://www.23andme.com/topics/health-predispositions/hereditary-hemochromatosis/">Hereditary hemochromatosis</a> is a common genetic condition that makes a person more prone to absorbing too much iron. Premenopausal women are largely protected from iron overload because of menstruation and pregnancy, but typically around menopause some women begin to experience symptoms of the condition.
A <a href="http://annals.org/article.aspx?articleid=710670">study</a> published in the late 1990’s with 176 women and 176 men with hemochromatosis, matched by age, found that a significant number of the women suffered serious complications from hemochromatosis, and developed their first symptoms only a little later than the men. On average, the women in the study showed symptoms around age 50, while the men showed signs nearly two years earlier. Roughly half of the women had stopped menstruating at the time of diagnosis, but the other half were technically premenopausal at diagnosis. There was some evidence that women who stopped menstruating before the age of 50 had higher levels of iron in their bodies.
For certain conditions*, like cirrhosis and diabetes, rates were higher in men, but for others, like fatigue and arthritis, rates were higher in women. Roughly 94 percent of the women, versus 100 percent of men, had abnormal measures of iron stores in the body.
<div style="float: right; text-align: justified; width: 200px; padding: 15px; border: 1px solid #ccc; margin-left: 10px;">Women and Men Have the Same Genetic Risk for Hemochromatosis 
Hereditary hemochromatosis affects women and men equally with respect to how the condition is inherited: you must inherit a mutated gene from each parent to have the condition and the gene involved in most forms of hereditary hemochromatosis, the HFE gene, is not located on the sex chromosomes. (This condition is autosomal recessive.) 
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Thus, the results from this study suggest that women can suffer overt symptoms of hereditary hemochromatosis and at roughly the same age as men. And once a woman goes through menopause and loses her natural way of expelling iron, she appears to have more or less the same risk as a man for suffering serious complications including arthritis and liver disease.
For most women menopause is associated with <a href="http://my.clevelandclinic.org/disorders/menopause/hic_menopause_the_short-term_effects_and_long-term_risks.aspx">various changes in health</a>. In the short term women can attest to unpleasantries that result from drops in estrogen levels. High on the list are hot flashes, changes in sex drive, and mood changes. But there are also serious long term risks for conditions like osteoporosis and heart disease. For women with hereditary hemochromatosis, increased risk for absorbing too much iron should also be added to the list. Women should take note that the symptoms of menopause and hemochromatosis can sometimes overlap, for instance fatigue is common to both.
Whether before or after menopause, it’s important for women with hereditary hemochromatosis to monitor the iron levels in their body. Physicians can order blood tests to measure transferrin saturation and serum ferritin levels in blood, which together provide a good picture of iron absorption and storage in the body. If these markers are elevated, additional testing to determine the impact on organs may also be warranted.
*Liver cirrhosis occurred in ~14 percent of the women and 26 percent of the men; diabetes occurred in ~7 percent of the women and ~16 percent of the men; fatigue occurred in ~65 percent of the women and 42 percent of the men; arthritis occurred in ~45 percent of the women and ~35 percent of the men.

&nbsp;

