A team of researchers found more than 60 genetic variants associated with resting heart rate, a known predictor of overall mortality.<img loading="lazy" decoding="async" class="wp-image-2759 size-full alignright" src="http://35.88.189.111/wp-content/uploads/2009/02/heartman.jpg" alt="" width="350" height="260" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/02/heartman.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/02/heartman-300x223.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Scientists from the University Medical Center Groningen in the Netherlands led the study, which was published in the journal Nature Genetics.
<h2>Many Variants</h2>
The researchers noted that while the effect of these genetic variants individually was small, taken together, they explained as much as 2.5 percent of the variance in resting heart rate. According to the study, a genetically predicted increase in heart rate is associated with shorter life expectancy.
“It is even more interesting to look at life expectancy,” said Ruben Eppinga, a study co-author. This study also suggested that an increase in heart rate of five beats per minute reduces life expectancy by 2.9 years in men and 2.6 years in women.”
According to cardiologist Pim van der Harst, who led the study, the findings offer evidence that there are shared genetic influences on resting heart rate and on all causes of mortality.
<h2>Data Contributions</h2>
In conducting the genome-wide association study for this research, the scientists used data from more than 134,000 people who participated in the<a href="http://www.ukbiobank.ac.uk/about-biobank-uk/"> UK Biobank</a>. Then, they were able to replicate their findings by looking at four other data sets that included more than 130,000 individuals’ data, including 51,000 23andMe customers who consented to participate in research.
“This work highlights the unprecedented opportunity provided by large-scale projects such as UK Biobank, the<a href="https://www.genomicsengland.co.uk/the-100000-genomes-project/"> 100,000 Genomes Project</a>, and the<a href="https://www.nih.gov/precision-medicine-initiative-cohort-program/scale-scope"> Precision Medicine Initiative</a> to discover novel genetic associations and to study links with outcomes and mortality,” the researchers said.
The researchers also found an association between a genetically higher resting heart rate and a person&#8217;s higher body mass index, blood pressure, and diabetes. The researchers suggest that genes or gene regions involved in cardiac development and structure may influence the association between resting heart rate and mortality. Still, more needs to be done to study the underlying biology.
Find the study in the journal <a href="https://www.nature.com/ng/journal/v48/n12/full/ng.3708.html">Nature Genetics</a>.

