Venus and Serena Williams, the Marx brothers, or our very own CEO Anne Wojcicki and her sisters Susan and Janet — our connections with siblings can be one of the strongest bonds in our lives. Finding those connections is one of the things that make 23andMe so special, our ability to reunite long-lost siblings — some have been looking for each other for years, while others never knew one another existed. 
Today on <a href="https://en.wikipedia.org/wiki/Siblings_Day">National Siblings Day</a>, we wanted to revisit a few of our favorite stories about brothers and sisters who built new connections with the help of 23andMe.

<a href="http://people.com/human-interest/identical-twin-sisters-separated-birth-find-each-other-33-years-later/">Amanda and Katey</a>
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2018/04/Amanda-Kay-1024x620.jpg" alt="" class="aligncenter size-large wp-image-26115" width="1024" height="620" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/04/Amanda-Kay-1024x620.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2018/04/Amanda-Kay-300x182.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2018/04/Amanda-Kay-768x465.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/04/Amanda-Kay-880x533.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2018/04/Amanda-Kay-1180x715.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2018/04/Amanda-Kay.jpg 1311w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />The story of identical twin sisters Amanda and Katey finding each other still gives us goosebumps. The pair were both born in Seoul, South Korea, but separated after being adopted to two separate American families. Amanda grew up in California, while Katey was raised in Arizona. They found each other using 23andMe after 33 years being apart. They soon discovered uncanny parallels in their lives — from failing algebra the same year in school, to passing their driving test on the second try. After decades apart the two sisters are now making up for lost time.

<a href="https://www.youtube.com/watch?v=Hw8G1JCr47w">Winnie and Meta</a>
<iframe loading="lazy" width="640" height="360" src="https://www.youtube.com/embed/Hw8G1JCr47w" frameborder="0" allow="autoplay; encrypted-media" allowfullscreen="allowfullscreen"></iframe>
Winnie always knew she was adopted. The 76-year-old always felt supported, had children and grandchildren who loved her, but always felt something was missing. Winnie spent decades searching for her birth family, pouring over her adoption records, and searching through tens of thousands of names she thought might lead her to her birth mother or father. Winnie’s big break didn’t come until she took 23andMe’s DNA test, which helped her find a nephew, and ultimately her half sister, Meta. This led her to two more half sisters and her half brother, who were overjoyed to meet her. Winnie shared with us when she found her family, “To actually hug someone you are biologically related at 75 years old, is just amazing.” 

<a href="https://www.today.com/video/watch-3-siblings-reunite-with-their-long-lost-sister-on-megyn-kelly-today-1185580099728">Laurie, Amber, Christine and Brian</a>

<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2018/04/Siblings-Laurie-Christine-Brian-and-Amber-1024x566.jpg" alt="" class="aligncenter size-large wp-image-26116" width="1024" height="566" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/04/Siblings-Laurie-Christine-Brian-and-Amber-1024x566.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2018/04/Siblings-Laurie-Christine-Brian-and-Amber-300x166.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2018/04/Siblings-Laurie-Christine-Brian-and-Amber-768x424.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/04/Siblings-Laurie-Christine-Brian-and-Amber-880x486.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2018/04/Siblings-Laurie-Christine-Brian-and-Amber-1180x652.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2018/04/Siblings-Laurie-Christine-Brian-and-Amber-271x149.jpg 271w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />
Siblings Laurie, Christine, Brian and Amber were adopted at a very young age. While Laurie, Christine and Brian stayed together, Amber, the youngest, was adopted by a separate family. The four were separated for decades. Then Laurie took the 23andMe genetic test and got an unexpected message, “you have one direct family member” in her DNA Relatives report. For decades the four siblings had no means of finding each other. Now that they’ve connected, they are talking non-stop. Best of all, Amber is pregnant and she will be giving her child the gift of additional family, two aunts and an uncle. 

<a href="https://www.youtube.com/watch?v=6eYt9CESTq4">Pat and Angel</a>
<iframe loading="lazy" width="640" height="360" src="https://www.youtube.com/embed/6eYt9CESTq4" frameborder="0" allow="autoplay; encrypted-media" allowfullscreen="allowfullscreen"></iframe>
Pat was adopted as a baby, and never knew any of her birth family. Her daughter Kelle used 23andMe not knowing she would find her mother’s sister, Angel. For years Pat’s fear of being rejected by her birth family, prevented her from searching for them. But after she and her sister Angel connected in December 2016, she was welcomed with open arms and has never looked back.

Anyone with a brother or sister knows the bonds siblings can share. That’s what makes these stories of siblings finding each other so powerful. Not everyone is looking for long lost family, but we all have our own DNA stories. What’s your 23andMe story? We’d love to hear it. Please share it with us at <a href="mailto:stories@23andMe.com">stories@23andMe.com</a>.

23andMe Blog

23andMe Blog Team

23andMe Celebrates Siblings Day

Earlier this month 23andMe added a new <a href="https://www.23andme.com/dna-health-ancestry">Carrier Status* report</a> on a serious but rare condition that can lead to excessive insulin production.
Known as familial hyperinsulinism (FHI), this congenital disease is most commonly found in people with Ashkenazi Jewish, central Finnish and Saudi ancestry. FHI causes overproduction of insulin that in turn can lead to low blood sugar, low energy, irritability, seizures, and if left untreated, brain damage. But the condition can be treatable if caught early. FHI is usually diagnosed in infancy or early childhood.<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/FHI-Detail-1024x606.jpg" alt="" class="aligncenter wp-image-26107 size-large" width="1024" height="606" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/FHI-Detail-1024x606.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2018/03/FHI-Detail-300x178.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2018/03/FHI-Detail-768x455.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/03/FHI-Detail-880x521.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2018/03/FHI-Detail-1180x699.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2018/03/FHI-Detail.jpg 1687w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />
This newly added Carrier Status* report doesn’t diagnose FHI. Instead, it reports on whether you are a carrier of one of three variants in the ABCC8 gene. The report is called “Familial Hyperinsulinism (ABCC8-Related), and it tests for three variants in the ABCC8 gene that can cause FHI. These three variants cover about 97 percent of ABCC8-related FHI variants in people of Ashkenazi Jewish descent, and about 41 percent of variants in people of Finnish descent.
<div style="float: right; text-align: justified; width: 300px; background-color: #eee; padding: 15px; margin-left: 10px;">
What’s a Carrier Status* Report?
Carrier status tests are a type of genetic test used to find out if you carry a genetic change – or variant. For the types of conditions included in a carrier status test, having one genetic change – being a carrier – typically means you do not have that condition, but you could pass the variant on to your each of your children.
 
Carrier status tests are typically offered for autosomal recessive conditions [or disorders]. For these conditions, a child needs to inherit a variant from both parents in order to have the condition. If both parents are carriers, each child has a one in four, or 25 percent, chance of being affected with the condition. 
(It’s important to note that this also means that each child has a 75 percent chance of not being affected.)
 