Hemochromatosis in Women Before and After Menopause

<div id="age_calculactor">
For a long time prospective fathers could wile away the years without much worry about when to have kids, while prospective moms were constantly checking their ticking biological clocks.
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<div></div>
<div>A<a href="https://www.nature.com/nature/journal/v488/n7412/full/nature11396.html"> recent study</a> may turn the tables a bit. It may push men to think a little more about how long they wait to start a family.The study by DeCODE in Iceland shows that each year a man delays fatherhood he increases the number of new genetic mutations that he passes on to his children.
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<h2>A Calculation</h2>
<div>These “de novo” mutations are not ones that the father was born with. Therefore they are unrelated to any previous family history or condition. They occur spontaneously in the father’s sperm cells.Using the data from the study, 23andMe’s Emily Chang lead the team that  created a simple tool that uses a man’s age to calculate the number of mutations he might pass on to his children.
<img loading="lazy" decoding="async" class="aligncenter wp-image-15995 size-full" title="mutation small" src="http://35.88.189.111/wp-content/uploads/2012/09/mutation-small.jpg" alt="" width="253" height="406" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/09/mutation-small.jpg 253w, https://blogcms.23andme.com/wp-content/uploads/2012/09/mutation-small-187x300.jpg 187w" sizes="auto, (max-width: 253px) 100vw, 253px" />
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<div>So what does the number mean?</div>
<div></div>
<div>The<a href="https://www.nytimes.com/2012/08/23/health/fathers-age-is-linked-to-risk-of-autism-and-schizophrenia.html"> implication from the study</a> is that the longer a man waits the more he increases the chances his child might develop certain kinds of conditions, such as autism. While the risk may increase, it is still very low.Also, keep in mind that despite the name, mutations are not necessarily bad. In fact, these different spellings within a person’s genetic code are largely benign. Some may even be beneficial and lead to long term genetic diversity among people.
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<h2>A Risk for Autism?</h2>
Science writer Alok Jha pointed out in a<a href="http://www.guardian.co.uk/science/2012/aug/22/older-fathers-genetic-mutations-research"> piece in the Guardian</a> that a single mutation in the APP gene actually protects against Alzheimer’s disease. It also helps people live longer. At the same time, some preliminary studies suggest that the more de novo mutations passed onto a child the higher the risk that child could develop certain types of conditions, such as autism and schizophrenia.
<div>Or as lead author Kari Stefansson, deCODE’s chief executive,<a href="https://www.nature.com/news/fathers-bequeath-more-mutations-as-they-age-1.11247"> told Ewen Callaway at Nature</a>:</div>
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“The older we are as fathers, the more likely we will pass on our mutations. The more mutations we pass on, the more likely that one of them is going to be deleterious.”
For women, who pass on other risks to their children with age, the number of de novo mutations a mom passes on to a child is constant at about 14. The number of new mutations a father passes to a child goes up by two each year. That means that a 50-year-old new father might pass on about 65 new mutations to his child. A father half his age would pass on about 35 mutations. The reason the number of de novo mutations women and men pass on to their children is so different is because women are born with all their eggs. Men on the other hand produce sperm throughout their lifetime, offering more opportunities for mutations to occur.
This doesn’t necessarily mean that men should start having kids or having their sperm frozen right out of college. But it does add more information for prospective fathers to consider. It also gives us a little more understanding about complex conditions like autism.
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Older Dads

<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-5677" title="alzheimers" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2009/12/alzheimers-150x150.jpg" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/12/alzheimers-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2009/12/alzheimers-271x271.jpg 271w" sizes="auto, (max-width: 150px) 100vw, 150px" />
In honor of World Alzheimer’s Day, we’re linking to a few posts and stories about the disease. Alzheimer’s disease is the most common form of dementia and affects more than 35 million people worldwide.
23andMe first began allowing customers to learn about their genetic risk for late-onset Alzheimer’s disease a little more than a year ago. We report on variants of the<a href="https://www.23andme.com/health/alzheimers/"> APOE</a> gene (e2, e3, and e4) and provide a risk estimate for the disease for customers with European ancestry. The 23andMe report also includes detailed background information on Alzheimer’s including other known risk factors for the disease, such as obesity and high cholesterol.
Although some are critical of giving people access to this information, many people say that despite their fear of Alzheimer’s they<a href="https://www.washingtonpost.com/national/health-science/despite-fears-of-alzheimers-many-would-like-to-know-their-risk-for-the-disease/2012/08/10/438eb3ba-6a2c-11e1-acc6-32fefc7ccd67_story.html"> would rather know</a> their risk than remain in the dark about the danger. For some knowing their APOE status and Alzheimer’s risk may encourage them to engage in <a href="http://well.blogs.nytimes.com/2012/01/18/how-exercise-may-keep-alzheimers-at-bay/">activities to stave off</a> the disease, or prompt them to participate in clinical research that could lead to more information about the causes and possible cures for Alzheimer’s.
Recently, scientists discovered a rare genetic variant that may be protective against the disease. In people of Icelandic descent, the T version of the variant (also known as the A673T variant in the APP gene) was associated with about five times lower odds of Alzheimer’s. This finding was <a href="https://www.nature.com/nature/journal/v488/n7409/abs/nature11283.html">first reported in the journal Nature</a> over the summer.
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World Alzheimer’s Day