23andMe Blog

23andMe Blog Team

Genetics found to influence resting heart rate

As modern humans migrated out of Africa, they interbred with Neanderthals. All non-Africans carry some remnant of those ancient encounters, and <a href="http://journals.plos.org/plosgenetics/article?id=10.1371%2Fjournal.pgen.1006340&amp;utm_source=feedburner&amp;utm_medium=feed&amp;utm_campaign=Feed%3A+plosgenetics%2FNewArticles+(PLOS+Genetics+-+New+Articles)">new research </a>by scientists at the University of California, Davis, shows how natural selection has purged all but the smallest bits of that ancient DNA. <img loading="lazy" decoding="async" class="alignnone size-medium wp-image-20253" src="https://blog-api.23andme.org/wp-content/uploads/2014/01/Neanderthal_model.jpg" alt="" width="1" height="1" srcset="https://blogcms.23andme.com/wp-content/uploads/2014/01/Neanderthal_model.jpg 260w, https://blogcms.23andme.com/wp-content/uploads/2014/01/Neanderthal_model-150x150.jpg 150w" sizes="auto, (max-width: 1px) 100vw, 1px" /><img loading="lazy" decoding="async" class="alignright size-medium wp-image-25884" src="https://blog-api.23andme.org/wp-content/uploads/2016/11/AN_38417240-300x200.jpg" alt="" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2016/11/AN_38417240-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2016/11/AN_38417240-768x512.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2016/11/AN_38417240-880x587.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2016/11/AN_38417240.jpg 900w" sizes="auto, (max-width: 300px) 100vw, 300px" />
In one of the first efforts to estimate the impact of hybridization between humans and Neanderthals, Ivan Juric and his former colleagues at Graham Coop’s Lab at UC Davis used a new method for estimating the strength of natural selection against Neanderthal genetic variants. These variants would have been deleterious for the success of modern human survival.
<h2>Mixing with Neanderthal</h2>
The work also offers new insight into early interbreeding and why only a small amount of Neanderthal DNA remains in all non-Africans today.
While modern humans may have benefited from that early interbreeding, Neanderthal DNA included some deleterious gene variants, and over time, natural selection removed large numbers of those variants that would have had mildly negative impacts, said Ivan, who is now a statistical biologist and population geneticist at 23andMe.
If those gene variants were problematic, then why weren’t they weeded out of Neanderthals through the same process of natural selection?<img loading="lazy" decoding="async" class="alignright wp-image-23695" src="https://blog-api.23andme.org/wp-content/uploads/2016/03/Ivan-Juric-208x300.jpg" alt="Ivan Juric, PhD" width="300" height="434" srcset="https://blogcms.23andme.com/wp-content/uploads/2016/03/Ivan-Juric-208x300.jpg 208w, https://blogcms.23andme.com/wp-content/uploads/2016/03/Ivan-Juric-768x1110.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2016/03/Ivan-Juric-709x1024.jpg 709w, https://blogcms.23andme.com/wp-content/uploads/2016/03/Ivan-Juric-609x880.jpg 609w, https://blogcms.23andme.com/wp-content/uploads/2016/03/Ivan-Juric-817x1180.jpg 817w, https://blogcms.23andme.com/wp-content/uploads/2016/03/Ivan-Juric-scaled.jpg 1772w" sizes="auto, (max-width: 300px) 100vw, 300px" />
According to Ivan, it all has to do with numbers.
The population of Neanderthals was very small, while the humans who migrated out of Africa reached a much larger population. As the two distinct populations interbreed, the deleterious Neanderthal genetic variants that entered the larger modern human population were subject to a stronger natural selection than they were in Neanderthals.
<h2>Neanderthal DNA</h2>
While some Neanderthal genetic variants remained that would have been beneficial for human survival, most of the ones that had a negative impact disappeared.
While explaining why so little Neanderthal DNA remains in modern humans, the research also confirms previous reports that East Asian people had somewhat higher initial levels of Neanderthal ancestry than Europeans. These findings shed new light on the role of population size in losing or maintaining Neanderthal ancestry in humans and add to our understanding of our close relatives—the Neanderthals.
Here&#8217;s a <a href="https://www.nytimes.com/2016/11/09/science/neanderthal-dna-natural-selection.html?action=click&amp;contentCollection=science&amp;region=rank&amp;module=package&amp;version=highlights&amp;contentPlacement=2&amp;pgtype=sectionfront">New York Times article </a>on the new research.
23andMe customers can explore their own Neanderthal DNA <a href="https://you.23andme.com/reports/neanderthal/">here</a>. Not yet a customer? Find out more <a href="https://www.23andme.org/dna-ancestry/#toc-neanderthal">here</a>.

New Neanderthal Research

Researchers have identified a genetic variant associated with severe menstrual cramps.<img loading="lazy" decoding="async" class="alignright wp-image-24518" src="https://blog-api.23andme.org/wp-content/uploads/2016/09/femalelog.jpg" alt="femalelog" width="200" height="289">
This is the first genome-wide association <a href="https://urldefense.proofpoint.com/v2/url?u=https-3A__www.ncbi.nlm.nih.gov_pubmed_27454463&amp;d=DQMFaQ&amp;c=UE1eNsedaKncO0Yl_u8bfw&amp;r=yIEbbFV-uqmMfsvimyJmaN3PWvyt_YZu77IupqdRYgQ&amp;m=qeGp7zXkxvv_tTvSZVQiMuN7567yj3qeMt22WM8sYWc&amp;s=o7oSWYiEBZD26QuppR_qZDJbKJ_ZJiSzToO2RBhJfxc&amp;e=">study</a> of this form of chronic pain. Known as dysmenorrhea, it is the most common gynecological condition among women over 18 and can be debilitating in certain cases.
According to a physician’s handbook description of dysmenorrhea, the pain can be severe enough to interfere with daily activities in up to <a href="http://www.aafp.org/afp/2012/0215/p386.html">20 percent of women</a> who suffer from the condition.
&#8220;To date the genetic basis of pain severity for dysmenorrhea remains largely unknown,” said Nick Furlotte, senior scientist at 23andMe. “Our findings could provide deeper insight into potential treatments for what is a chronic and debilitating condition for many women.&#8221;
The study, conducted by scientists at Pfizer Inc. and 23andMe, found a single variant in the gene encoding nerve growth factor (NGF) associated with the condition in women of European ancestry. The researchers looked at data from more than 11,800 female customers of 23andMe, who consented to participate in research and answered survey questions ranking the severity of their menstrual cramps.
NGF is located in a region of the genome that also regulates ovarian and fat tissues, and has been linked to other pain disorders, although the function of the NGF gene as it relates to dysmenorrhea is not entirely known. The pain from menstrual cramps is mostly a function of the increased production of lipids known as prostaglandins during menstruation.
Although nonsteroidal anti-inflammatory drugs (NSAIDs) – such as ibuprofen or aspirin – are often effective in treating the pain, in about 15 percent of women the drugs are either ineffective or trigger adverse side effects.*
*Campbell MA, McGrath PJ. Non-pharmacologic strategies used by adolescents for the management of menstrual discomfort. The Clinical journal of pain 1999;15(4):313-320.
You can find the study in the journal <a href="https://www.ncbi.nlm.nih.gov/pubmed/27454463">Pain</a>.