Autosomal recessive conditions for which carrier testing is commonly offered by healthcare providers include cystic fibrosis, Tay-Sachs disease, and sickle cell anemia, among many others.<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/Carrier-Status-300x239.jpg" alt="" class="aligncenter size-medium wp-image-26106" width="300" height="239" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/Carrier-Status-300x239.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Carrier-Status-768x612.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Carrier-Status-1024x816.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Carrier-Status-880x701.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Carrier-Status.jpg 1137w" sizes="auto, (max-width: 300px) 100vw, 300px" />
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Carriers have a slight risk of developing a form of FHI. But the report is most relevant for prospective parents, who could pass the variant on to their children.
About one in 52 people of Ashkenazi Jewish descent are carriers of ABCC8-related FHI. And as we noted earlier, unlike with our other Carrier Status* reports, being a carrier of one of the three variants in our report does carry a small risk (less than 1 percent) of developing a form of FHI. 
The FHI report is the latest in a regular cadence of new FDA-authorized health-related reports 23andMe offers customers. This brings the total number of Carrier Status* reports to 43. 23andMe also includes Genetic Health Risk* reports, and next month, 23andMe will add a BRCA1/BRCA2 (Selected Variants)* report to its list of Genetic Health Risk* reports. The BRCA1/BRCA2 (Selected Variants)* report is the first-ever direct-to-consumer genetic health report on cancer risk.
As with other health-related reports, 23andMe has a tutorial customers can go through before viewing their Familial Hyperinsulinism (ABCC8-Related) report. In addition to the tutorial, the report itself offers details on the condition, the specific variants tested for and the scientific details supporting the report. There are also links to information about genetic counseling and support group resources.
*The 23andMe PGS test uses qualitative genotyping to detect select clinically relevant variants in the genomic DNA of adults from saliva for the purpose of reporting and interpreting genetic health risks and reporting carrier status. It is not intended to diagnose any disease. Your ethnicity may affect the relevance of each report and how your genetic health risk results are interpreted. Each genetic health risk report describes if a person has variants associated with a higher risk of developing a disease, but does not describe a person’s overall risk of developing the disease. The test is  not intended to tell you anything about your current state of health, or to be used to make medical decisions, including whether or not you should take a medication, how much of a medication you should take, or determine any treatment. Our carrier status reports can be used to determine carrier status, but cannot determine if you have two copies of any genetic variant. These carrier reports are not intended to tell you anything about your risk for developing a disease in the future, the health of your fetus, or your newborn child&#8217;s risk of developing a particular disease later in life. For certain conditions, we provide a single report that includes information on both carrier status and genetic health risk. Warnings &amp; Limitations: The 23andMe PGS Genetic Health Risk Report for BRCA1/BRCA2 (Selected Variants) is indicated for reporting of the 185delAG and 5382insC variants in the BRCA1 gene and the 6174delT variant in the BRCA2 gene. The report describes if a woman is at increased risk of developing breast and ovarian cancer, and if a man is at increased risk of developing breast cancer or may be at increased risk of developing prostate cancer. The three variants included in this report are most common in people of Ashkenazi Jewish descent and do not represent the majority of BRCA1/BRCA2 variants in the general population. This report does not include variants in other genes linked to hereditary cancers and the absence of variants included in this report does not rule out the presence of other genetic variants that may impact cancer risk. The PGS test is not a substitute for visits to a healthcare professional for recommended screenings or appropriate follow-up.  Results should be confirmed in a clinical setting before taking any medical action. For important information and limitations regarding other genetic health risk reports and carrier status reports, [visit <a href="https://www.23andme.com/test-info/">https://www.23andme.com/test-info/]</a>

23andMe Adds A New Carrier Status Report on Familial Hyperinsulinism

By Jey McCreight, Ph.D., Research Communications Scientist
It takes a village to do research. 23andMe’s scientific discoveries are made possible by our more than three million customers who’ve consented to participate in research and by our collaborators. Those collaborators include people like Varun Warrier, MPhil, a graduate student in the laboratory of Simon Baron-Cohen at the University of Cambridge. Warrier has led several collaborative studies with 23andMe, including most recently two studies on empathy published in Translational Psychiatry and Molecular Psychiatry and another on “theory of mind” published in Scientific Reports.
<img loading="lazy" decoding="async" class="aligncenter size-large wp-image-26099" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-1024x1024.jpg" alt="" width="1024" height="1024" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-1024x1024.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-768x768.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-880x880.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-1180x1180.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier-980x980.jpg 980w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Varun-Warrier.jpg 1481w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />
<h2>Autism, Genetics, and Neuroscience</h2>
JM: What motivated you to start studying autism first?
VW: I don&#8217;t think anything specifically motivated me to study autism. I was interested in genetics and neuroscience, and during my undergraduate and master&#8217;s, I tried to choose between the two of them. Then, at some point, I realized that I didn&#8217;t have to choose — I could use methods in genetics to investigate the biology of mental health conditions. I wrote to Simon and asked if I could join his lab to do this research. What really attracted me to the Autism Research Centre was the fact that they were looking at the dimensional aspect of autism, which, to me, was a lot more exciting than thinking of mental health conditions as existing in silos.