by Emily Chang, Joanna Mountain, and Mike Macpherson
<img loading="lazy" decoding="async" class="alignright wp-image-15198 size-medium" src="http://35.88.189.111/wp-content/uploads/2012/08/Haplogroup10-300x193.jpg" alt="" width="300" height="193" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/08/Haplogroup10-300x193.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/08/Haplogroup10-768x495.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/08/Haplogroup10-1024x660.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2012/08/Haplogroup10-880x567.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2012/08/Haplogroup10-1180x760.jpg 1180w" sizes="auto, (max-width: 300px) 100vw, 300px" /> 
 Click on the image above for a larger version of this chart, which shows that some ancestry combinations are more common than others in the 23andMe database.
Given the United States&#8217;s “melting pot” nature, it is not surprising that most Americans have mixed ancestry.
Like many of my fellow citizens, my ancestry is a long recipe: a bit of English, a dash of German, a pinch of Hungarian. Should my husband and I have kids, my children will have Chinese ancestry, too. Such mixed ancestry is becoming increasingly the norm, and genetics turns out to be a very useful tool to explore it.
Traditionally, genetic ancestry focused on two particular pieces of DNA, mitochondrial DNA and the Y-chromosome.  Your maternal line includes your mother, your maternal grandmother, her mother before her, and so on; likewise, your paternal line includes your father, your paternal father, his father before him, and so on. The paternal line is determined using the Y chromosome, which determines whether a person is male and only men can pass down. The maternal line is determined using the DNA found inside mitochondria, small energy-producing cellular machines with their own genetic blueprints.
Both men and women have mitochondrial DNA, but only women pass on their mitochondrial DNA to children.
These days, genetic ancestry tools like 23andMe use DNA from all of your 23 pairs of chromosomes to offer insights into your heritage.  However, information about maternal and paternal lines, which can reflect ancestral origins, can yield interesting insights.
<img loading="lazy" decoding="async" class="alignright wp-image-15199 size-medium" src="http://35.88.189.111/wp-content/uploads/2012/08/MaternalPaternalLines-300x283.jpg" alt="" width="300" height="283" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/08/MaternalPaternalLines-300x283.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/08/MaternalPaternalLines.jpg 400w" sizes="auto, (max-width: 300px) 100vw, 300px" /> This figure shows the paternal line in blue and the maternal line in pink. Your maternal grandmother and paternal grandfather are members of your maternal and paternal lines, respectively.
Our large customer database shows that some ancestry combinations are more common than others among our customers. Given a pair of ancestral origins, there are two ways to combine the maternal and paternal lines: a maternal line of the first ancestry with a paternal line of the second ancestry or a paternal line of the first ancestry with a maternal line of the second ancestry.
Our database shows that these two ways of combining the maternal and paternal lines are not equally common, indicating gender trends in mating. For instance, about 3.5 times as many 23andMe customers have a maternal line indicative of African ancestry and a paternal line indicative of European ancestry than the reverse. This mating trend probably reflects, in part, a disgraceful period in the United States&#8217; past in which white male slave owners fathered children with enslaved African American women rather than recent trends in interracial marriages. More recent marriage patterns actually reflect a trend in the opposite direction.
The 2010 US census shows that a “white” wife and “black” husband is 2.3 times more common than a “white” husband and “black” wife [note: the terms “black” and “white” were the descriptors used in the US census report].
The maternal and paternal lines of the 23andMe customers, thus, tell the sad truth of the treatment of enslaved African American women. In one episode of the television program Finding Your Roots, Condoleezza Rice says this aspect of United States history is an “unhealed wound in America” and that we have trouble talking about what really happened during slavery. She is right. Most of us would rather not talk about the rape of enslaved African American women, but DNA isn’t shy about addressing this ugly truth. As we study and learn about these genetic patterns, we face one of the most disturbing aspects of United States history &#8212; a vital step towards healing that unhealed wound to which Rice referred.
<div style="border: 1px solid #000; padding: 15px; font-style: italic; margin-bottom: 15px; width: 300px; float: right; margin-left: 15px; margin-top: 5px;">
<img loading="lazy" decoding="async" class="alignleft size-full wp-image-12163" style="float: left; margin-right: 15px;" src="https://blog-api.23andme.com/wp-content/uploads/2012/04/JRBgdIBXKIeVIdETJrxYIw_ttam_logo.jpg" alt="" width="24" height="40" /> Learn more about <a href="https://www.23andme.com/you/ancestry">your ancestry</a> in your  23andMe account.
Not yet a customer? Visit our <a href="https://www.23andme.com/store/cart/">store</a> or <a href="https://www.23andme.com/ancestry">learn more</a>.
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A similar but less extreme pattern was observed for individuals of Asian and European ancestry; about 1.7 times as many 23andMe customers have a European paternal line in conjunction with an Asian maternal line than have an Asian paternal line with a European maternal line. The reason for this particular mating trend can not be traced to slavery and may have more complex sociological and historical origins.  Regardless of its source, however, the trend is supported by other studies. The large <a href="http://www.pewsocialtrends.org/2012/02/16/the-rise-of-intermarriage/">PEW study</a> on interracial marriage released this past February which observed that Asian American women were more likely to have an interracial marriage than Asian American men, and the US Census Bureau, which captures a wider segment of our society than the 23andMe database, shows an even stronger trend &#8212; a “white” husband and “Asian” wife is 2.4 times more common than a “white” wife and “Asian” husband [note: the terms “Asian” and “white” were the descriptors used in the US census report].
Our DNA holds a lot of information. It tells us who we are and who we, collectively, were. The mating trends seen in the maternal and paternal lines of 23andMe customers reflect complex sociological and historical truths, even some historical truths that are difficult to face. Genetics helps us learn more about who we are and who we were, hoping that such knowledge will translate into less racism and more appreciation for people who are different from ourselves.

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