Genetics found to influence menstrual cramps severity

As part of a massive study that includes the contributions from scores of researchers across the globe, scientists have found a dozen genetic markers linked to fertility, offering hope to the more <img loading="lazy" decoding="async" class="alignright size-medium wp-image-19130" src="https://blog-api.23andme.org/wp-content/uploads/2013/08/Pregnancy-Belly-300x207.jpg" alt="Pregnancy Belly" width="300" height="207" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/08/Pregnancy-Belly-300x207.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/08/Pregnancy-Belly-768x530.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2013/08/Pregnancy-Belly.jpg 834w" sizes="auto, (max-width: 300px) 100vw, 300px" />than 48 million couples worldwide who struggle to conceive.
Published today <a href="https://www.nature.com/articles/ng.3698">the research</a> is the largest genetic epidemiological study on human reproduction ever done involving data from 62 studies. Those studies included information from 251,151 men and women regarding the age when they first had children, and another 343,072 men and women regarding the number of children they’ve had. All individuals were of European descent.
As modern couples increasingly wait until they are older to start families – which in and of itself can make it harder to conceive – the findings in this study may help couples determine how late is too late to have children, researchers said.
&#8220;One day it may be possible to use this information so doctors can answer the important question: “How late can you wait?” based on the DNA variants,” <a href="http://www.ox.ac.uk/news/2016-10-31-twelve-dna-areas-linked-age-which-we-have-our-first-child-and-family-size">said Melinda Mills</a>, the lead author of the paper and a professor at the University of Oxford. “It is important to put this into perspective, however, as having a child still strongly depends on many social and environmental factors that will always play a bigger role in whether or when we have babies.”

<div style="float: right; text-align: justified; width: 300px; background-color: #eee; padding: 15px; margin-left: 10px;">
More To Come
This massive study, that included data collected over several years, illustrates the potential for research into fertility.
23andMe contributed a small part of data used in this study, but the work is an example of the potential for breakthroughs in research into the genetics involved in human reproduction.
Early in 2016, 23andMe began a collaboration with the personalized medicine company Celmatix focusing specifically on discovering genetic factors to dramatically improve the diagnosis and treatment of infertility.
You can read more about that collaboration <a href="https://blog.23andme.org/articles/collaboration-to-create-better-treatments-for-infertility">here</a>.
We expect to announce more on this promising collaboration in the near future.
</div>
Estimates are that between 10 and 15 percent of couples have trouble conceiving. Researchers said that the genetic markers identified in this study could potentially serve as drug targets for preventing or delaying age-related declines in fertility and sperm quality, or the markers might be useful for improving the outcomes in fertility treatments.
Led by scientists at Oxford University and University Medical Center Groningen in the Netherlands, the study focused on two common measures of reproduction – age of first birth and number of children born. What the researchers found were 12 genetic markers associated with reproduction, ten of those have never before been associated with fertility. In addition, many of the markers are in genes – or affect the expression of genes – involved in the development of reproductive organs or are tentatively linked to a variety of gynecological disorders. The two indicators for human reproduction used in this study – age of first birth and number of children ever born – have a strong relationship with fitness, human development, infertility and risk of neuropsychiatric disorders.
This gives scientists more insight into the underlying biology of infertility, researchers said. For example, one of the markers is linked to genes involved in sperm development and is also important in the development of ovaries, the uterus, and placenta.
The study authors point out that genetics is just one of many things that influence fertility in men and women. Personal choices, as well as cultural, economic and social environments also clearly play an important role. But the insights gained in this study could help what the researchers call “reproduction awareness,” a more grounded look at what is possible as couples wait longer and longer to have children.
23andMe principal scientist and statistical geneticist Dave Hinds, said the research is promising on many levels.
&#8220;Insights driven by this important research could help in treating the many couples who have difficulty conceiving a child,” he said.
And beyond these specific findings this kind of research is a good example of what else can be done, by combining genetic studies from around the world.
“It is why 23andMe is involved in this and other similar kinds of research. It’s another way to make the contributions from our own customers, who voluntarily participate in research, have an even greater impact in scientific discovery.&#8221;
The study appears in the journal <a href="https://www.nature.com/articles/ng.3698">Nature</a>.
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New genetic variants found to influence fertility