JM: How has the rapidly increasing availability of large datasets changed the field of psychiatric genomics?
VW: The progress has been immense. The earliest genome-wide association study (GWAS) of a psychiatric condition was a decade ago. Until about 2013 or so, we had a handful of genetic variants associated with any psychiatric condition or related traits. Thanks to large datasets like 23andMe and the UK Biobank, the number of variants discovered has seen a massive jump in the last five years. For instance, just about a month ago, a preprint was posted on BioRxiv that identified more than 600 genetic regions associated with risky behavior. We&#8217;ve crossed a milestone in psychiatric genetics. The next challenge is to link this to biology and use these polygenic scores to inform diagnosis and interventions.
<h2>Genome-Wide Association Studies and Autism</h2>
JM: What are the benefits of using GWAS to investigate autistic behavioral traits? Are there any limitations?
VW: First, the limitations. The underlying risk for developing autism is only partly genetic (60 to 80 percent). With traits like empathy or theory of mind, genetics account for an even smaller proportion of the variance. So we are very much working within that fraction of variance when we look at genetics. The other thing to bear in mind is that the environment plays a vital role in whether someone chooses to receive an diagnosis or not. For instance, if you&#8217;re in a supportive environment that allows you to flourish and have high autistic traits, then you may choose not to receive a diagnosis. There are quite a few other factors besides genetics that determine the relative wellbeing of an individual.
That said, the benefits far outweigh the limitations. Personally, I think trying to delineate the genetic mechanisms underlying autism is vital for us to understand anything else about the condition. The interesting thing about genetics is that, by and large, we can assume that reverse causality is absent. With almost anything else, you aren&#8217;t entirely sure if what you&#8217;re observing is a cause or a consequence of the condition. Once you better understand the genetic mechanisms of a condition like autism, you can use that to better understand things like neural circuits or methylation signatures in autism and understand causality.
<h2>Empathy and Autism</h2>
JM: Your recent papers investigate different processes contributing to autism, such as <a href="https://www.nature.com/articles/s41598-018-21737-8">theory of mind</a>, <a href="https://www.biorxiv.org/content/early/2017/11/14/050682">empathy</a>, <a href="https://www.biorxiv.org/content/early/2017/12/03/228254">systemizing</a>, and <a href="https://www.biorxiv.org/content/early/2017/10/05/196071">relationship satisfaction</a>. Why is it important to look at these individual processes rather than autism?
VW: Autism is an umbrella term for a heterogeneous group of conditions. We can think of it in two ways. In the first scenario, we can go by the diagnostic label of autism for research. However, we know that there is immense heterogeneity within the condition, which we may not be able to dissect genetically unless we look at it from other perspectives. An alternative is to investigate traits that are typically distributed in the general population but in which autistic individuals, on average, have strengths or difficulties in — or in other words, thinking of autism as being along multiple different dimensions. Our lab has a longstanding interest in investigating the dimensional nature of autism, and thanks to 23andMe and other genetic biobanks like the UK Biobank and ALSPAC, we could do just that using genetics.
<h2>The Role of Systemizing</h2>
JM: You recently identified three loci significantly associated with systemizing, a non-social autistic trait. What is systemizing, and why is it important to consider both social and non-social traits when investigating the genetic architecture of autism?
VW: Systemizing is an interest in or a talent for analyzing or building systems. If we think of all the information around us, we can try and classify them or order or group them based on some intrinsic properties in the natural world. For example, think of colors. When we think of colors, we don&#8217;t necessarily go and classify them. But if we wanted to, we could order them based on the natural visible spectrum. We could group them into warm or cold colors. We could order them based on brightness. Scientists like to find order and pattern in things to better understand them. The same seems to be true, on average, with autistic individuals. Research from our lab and others has demonstrated that, on average, autistic individuals have superior interests in systems. While most people think of autism as a social condition, there is also a non-social aspect to it that&#8217;s necessary for a diagnosis — unusually restricted or repetitive patterns of interest and behavior. We think that it is aspects of these that are reflected in the superior systemizing skills that are frequently observed in autistic individuals.
JM: Two of your recent GWAS did not find any significant loci associated with “empathy” or “theory of mind” (the ability to attribute mental states to oneself and others and to use such mental state attribution to make sense of behavior and predict it). Why do you think this is so?
VW: This essentially boils down to sample size. We know that there is a genetic signal in these GWAS. Differences in the theory of mind and empathy are heritable. Twin studies show that approximately a third of the differences in how empathetic people are are due to genetics. Our studies have also identified a small but significant additive SNP heritability. However, the variance explained by each individual SNP is small. To find these minimal effects, we need large sample sizes.
<h2>Theory of Mind and Cognition</h2>
JM: Your studies suggest shared genetic architecture between different measures of theory of mind and cognition, as well as between empathy and autism, schizophrenia, and anorexia nervosa. Why are psychological traits so interconnected? Does this present any challenges or opportunities for your research?
VW: We can think of any psychiatric condition or cognitive and behavioral trait as emergent neural network properties. Genes contribute to these phenotypes primarily by altering these neural networks. They alter development, synaptic signaling, glial function, and so on, all of which contribute to altered information processing in the brain. Suppose a handful of these neural networks are altered. In that case, they will contribute to differences in multiple phenotypes, which probably explains the shared genetics we see between all these different conditions and behaviors. It&#8217;s challenging in that we need to figure out why some people get diagnosed with autism, and some others get diagnosed with ADHD when we know that there is considerable overlap in common and rare variants associated with the conditions. It&#8217;s a lot more tricky than anticipated, and we will have to investigate both interactions between genetic variants and interactions between genetic variants and other factors to better predict the differences in these conditions. On the other hand, we can leverage the shared genetics between multiple conditions to increase the statistical power in our studies and identify genetic variants.
<h2>Sex Bias in Autism</h2>
JM: Across the number of autistic traits you measure, women consistently score less autistic than men. Why do you think we see this sex bias in autism?
VW: We think there are multiple reasons for the sex bias. Some of it is biological. We know that women diagnosed with autism have, on average, a larger number of rare, usually de novo, protein truncating variants associated with autism compared to men diagnosed with autism. We have some evidence for sex differences in the genetic variants that contribute to some of the traits associated with autism, such as empathy. There could be other biological reasons — studies have demonstrated that elevated prenatal androgens are associated with increased risk for autism.
There are also other non-biological factors. Women are less likely to be diagnosed with autism as many clinicians may think that autism is primarily a condition seen in men. There is evidence that autism manifests differently in women. Women often need more autistic traits than men to receive a diagnosis. Finally, the diagnostic criteria for autism may not recognize how autism manifests in women. We need to explore all these factors, and both the biological and social factors likely contribute to the sex bias in autism.
<h2>Collaboration with 23andMe</h2>
JM: What made you first interested in collaborating with 23andMe?
VW: A few years ago, 23andMe approached the Autism Research Centre to include some of the tests developed by researchers there in the customer website. At some point in 2012, when the early GWAS studies on autism were published, we realized that we needed to investigate the dimensional nature of autism. We contacted 23andMe to see if they&#8217;d be happy to collaborate again on these phenotypes and conduct a GWAS.
JM: What’s your opinion now that you have collaborated with 23andMe?
VW: We&#8217;ve had a series of fruitful collaborations with 23andMe. I remain highly positive in general of collaborations with a consumer genetics company.
JM: Your advisor, Simon Baron-Cohen, has developed autism support services such as The Transporters, an animated DVD series that teaches emotion recognition to children with autism. Does your lab have any further plans to develop autism support services based on your research?
VW: Yes, our lab is conducting randomized control trials on various interventions, including apps that can help minimally verbal autistic children.
JM: What other research projects do you have planned for the future?
VW: We want to continue our work on the genetics of dimensional measures associated with autism. I am particularly interested in seeing if this can be used to stratify individuals within the autism spectrum.