23andMe reached another milestone earlier this month by completing enrollment in what is now one of the largest genetic studies of <img loading="lazy" decoding="async" class="alignright size-medium wp-image-22692" src="https://blog-api.23andme.org/wp-content/uploads/2015/07/Lupus-Logo-300x296.jpg" alt="Lupus Logo" width="300" height="296" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/07/Lupus-Logo-300x296.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Lupus-Logo.jpg 572w" sizes="auto, (max-width: 300px) 100vw, 300px" />lupus in the world.
As part of the Lupus Research Study, 23andMe and its collaborator in this study, Pfizer, Inc., have enrolled 5,000 people with lupus.
Using genetic and survey data gathered from participants, researchers hope to gain insight into the genetics of lupus, an autoimmune disease that impacts 1.5 million people in the United States alone. The hope is that those research insights will in turn lead to new and better ways of treating the condition, including the development of new drugs to treat the disease.
&#8220;We believe that by studying human genetics alongside environmental and health history factors it will ultimately help inform better treatment options for lupus patients, and make important discoveries,” said 23andMe CEO and co-founder Anne Wojcicki.

Currently those living with lupus face many challenges. The condition is both chronic but also hard to diagnose. It often impacts different parts of the body such as the skin, joints and various organs. But because the symptoms often vary depending on the individual, making a diagnosis can be difficult. Although its cause is unknown, research indicates that genetics, hormones and environmental factors all play a role. Currently there is no known cure for the disease.
Now that 23andMe’s <a href="https://www.23andme.org/lupus/">Lupus Research Study</a> has reached its enrollment goal, the scientific work can begin in earnest.
Researchers are incorporating genotypic information from participants, as well as information about other traits and conditions participants may have, in addition to  medical health records for the analysis of longitudinal surveys with participants.
For many participants in this study like, <a href="https://www.youtube.com/watch?v=NOoOoWH2BuU">Mary Frances</a>, a California mother who was first diagnosed with lupus in college, this is important work.
“23andMe is trying to understand on a genetic level what causes these diseases,” Mary Frances said.
You can learn more about <a href="https://www.23andme.org/lupus/">23andMe’s Lupus Research Study here</a>.
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23andMe Reaches Enrollment Goal for Lupus Research

A lot of people bite their nails. It’s not that unusual, but researchers looking at the underlying biology for individuals who do it often are learning that frequent nail-biting may point to more serious conditions.<img loading="lazy" decoding="async" class="size-full wp-image-21024 alignright" src="https://blog-api.23andme.org/wp-content/uploads/2014/05/@PITER-23andMe-ChaoTian-25.jpg" alt="@PITER-23andMe-ChaoTian-25" width="199" height="287" />


For people who frequently bite their nails, the habit is associated with higher chances of having some psychiatric disorders or compulsive behaviors, according to new research by 23andMe senior statistical geneticist Chao Tian. In a short talk at the annual American Society of Human Genetics meeting in Vancouver, Chao presented findings showing   genetic associations with frequent nail-biting as well as other associations with the habit.
Before diving into her findings, it’s important to note again that in most cases nail-biting is not out of the ordinary. In children and teens, it <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556753/">isn’t associated</a> with any psychiatric disorder. It is more a reflection of boredom, stress or even behavior modeled from parents, according to psychiatrists who study the condition.
The habit is fairly common. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556753/">Estimates</a> are that about 30 percent of children and 45 percent of teens bite their nails, and as people move into adulthood the percent of people who bite their nails diminishes.
But where there are interesting associations are among those who report that they frequently bite their nails. For those individuals the habit is associated with higher chances of having some psychiatric disorders or compulsive behavior, according to new research by 23andMe senior statistical geneticist Chao Tian.
In her talk at the annual American Society of Human Genetics meeting in Vancouver this week, Chao presented findings showing both genetic associations with frequent nail-biting as well as associations between the habit and certain psychiatric disorders.


For this study, Chao looked at data from 180,000 23andMe customers of European ancestry who consented to research. About 37 percent of whom reported that they bite their nails, with about seven percent of the total saying they did so frequently.<img loading="lazy" decoding="async" class="alignright size-full wp-image-24474" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/Nail-biter-1.jpg" alt="nail-biter" width="147" height="193" />
Chao and other researchers at 23andMe found two dozen genetic associations with nail-biting, known by the medical term onychophagy.
While nibbling on nails during times of stress doesn’t mean one has a psychiatric disorder, among those who report that they frequently bite their nails the picture changes a bit.
Data shows that frequent nail biters are more likely to have certain disorders and habits such as depression, anxiety, and trichotillomania, the scientific name for the urge to pull out one’s own hair.
What’s also interesting is that the function of some of the genes in which nail biting associations were found point to links with things like nail structure, BMI, taste perception and neuronal regulation in the brain, Chao said.


What’s important to note here is that most cases of nail biting among children and teens isn’t associated with any psychiatric disorder, but rather a sign of boredom, stress or even behavior modeled from parents. About 30 percent of children and 45 percent of teens bite their nails. Nail-biting tends to diminish as people move into adulthood.
In this study, Chao also looked other characteristics like conscientiousness, openness, neuroticism, agreeableness and perceived stress, and found that those people who reported biting their nails often were also more likely to be neurotic and stressed. On the other hand, her research showed that people who didn’t bite their nails were more likely to be conscientious.


In and of itself this study is interesting, but it also illustrates the power of collecting large amounts of phenotypic data with genotypic data to study the underlying biology of many different kinds of conditions.

A Real Nail Biter

For fans of HBO’s hit show Silicon Valley, you may be familiar with this formula for innovation – put a bunch of smart
<div id="attachment_24451" style="width: 210px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-24451" class="size-thumbnail wp-image-24451" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/IMG_4099-200x200.jpg" alt="Mike Polcari, vice president and chief architect, laying out the schedule on the first day of the hackathon." width="200" height="200" />Mike Polcari, a 23andMe vice president and its chief architect, lays out the schedule on the first day of the hackathon.</div>
people together in a room and give them 48 hours, with the freedom to pursue their own ideas, and raise the stakes with a little friendly competition.


This formula is known as a “hackathon”– focused design sprints that involve engineers, scientists, designers, product managers and others. It’s an event we’ve embraced annually at 23andMe, where the hackathons have helped spawn new products and novel ideas.
“My hope with the hackathon was manifold – to foster innovation within the building, get everyone thinking about exciting opportunities to deliver new ideas to the customer, to get people to break out of their routine, and to get them to collaborate with different people on something they’re passionate about,” said Mike Polcari, our VP, Chief Architect.


This year’s 23andMe hackathon didn’t disappoint, with groups developing everything from a simple way to track the progression of Parkinson&#8217;s by using a patient’s own phone, to creating an online tool to see what traits you and your partner might pass onto your baby, to integrating 23andMe’s phenotypic data collection into <img loading="lazy" decoding="async" class="alignright wp-image-23719 size-medium" src="https://blog-api.23andme.org/wp-content/uploads/2016/03/23andMe-ResearchKit-147x300.png" alt="23andMe-ResearchKit" width="147" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2016/03/23andMe-ResearchKit-147x300.png 147w, https://blogcms.23andme.com/wp-content/uploads/2016/03/23andMe-ResearchKit-768x1569.png 768w, https://blogcms.23andme.com/wp-content/uploads/2016/03/23andMe-ResearchKit-501x1024.png 501w, https://blogcms.23andme.com/wp-content/uploads/2016/03/23andMe-ResearchKit-431x880.png 431w, https://blogcms.23andme.com/wp-content/uploads/2016/03/23andMe-ResearchKit-578x1180.png 578w, https://blogcms.23andme.com/wp-content/uploads/2016/03/23andMe-ResearchKit.png 863w" sizes="auto, (max-width: 147px) 100vw, 147px" /> Apple’s open source ResearchKit ®framework.