Researcher Varun Warrier’s Work on Empathy

Editor’s note: This is another in a series of posts that first appeared in a student quarterly magazine called the DNA Decoder — a magazine written by students, for students. The magazine is designed to help students across the nation connect with each other and share interesting ideas around genetics. We in turn want to share a few of those stories with you on 23andMe’s blog. 
By Ava Daniel
In this article, we’ve highlighted some useful tips for how undergraduates can become more involved in genetics and academic research, both at their home institutions and around the country. Knowing how to join a laboratory as a research assistant can be a confusing task, so we’ve provided a comprehensive summary of advantageous steps to take that can make the process easier. Joining a research laboratory is a both a fun and extremely rewarding experience, and we’d love to explain why. 
<h5>What can Undergraduates Gain from Participating in Laboratory Research?</h5>
<div id="attachment_26072" style="width: 1034px" class="wp-caption aligncenter"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-26072" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/Abagail-and-Ava-1024x768.jpg" alt="" class="wp-image-26072 size-large" height="768" width="1024" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/Abagail-and-Ava-1024x768.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Abagail-and-Ava-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Abagail-and-Ava-768x576.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Abagail-and-Ava-880x660.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Abagail-and-Ava.jpg 1152w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />Ava Daniel, l, and Ann Serbin working in the Tjian Lab at the University of California Berkeley during the summer of 2016.</div>
<h5> </h5>
Exposure to the field of laboratory research. This is a great way to find out if research could be a suitable career choice for you, especially in this era of scientific and technological innovation. Even if you may not foresee yourself working in a lab as a career, many areas of science (ex: medicine, biomedical engineering, technology) may call on you to engage in a lab environment at some point; so, it could only benefit you to get acquainted with even the most basic kinds of research.
Mentorship. A formative mentoring experience will help you to learn hands-on skills that you may not have the opportunity to gain otherwise. Having a mentor can be extremely beneficial for guidance, advice, and even letters of recommendation for your future learning and career opportunities as you progress through university and employment. 
Advantages in your different academic science courses. You will be able to personally see the applications of experimental techniques as they pertain to real-life laboratory and clinical uses.
A chance to be involved in groundbreaking research, either by witnessing it firsthand or even participating in it. This gives you the chance to potentially be included as an author on a publication or symposium presentation.
<h5>How can I participate in Laboratory Research? Where do I even start?</h5>
STEP 1 Try to think about what field of science interests you. Ex: genetics, cell biology, developmental biology, evolutionary biology, endocrinology (hormones), oncology (cancer), immunology (immune system), pathology (diseases), etc. 
STEP 2  Try to gain a foundational set of practical skills relevant to laboratory work, if possible. Take a lab course in the type of research you’re interested in (molecular biology, genetics, biochemistry, etc.) or find out if your university offers any “Lab Fundamentals Bootcamps.” While not required, having a set of basic skills and familiarity with lab work will set you apart from other applicants. 
STEP 3  Approach instructors and graduate teaching assistants (TAs) in classes that you are especially excited about and ask if there are any research opportunities for undergraduates in their labs (or in other labs they may know of). If you perform well in the course or go out of your way to be especially thoughtful and curious, your teachers will likely be excited to welcome you into their labs.
STEP 4 Look into the labs that are thriving at your university. You can find labs by attending undergraduate journal clubs and/or research talks, doing online research, or talking to professors or TAs that are in the field of study you’re interested in.
You can then see what labs are run under which principal investigators (PIs) (via Google Scholar). 
<ul>
<li>How many articles have been published? </li>
<li>How many citations? </li>
<li>How recent? </li>
</ul>
If any of those PIs stick out to you, try to read some of their papers to familiarize yourself with the work. 
<h5>How to Choose a Lab </h5>
<ul>
<li>Look for a lab with a strong record of welcoming undergraduate students in their research. You can find this out by exploring the lab’s website.</li>
<li>Search for labs who have graduate students or post-doctoral researchers, as they may be able to answer questions and offer help while you work, or potentially act as mentors to you.  </li>
<li>Consider talking to other students further along in the major you want to pursue and see if they have any research experience or recommendations, either in a lab you want to work in or labs similar to it.  </li>
<li>Asking your peers for advice can be a great first step in identifying what you want to do. </li>
<li>Keep in mind that any kind of exposure can be beneficial to you. Although your lab of interest may not have openings for research positions right away, ask if you can do some periodic shadowing.  </li>
<li>Continue to check in with the lab to see if anything opens up over time.  </li>
<li>Don’t concern yourself too much about finding the perfect experience, especially right away.</li>
<li>You will learn over time, and you never know where or when a perfect opportunity may arise.</li>
<li>Take advantage of the resources already available to students who are looking for research opportunities.  </li>
<li>Many educational programs and departments have staff members who are dedicated to helping students find on-campus research opportunities.  </li>
<li>Take time to identify if there are such staff members in your program and set up an appointment to meet with them to discuss your interests. </li>
</ul>
<h5>How do I contact a lab that I&#8217;m really interested in?</h5>
Once you&#8217;ve narrowed down a lab you are very interested in, reach out to the Principal Investigator (PI) of the lab via email and attach your CV (see below).
If you choose to reach out by email, make sure to show them that you are interested in the specific work that they do by familiarizing yourself with their research, but not repeating the exact wordings from their lab website. Express interest in what you would hope to gain from working in their lab, and in what ways you could contribute to the work they do.<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/Ava-264x300.jpg" alt="" class="alignright size-medium wp-image-26071" height="300" width="264" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava-264x300.jpg 264w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava-768x873.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava-900x1024.jpg 900w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava-774x880.jpg 774w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava-1038x1180.jpg 1038w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava.jpg 1407w" sizes="auto, (max-width: 264px) 100vw, 264px" />
Come off as knowledgeable, informed, and professional. Feel free to reach out to a trusted professor, advisor, or TA to look over the email before you send it. 
If at first you don’t succeed, try again! PIs are often very busy traveling and running their lab. 
Try to reach out to multiple labs at once and wait to see who contacts you back. This way, you have more options in case something does not work out. 
You can try to reach out to individual researchers (graduate students and postdoctoral researchers) within the lab that are not the PI that you may want to personally work with. You can find the contact information of these researchers on the lab’s website, and you can reach out by sending them an introductory email similar to what you sent the PI. 
Remember, it is okay to reach out to a PI even if you have no lab experience. Labs are encouraged to be educational spaces, so do not feel intimidated if you have never had prior lab or hands-on science exposure.
<h5>What if you do not have access to research opportunities at your university? </h5>
At some universities, undergraduate research positions may be few and far between, or you may not find a research lab that peaks your exact interests. Also, it may be possible that your university may not have a strong laboratory science presence. 
There are other options for how you can get exposed to laboratory research. For example, you can look into paid summer internship opportunities at the National Institute of Health (NIH), The Broad Summer Research Program (BSRP), Amgen Research Scholars,  National Science Foundation (NSF) funded Research Experiences for Undergraduates (REUs), Cold Springs Harbor Undergraduate Research Program, and other similar programs at other universities. These programs may offer you with funding for summer lab internship opportunities, or with alternative ways to apply to separate fellowships or grants that could provide you with funding. 
You should start applying to these opportunities as soon as you can, even in your freshman or sophomore years. By experiencing research early, you can make the decision for yourself if you want to continue to pursue it, or spend your time exploring something else. Always remember that you can and should reach out for help! Never be afraid of asking for guidance, recommendations, or general advice from professors, advisors, TAs, and peers in whatever area of study appeals to you. Your undergraduate years are meant for exploration and inquiry, so take advantage of as many resources and opportunities as you can.
<h5>Guidelines for a good CV </h5>
<ul>
<li>Break up your CV into sections: </li>
<li>Name and contact information</li>
<li>Experience Summary &#8211; brief overview of who you are</li>
<li>Education &#8211; list your institutions, GPA and activities done at each institution</li>
<li>Experience &#8211; describe each relevant work experience, the duration of the work experience, and whether you have a letter of recommendation available</li>
<li>Honors and Awards &#8211; list your awards, prestigious positions, fellowships, etc.</li>
<li>Skills Summary &#8211; list any of your best skills not highlighted in the previous sections</li>
</ul>
<h5>Useful Links </h5>
<a href="https://www.training.nih.gov/programs/sip">NIH Summer Internship Program (SIP)</a>
<a href="https://www.broadinstitute.org/bsrp/broad-summer-research-program-bsrp">The Broad Summer Research Program (BSRP</a>)
<a href="http://www.amgenscholars.com/">Amgen Research Scholars</a> 
<a href="https://www.nsf.gov/crssprgm/reu/reu_search.jsp">NSF Research Experience for Undergraduates</a> 
<a href="https://www.cshl.edu/education/undergraduate-research-program/">Cold Springs Harbor Undergraduate Research</a> 
&nbsp;
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/Ava-2-225x300.jpg" alt="" class="alignright size-medium wp-image-26070" height="300" width="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava-2-225x300.jpg 225w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava-2-768x1024.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava-2-660x880.jpg 660w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava-2-885x1180.jpg 885w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Ava-2.jpg 1200w" sizes="auto, (max-width: 225px) 100vw, 225px" />Ava Daniel is a sophomore at Yale University majoring in Molecular, Cellular and Developmental Biology. She is a Yale Freshman Research Fellowship recipient and a research assistant at the Yale School of Medicine. Aside from academics, Ava is a Community Health Educator, for which she teaches health education in New Haven public schools, as well as an active mentee of neurosurgery at Yale-New Haven Hospital. She is excited to be a Genetics Education Student Leader and create educational content to inspire students across the country in genetics and other areas of STEM. She is originally from Millbrae, California and hopes to attend medical school after Yale.

Ava Daniel

An Undergraduate’s Guide to Gaining Research Experience

Researchers have found genetic associations for morning sickness, offering important insight into what — in the most severe cases — is the second leading cause of hospitalization among women during pregnancy.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-26094" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/morning-sickness-300x200.jpg" alt="" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/morning-sickness-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2018/03/morning-sickness-768x512.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/03/morning-sickness-1024x682.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2018/03/morning-sickness-880x586.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2018/03/morning-sickness-1180x786.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2018/03/morning-sickness.jpg 1255w" sizes="auto, (max-width: 300px) 100vw, 300px" />
<h2>Potentially Serious</h2>
Although morning sickness is very common — up to 90 percent of women have some form of nausea or vomiting during pregnancy — its causes remain elusive. Up to 2 percent of pregnant women endure the most severe form of morning sickness, called hyperemesis gravidarum or HG.
HG can be so severe and intractable that women begin losing weight, become dehydrated, and ultimately must be hospitalized. In those cases, the condition can also be problematic for the baby.
Before the advent of intravenous hydration in the 1950s, HG was the leading cause of death during pregnancy — for example, it led to the death of author Charlotte Bronte. More recently Kate Middleton, Duchess of Cambridge, was <a href="https://www.forbes.com/sites/brucelee/2017/09/04/kate-middleton-is-pregnant-and-suffering-hyperemesis-gravidarum-again/#3c00e632b50c">hospitalized</a> after suffering from HG during both of her pregnancies. Even now, it is the second leading cause of hospitalization for pregnant women, behind preterm labor. And yet, despite years of study, researchers haven’t pinpointed a cause or even a safe and effective treatment for this severe form of morning sickness.
<h2>New Study</h2>
However, a new study published in <a href="https://www.nature.com/articles/s41467-018-03258-0">Nature Communications</a> offers promising clues on the causes of morning sickness. Researchers from UCLA, USC, and 23andMe found the strongest genetic associations in the genes GDF15 and IGFBP7. GDF15 plays a role in the development of the placenta, and low expression of GDF15 is associated with miscarriages. The gene IGFBP7 controls appetite.  The study also looked at less severe cases of morning sickness and found that these same genes are also associated with nausea and vomiting in pregnant women.

Researchers said that the variants in GDF15 associated with the condition were over 1000-fold more significant than the variants in the gene with the next closest association.
<h2>Some Surprises</h2>
The findings are surprising, in part, because up until now, much of the focus of research around HG has been on hormonal fluctuations in the body. This study found no evidence for that link and instead suggests that the expression of the gene involved in placenta formation may play more of a role.
“It has long been assumed that the pregnancy hormones, human chorionic gonadotropin or estrogen, were the likely culprits of extreme nausea and vomiting, but our study found no evidence to support this,” <a href="http://newsroom.ucla.edu/releases/two-genes-likely-play-key-role-in-extreme-nausea-and-vomiting-during-pregnancy">said Marlena Fejzo</a>, the lead author of the study and an associate researcher at the David Geffen School of Medicine at UCLA.  Fejzo herself had hyperemesis gravidarum and lost a pregnancy to the condition in 1999.
The two genes identified in the study are also linked to cachexia, a weight loss and muscle wasting condition that leads to death in about 20 percent of cancer patients and has similar symptoms to hyperemesis gravidarum.
<h2>Theories</h2>
As for why the expression of GDF15 is implicated in morning sickness, the authors theorize that perhaps the protein triggers vomiting during the early stages of pregnancy so women aren’t tempted to eat anything that might hurt the developing fetus.
For this study researchers conducted their work in two stages. The first used about 1,300 women with the most severe form of morning sickness and another 15,700 who did not have the condition. All the women were 23andMe customers who consented to participate in research. The second stage looked at data from more than 50,000 women — also 23andMe customers who consented to participate in research — across a range of symptoms from no nausea to slight to very severe. Again, the researchers found the strongest signal in the genes GDF15 and IGFBP7.
The study also provides the first evidence that HG, the most severe form of morning sickness, is not a separate disease, but more of an end of the spectrum for nausea and vomiting during pregnancy, as they are all influenced by the same genes.