Earlier this month, 23andMe-ers from across the company assembled into teams centered on a variety of ideas. Some let out their inner artists, focusing on ways to artistically represent genetic information. Others proposed ways to take a deeper dive into 23andMe’s existing database, finding opportunities to offer customers more information with results.


While some got down and dirty with the microbes found in your mouth (did you know that as much as 10 percent of the DNA found in your saliva isn&#8217;t human!?), all of the teams shared the same goal, to create something new and useful for 23andMe customers.
For most participants, this was a chance to push aside some of their day-to-day workload and to develop long-time passion projects.
“I’ve had this idea for a while and felt that the hackathon was the right opportunity to get some momentum and bring the idea to fruition,” said Olga Sazonova, a 23andMe computational biologist.


Olga worked on an idea to extract microbiome data from saliva. Her idea would then use the information gleaned from the microbiome data to add to what customers can already learn about themselves from the DNA that is extracted from their spit.
Another scientist, who worked with a team on a hack he called “super color sensor,” meant to detect if a customer could see small variations in color shades, said he’d been thinking about this idea even before his time at 23andMe. The freedom of the hackathon gave him an opportunity to see if he could bring this idea to life.
<div id="attachment_24453" style="width: 210px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-24453" class="wp-image-24453 size-thumbnail" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/IMG_4129-200x200.jpg" alt="img_4129" width="200" height="200" />As part of the two-day hackathon, a team working on a new app for educators map out ideas and the flow of the design on post-it notes.</div>
Whether the teams were successful or not, the process was also about collectively energizing the company, so that when everyone goes back to their routine work they can apply that same level of passion and focus.
Although the winning prize of a fancy dinner in downtown Mountain View certainly enticed our hackers to bring their projects to life over this short window of time (and a company-wide rooftop Happy Hour at the conclusion didn’t hurt either), the real prize is producing something that not only the employees at 23andMe can explore, but one that can help our customers in some way.


This year, three of the 24 different projects rose to the top: one that further integrates 23andMe’s collection of data for research into Apple’s open source ResearchKit* framework; another one focused on diet; and the third one that includes an interactive map of the human body to allow customers to see parts of the body for which 23andMe offers reports.
Reflecting on all the different ideas developed in this year’s hackathon, Mike said he was impressed.
“People found that having this kind of ownership over the end product was engaging, motivating, and exhausting,” he said. “But also the most fun they’ve had. There’s something magical about offering people the autonomy, creative license and control that makes our hackathon an unparalleled opportunity for real innovation.”

&nbsp;

*ResearchKit is a registered trademark of Apple Inc.

Hacking Away at Health and Ancestry

As part of a series on cutting edge women, The Today Show featured Anne Wojcicki, 23andMe&#8217;s CEO and co-founder.


The NBC crew followed Anne as she hustled through a typical day, juggling family life, and work meetings. The crew also got a glimpse of 23andMe&#8217;s Therapeutics lab, and sat down with her to talk about her vision for the future.


Check out the segment.

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23andMe’s CEO Featured On The Today Show

Attending the annual American Society of Human Genetics meeting in Vancouver next week?<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-6586" src="https://blog-api.23andme.org/wp-content/uploads/2010/05/23andMe_Logo_blog-200x200.jpg" alt="23andMe_Logo_blog" width="200" height="200" />
We&#8217;d love to hear from you! Attend our talks, come by our posters, and find us at our booth.
The 23andMe research team has a full slate of presentations and posters at ASHG this year.


Wednesday, Oct 19

TALK 
11:30am &#8211; 12:00pm


From GWAS and Mendelian Genes to Therapeutic Drug Targets

Richard Scheller, 23andMe Chief Science Officer and Head of <img loading="lazy" decoding="async" class="alignright size-full wp-image-24403" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/richard-small.jpg" alt="richard-small" width="100" height="94" />Therapeutics 
The Therapeutics group at 23andMe is using human genetic data as the starting point for identifying new therapies for both common and rare diseases.