Researchers find genetic associations for morning sickness

Overturning long-held beliefs about the past, new insights from ancient DNA have revealed exciting surprises about who we are as people and how we got here.
In just the last few years, the ability for scientists to extract and sequence DNA from bones that are tens of thousands of years old has changed our understanding of the human story. Perhaps there are few better to tell that tale than the population geneticist David Reich.<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/jackethighres-199x300.jpg" alt="" class="alignright size-medium wp-image-26087" width="199" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/jackethighres-199x300.jpg 199w, https://blogcms.23andme.com/wp-content/uploads/2018/03/jackethighres-768x1160.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/03/jackethighres-678x1024.jpg 678w, https://blogcms.23andme.com/wp-content/uploads/2018/03/jackethighres-583x880.jpg 583w, https://blogcms.23andme.com/wp-content/uploads/2018/03/jackethighres-781x1180.jpg 781w, https://blogcms.23andme.com/wp-content/uploads/2018/03/jackethighres.jpg 1500w" sizes="auto, (max-width: 199px) 100vw, 199px" />
In his new book, Who We Are and How We Got Here, Ancient DNA and the New Science of the Human Past, Reich explains the significance this new technical innovation has had in the study of human history and prehistory. He has packed into this book, not just an explanation of the difficulty in initially finding and sequencing DNA from these samples, but also what it means and how it has changed what we know about out our history.
“Basically, it’s a gold rush right now;” Reich said in a February 2016 interview with <a href="http://edge.org/conversation/david_reich-the-genomic-ancient-dna-revolution">The Edge</a>. “It’s a new technology, and that technology is being applied to everything we can apply it to, and there are &#8230; many gold nuggets strewn on the ground that are being picked up very rapidly. That’s what’s happening now.”
In his book, Reich describes ancient DNA researchers like himself as barbarians overturning the old and long standing approaches to studying human history.
<div id="attachment_26088" style="width: 968px" class="wp-caption aligncenter"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-26088" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/Reic_9781101870327_jkt_ap1_r1-e1521242394539.jpg" alt="" class="wp-image-26088 size-full" width="958" height="1146" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/Reic_9781101870327_jkt_ap1_r1-e1521242394539.jpg 958w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Reic_9781101870327_jkt_ap1_r1-e1521242394539-251x300.jpg 251w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Reic_9781101870327_jkt_ap1_r1-e1521242394539-768x919.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Reic_9781101870327_jkt_ap1_r1-e1521242394539-856x1024.jpg 856w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Reic_9781101870327_jkt_ap1_r1-e1521242394539-736x880.jpg 736w" sizes="auto, (max-width: 958px) 100vw, 958px" />David Reich &nbsp;&nbsp; Photo: Bizu Tesfaye (Howard Hughes Medical Institute)</div>
“Ancient DNA has allowed us to peer deep into time and force us to question our understanding of the past,” he writes.
A professor of Genetics at Harvard University and a Howard Hughes Medical Institute Investigator, Reich opened his own ancient DNA lab at Harvard in 2013, with the help of <a href="https://www.theguardian.com/science/2014/feb/15/svante-paabo-dna-neanderthal-genetics">Svante Paabo</a>, who was the first to use DNA extracted from ancient bones to sequence the Neanderthal genome. That has revealed the more than being just ancient cousins, early modern human and Neanderthal interbreed, and DNA fragments of those encounters live on today in all humans outside of Africa. Similar findings have been made around Denisovans, another ancient human cousin, and other “ghost populations” that have died out. And with each revelation comes a revision of human prehistory and mankind’s migration out of Africa and across the globe.
In his book, Reich also reveals in a chapter called “The Great Mixing” a refrain in of human history, that no matter how divergent the population, humans intermixed and that all populations today are mixed.
“The mixtures of highly divergent groups have happened time and time again,” he writes.
He uses examples <a href="https://www.nature.com/articles/nature08365">of populations in India</a>, that intermixed 2,000 to 4,000 years ago, as well as more recent mixing among <a href="http://www.cell.com/ajhg/pdfExtended/S0002-9297(14)00476-5">African Americans, Latinos and European Americans</a>. Some of that mixing also reflects the “deep history of inequality” among the different populations and sexes.
Toward the end of his book, Reich talks about his optimism that this work to highlight human connections, not their differences.
“[If] you actually take any serious look at this data, it just confounds every stereotype. It’s revealing that the differences among populations we see today are actually only a few thousand years old at most and that everybody is mixed,” he said in <a href="https://www.theatlantic.com/science/archive/2018/03/ancient-dna-history/554798/">a recent interview</a>.

Ancient DNA offers new insight into the human story

Note: As the manager of 23andMe’s Education and Academia Program, I absolutely love my job! Not only do I get to work with inspiring scientists and researchers at 23andMe, I also get to work with talented young people across the country, who are fascinated by the science of genetics. Over the last few months, I’ve spoken at many outreach events at university campuses across the country to support students to form <a href="https://education.23andme.org/genetics-club/?_ga=2.254976072.1309779101.1520270476-1940026374.1477938134">Genetics Clubs</a> on their campus. Along my journey, I met many inspiring college students, who have strong leadership skills and deep passions for science communication. So I invited a team of students to collaborate together and co-create a quarterly magazine called the DNA Decoder &#8212; a magazine written by students, for students. The magazine is designed to help students across the nation connect with each other and share interesting ideas around genetics. We in turn want to share a few of those stories with you on 23andMe’s blog. This is the first in a series of stories from our student contributors — Thao Do, Ph.D.
By Hannah Ericson
On the fourth Tuesday of each month, members of the DNA Interest Group gather at the Iowa Public Library to discuss personalized genetics testing. 
Started by Dr. Bryant McAllister, a professor of genetics and evolution at the University of Iowa, the DNA Interest Group meets to help educate members of the Iowa City community about personalized DNA testing.
<div id="attachment_26076" style="width: 522px" class="wp-caption aligncenter"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-26076" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/Iowa-City-DNA-Interest-Group.jpg" alt="" class="wp-image-26076 size-full" width="512" height="288" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/Iowa-City-DNA-Interest-Group.jpg 512w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Iowa-City-DNA-Interest-Group-300x169.jpg 300w" sizes="auto, (max-width: 512px) 100vw, 512px" />Dr. Bryant McAllister, above, explains genetic concepts to Iowa City community members during a DNA Interest Group meeting, at a local public library. Photo courtesy of Hannah Ericson.</div>
&nbsp;
Members of the interest group come from a wide range of ages and backgrounds, intermixing university students, and people from the general community.
The group’s mission is to “provide a forum to explore heredity and humanity through personal genomics.”

Since its creation early last year, the DNA Interest Group works to connect people interested in learning more about direct-to-consumer DNA tests, such as those offered by 23andMe, ancestry.com, and other companies.

During the meetings, a wide range of topics are discussed. Conversations have dealt with debunking the common myths about genetics, ways to use personalized DNA testing as a teaching tool in the classroom, as well as security concerns arising from using genetic testing services.
7
The group also sponsors a “Festival of Genetics” on National DNA Day. National DNA Day, held on April 25th every year, celebrates the completion of the Human Genome Project in 2003 along with Watson, Crick, Wilkins, and Franklin’s discovery of the DNA double helix in 1953. 