Session 20.
From GWAS and Mendelian Genes to Therapeutic Drug Targets 
Ballroom B, West Building, Convention Centre


POSTERS 
3 pm &#8211; 4 pm


<img loading="lazy" decoding="async" class="alignright size-full wp-image-24402" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/Karl-small.jpg" alt="karl-small" width="100" height="94" />

Karl Heilbron, 23andMe Post-doctoral Computational Biologist

Poster #: PgmNr 406

Convention Centre, Exhibit Hall B, West Building
<img loading="lazy" decoding="async" class="alignright size-full wp-image-24401" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/RobertB-1.jpg" alt="robertb-1" width="100" height="99" />

Robert Bell, 23andMe Bioinformaticist

Poster #: PgmNr 430

Convention Centre, Exhibit Hall B, West Building


<img loading="lazy" decoding="async" class="alignright size-full wp-image-24404" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/Aaron-Small.jpg" alt="aaron-small" width="100" height="97" />

Aaron Kleinman, 23andMe Senior Computational Biologist

Poster #: PgmNr 496

Convention Centre, Exhibit Hall B, West Building


<img loading="lazy" decoding="async" class="alignright size-full wp-image-24440" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/Nick-Small.jpg" alt="nick-small" width="100" height="83" />

Nicholas Furlotte, 23andMe Statistical Geneticist

Poster #: PgmNr 514

Convention Centre, Exhibit Hall B, West Building


Thursday, Oct 20 
EDUCATIONAL SEMINAR (registration required) 
1pm — 2:30pm


New Models in Genotyping: Incentivizing Recruitment, Engaging Participants and Accelerating Research Results

Location: Ballroom B, East Building, Convention Centre


Program includes:<img loading="lazy" decoding="async" class="alignright size-full wp-image-24437" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/Joyce-Small.jpg" alt="joyce-small" width="100" height="82" /> 
How the consumerization of genomics benefits research

Joyce Tung, 23andMe VP of R&amp;D


Reimagining genetic studies: Genotyping Services for Research

Robert Borkowski, 23andMe Product Manager<img loading="lazy" decoding="async" class="alignright size-full wp-image-24438" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/RobertB-small.jpg" alt="robertb-small" width="100" height="88" />


POSTERS 
2 pm &#8211; 3 pm
&nbsp;

<img loading="lazy" decoding="async" class="alignright size-full wp-image-24439" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/Olga-Small.jpg" alt="olga-small" width="100" height="89" />

Olga Sazonova, Computational Biologist

Poster #: PgmNr 1409 
Convention Centre,
Exhibit Hall B, West Building
3 pm &#8211; 4 pm

<img loading="lazy" decoding="async" class="alignright size-full wp-image-24436" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/Janie-Small-1.jpg" alt="janie-small" width="100" height="109" />

Janie Shelton, 23andMe Survey Methodologist

Poster #: PgmNr 350 
Convention Centre, Exhibit Hall B, West Building

&nbsp;

<a href="https://ep70.eventpilot.us/web/page.php?page=Speaker&#038;project=ASHG16&#038;id=341749">The impact of personal experience with direct ­-to- ­consumer genetic testing on physician readiness</a>

Erynn Gordon, 23andMe Director of Clinical Development<img loading="lazy" decoding="async" class="alignright size-full wp-image-24441" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/Erynn2-small.jpg" alt="erynn2-small" width="100" height="89" />

Poster #: PgmNr 3098

Convention Centre, Exhibit Hall B, West Building


Friday, Oct 21


POSTERS 
2 pm &#8211; 3 pm
<img loading="lazy" decoding="async" class="alignright size-full wp-image-24400" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/Mike-Small.jpg" alt="mike-small" width="100" height="102" />

Michael Multhaup, 23andMe Product Scientist

Poster #: PgmNr 477

Convention Centre, Exhibit Hall B, West Building


<img loading="lazy" decoding="async" class="alignright size-full wp-image-24399" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/Fah-small.jpg" alt="fah-small" width="93" height="99" />

Fah Sathirapongsasuti, 23andMe Computational Biologist

Poster #: PgmNr 1719

Convention Centre, Exhibit Hall B, West Building


Saturday, Oct 22
TALK 
9:15am &#8211; 9:30am

<img loading="lazy" decoding="async" class="alignright size-full wp-image-24398" src="https://blog-api.23andme.org/wp-content/uploads/2016/10/chao-small.jpg" alt="chao-small" width="100" height="121" />

Chao Tian, 23andMe Senior Statistical Geneticist

PgmNr 276 
Session 78.
Neuropsychiatric Diseases of the Young and Old 
Room 221, West Building, Convention Centre
You can also find us at our marketing booth #211.


<a href="https://blog.23andme.org/23andme-research/23andme-scientists-to-present-new-findings/">Read more</a> about our scientific presence at ASHG.

Latest Posts — Page 95