During the festival, members of the University of Iowa’s Personal Genome Learning Center set up different stations to teach community members about genetics, and they also offer support to anyone with questions about their DNA test results. 
<h5>Professor&#8217;s Perspective</h5>
During an interview for an episode of the Talk of Iowa radio program, Dr. McAllister got his first stroke of inspiration to start the DNA Interest Group. 
<div id="attachment_26075" style="width: 310px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-26075" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/Dr.-McAllistar-300x243.jpg" alt="" class="wp-image-26075 size-medium" width="300" height="243" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/Dr.-McAllistar-300x243.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Dr.-McAllistar.jpg 317w" sizes="auto, (max-width: 300px) 100vw, 300px" />Professor Bryant McAllister..</div>
While on the air, a community member called into the program to ask for help on how to understand his DNA test results. 

This experience opened Dr. McAllister’s eyes to the need for resources for community members to help them interpret their genetic test results, and deepen their understanding of genetics. 

In the future, Dr. McAllister says, “I would like to expand outside of Iowa City. 

One of the things I would like to do is to motivate people in other biology departments in other colleges and universities to do a similar thing in their communities, building the infrastructure and the interest outside of Iowa City so that other biology departments can support similar things in their own communities.”

For students thinking of starting a DNA Interest Group of their own, Dr. McAllister has some advice. 

He recommends, “I would try to get some kind of faculty buy-in. A faculty member would be essentially a sponsor that helps with some of the organization and making contacts,”as many students may not have the support network needed to start a project of this size. 

After that, he said it’s mostly about trying to connect to other community members or resources, in an effort to reach more people and to grow the group. 
<h5>Student&#8217;s Perspective</h5>
Abagail McKernan is a sophomore studying genetics and biotechnology at the University of Iowa and is a member of the DNA Interest Group. She first joined the DNA Interest Group through her involvement with another group at the University of Iowa, the Personal Genome Learning Center.<div id="attachment_26074" style="width: 250px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-26074" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/Abagail-McKernan-240x300.png" alt="" class="size-medium wp-image-26074" width="240" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/Abagail-McKernan-240x300.png 240w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Abagail-McKernan.png 361w" sizes="auto, (max-width: 240px) 100vw, 240px" />Abagail McKernan</div>
Abagail especially enjoys being able to interact with members of the community, with whom she normally would not have a chance to communicate with. 

“You wouldn’t think people, especially people from older generation, would be as interested in it [personalized genomics] as you are seeing at these meetings,” she says.

Abagail likes that everyone who comes to the meetings shares common interests, and she enjoys educating community members on genetics topics that they may not be completely familiar with. 

For example, on DNA day, Abagail held demonstrations on the processes of mitosis and meiosis (different ways that cells undergo division) using gummy worms—which participants were able to eat afterwards.

Abagail plans on continuing her involvement with the group in the future as she thinks that communicating with the public about science topics is important.

For students thinking about starting a similar group, Abagail recommends advertising the group in as many places throughout the community as possible. 

This would include putting up posters throughout the community. As a result, this group would help educate many community members, which helps foster a greater understanding of scientific topics in the community and beyond.
<div id="attachment_26073" style="width: 210px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-26073" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/Hannah-Ericson-200x300.jpg" alt="" class="size-medium wp-image-26073" width="200" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/Hannah-Ericson-200x300.jpg 200w, https://blogcms.23andme.com/wp-content/uploads/2018/03/Hannah-Ericson.jpg 341w" sizes="auto, (max-width: 200px) 100vw, 200px" />Hannah Ericson</div>
Hannah Ericson is a sophomore at the University of Iowa, studying genetics and biotechnology. Outside of class, she is active in the Iowa Comic Book Club and the fencing club, as well as the Personal Genome Learning Center, where she works to help educate other students as well as the general public about the world of personalized genomics. After graduating, Hannah would like to find a research position in a genetics lab. As part of the Genetics Education Student Leadership Team, she hopes to foster a love of genetics in others, who may not have had a prior opportunity to be exposed to the topic.

Hannah Ericson

The DNA Interest Group at the University of Iowa

Researchers at the University of Cambridge have found that it isn’t just your environment and experiences that influence your empathy for others, your genes also play a small but important role and this connection also sheds new light on the biology of autism.
“This is an important step towards understanding the small but important role that genetics plays in empathy,” said <a href="http://www.neuroscience.cam.ac.uk/directory/profile.php?vw260">Varun Warrier</a>, a Ph.D. student at the University Cambridge who led the study.
<div id="attachment_25991" style="width: 210px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-25991" src="https://blog-api.23andme.com/wp-content/uploads/2018/01/sm_vw260_phpHPqcmu.jpg" alt="" class="wp-image-25991 size-full" width="200" height="257" />Varun Warrier</div>
Warrier said that while the genetic influences are important they still only play a small role in empathy. Other, non genetic factors, like upbringing, environment and other non-biological factors explain 90 percent of the individual differences in empathy between people, he said.
The study, published in the journal <a href="https://www.nature.com/articles/s41398-017-0082-6">Translational Psychiatry,</a> also confirms previous research that shows that women on average are more empathetic than men. However, this difference is not due to our DNA, which in turn implies that the sex difference in empathy is the result of other non-genetic biological factors such as prenatal hormonal influences, or non-biological factors, such as socialisation, both of which also differ between the sexes.
Finally, the new study found genetic variants associated with lower empathy are also associated with higher risk for autism. In fact the paper is part of a series of papers looking at the genetics of autism by this same group of researchers at Cambridge.
For this study — led by Warrier and Professor <a href="http://www.neuroscience.cam.ac.uk/directory/profile.php?sb205">Simon Baron-Cohen</a>, the director of the <a href="https://www.autismresearchcentre.com/">Autism Research Centre</a> at Cambridge, and with contributions from researchers at 23andMe, the University Paris Diderot, and Institut Pasteur — scientists used data from more than 46,000 23andMe customers who consented to participate in research and completed the online survey that measures their Empathy Quotient, or EQ. It was scientists at Cambridge who first developed the tool to measure empathy 15 years ago.
“This new study demonstrates a role for genes in empathy, but we are have not yet identified the specific genes that are involved in empathy,” said Professor Thomas Bourgeron of the University of Paris. “Our next step is to gather larger samples to replicate these findings and to pinpoint the precise genes associated with individual differences in empathy.”
<div id="attachment_25992" style="width: 210px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-25992" src="https://blog-api.23andme.com/wp-content/uploads/2018/01/sm_sb205_phpdnwk32.jpg" alt="" class="wp-image-25992 size-full" width="200" height="271" />Simon Baron-Cohen, PhD</div>
23andMe is uniquely equipped for a study like this, said David Hinds, Ph.D., the company’s principal scientist and a statistical geneticist who worked on this study.
“We’re encouraged by these findings, which are the latest in <a href="https://blog.23andme.com/23andme-research/the-genetics-of-empathy/">a series of studies</a> we’ve collaborated on with researchers at Cambridge,” Hinds said. “Together they are are helping to reveal new insights into the genetics that influences autism.”
Empathy has two parts: “cognitive empathy,” the ability to recognize another person’s thoughts and feelings, and “affective empathy,” the ability to respond appropriately. EQ measures both parts.
Earlier studies have shown that some of us are more empathetic than others, and that women, on average, are slightly more empathetic than men. Studies have also shown that autistic people, on average, score lower on the EQ, and that this was because they struggle with cognitive empathy, even though their affective empathy may be intact.
“Finding that even a fraction of why we differ in empathy is due to genetic factors helps us understand those (like autistic people) who struggle to imagine another person’s thoughts and feelings,” said Professor Baron-Cohen.

New Research on the Genetics of Empathy, and How it Relates to Autism

We wear pink ribbons. We walk or run for the cause. We have a month for awareness, and yet many women who have a higher risk variant in the BRCA1 or BRCA2 genes remain unaware of their heightened genetic risk for breast and ovarian cancer until a doctor diagnoses them with cancer.<a id="a1" href="#f1">[1]</a> 
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2015/01/Anne_Color_-Seated-250x300.jpg" alt="" class="alignright size-medium wp-image-22084" width="250" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/01/Anne_Color_-Seated-250x300.jpg 250w, https://blogcms.23andme.com/wp-content/uploads/2015/01/Anne_Color_-Seated-768x923.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/01/Anne_Color_-Seated-852x1024.jpg 852w, https://blogcms.23andme.com/wp-content/uploads/2015/01/Anne_Color_-Seated-732x880.jpg 732w, https://blogcms.23andme.com/wp-content/uploads/2015/01/Anne_Color_-Seated-982x1180.jpg 982w" sizes="auto, (max-width: 250px) 100vw, 250px" />
That’s a failure. 
This is not a radical indictment of the American healthcare system; it’s just a fact. We are very good at treating illnesses, but not at preventing them. 

<h6>BRCA</h6>
Under the current system, there are specific guidelines for BRCA screening that limit who has access to BRCA testing. Family history of cancer and Ashkenazi Jewish ancestry are the most common criteria for screening guidelines. However we have seen at 23andMe that many people do not know their family medical history or their ancestry. So, many people fall through the cracks in the current screening system leaving them unaware of their risk. <a id="a2" href="#f2">[2]</a>
It doesn’t have to be that way.
<h6>23andMe&#8217;s BRCA1/BRCA2 Report</h6>
Today, 23andMe received the first-ever FDA authorization for a direct-to-consumer genetic test for cancer risk for its BRCA1/BRCA2 (Selected Variants) report. The report covers three variants in the BRCA1 and BRCA2 genes associated with increased risk for breast, ovarian, and prostate cancer. These variants are most common in people of Ashkenazi Jewish descent.
Worrying about the many current 23andMe customers who have one of or more of these variants has caused me sleepless nights. We believe they have the right to know about this risk, if they choose. And it&#8217;s more than just women — men with one of the BRCA1 or BRCA2 variants we test for are at higher risk for male breast cancer, and may have a higher risk of certain other cancers as well. Men who find out they have one of the tested BRCA variants can also alert female relatives who might benefit from knowing about their potential genetic risk.
<h6>Opportunities for Prevention</h6>
Importantly, studies have found women falling through gaps in breast cancer screening. In her 2015 recommendation for broader screening, <a href="http://www.ascopost.com/issues/february-10-2015/dr-mary-claire-king-proposes-population-screening-in-all-young-women-for-brca-mutations/">geneticist Mary-Claire King, Ph.D., said</a>, “Every breast cancer patient we identify after she develops cancer clearly represents a missed opportunity for prevention.”
A <a href="http://www.pnas.org/cgi/doi/10.1073/pnas.1415979111">2014 study</a> led by Dr. King found that 50 percent of families that had a BRCA1 or BRCA2 mutations had no history of breast or ovarian cancer that would have triggered clinical attention. Similarly our own data shows that a significant number of 23andMe customers who have one of the selected BRCA mutations for which we test, would likely not meet traditional guidelines for screening because they reported being unaware of their ancestry or a family history of cancer. 
Those customers — carriers of the selected BRCA1/BRCA2 variants who reported no family history of cancer and no Jewish ancestry — would likely never know about their risk because they’d never be offered screening under traditional guidelines. It’s a small but significant number of people, and for those individuals, this information could have a profound impact in their lives.<a id="a3" href="#f3">[3]</a>
<h6><img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080-300x300.png" alt="" class="alignright size-medium wp-image-26062" width="300" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080-300x300.png 300w, https://blogcms.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080-150x150.png 150w, https://blogcms.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080-768x768.png 768w, https://blogcms.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080-1024x1024.png 1024w, https://blogcms.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080-880x880.png 880w, https://blogcms.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080-271x271.png 271w, https://blogcms.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080-372x372.png 372w, https://blogcms.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080-574x574.png 574w, https://blogcms.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080-980x980.png 980w, https://blogcms.23andme.com/wp-content/uploads/2018/03/BRCA-Launch_1080x1080.png 1080w" sizes="auto, (max-width: 300px) 100vw, 300px" />Unexpected Findings</h6>
A few years ago, 23andMe studied how people react to<a href="https://peerj.com/articles/8/"> unexpected BRCA findings</a>.<a id="a4" href="#f4">[4]</a> Researchers found that the results didn’t induce anxiety, which was the concern of many. Instead, they sparked crucial conversations among families. These conversations, in turn, created what researchers call a “cascade effect.” These are benefits that extend beyond the person who tested. They extend to members of that person&#8217;s family. It gives each a warning of a potential risk not just for breast, but also ovarian as well as prostate cancer in men.
This was a small study, but since the paper was published a lot has happened. 23andMe had to suspend offering genetic health risk reports — including the BRCA1/BRCA2 report — to customers as we went through an FDA review of our ability accurately detect these variants. We also had to show to the FDA that we could report genetic health risk information to customers in a way that could be easily understood. We did that.
Let’s be clear. 23andMe’s new report, once it’s available, does not diagnose cancer and cannot rule out your chances of getting cancer. It doesn&#8217;t cover most of the thousands of BRCA1 and BRCA2 variants associated with increased cancer risk. There are also variants in other genes associated with hereditary cancer, or non-genetic factors such as environment and lifestyle. The report should not be used on its own to make medical decisions. Results should be confirmed with a healthcare provider in a clinical setting before taking any medical action. 
23andMe’s BRCA1/BRCA2 report is not going to be helpful for everyone, but it’s a step in the right direction. We already know of customers who benefited from this information.
<h6>Taking Action</h6>
I know some of these women. They are among the 23andMe customers who tested more than four years ago when we previously offered this report.
&nbsp;
Women like Hilary Hood, a photographer, and mother of three grown daughters, who was surprised to learn about her breast cancer risk after testing with 23andMe. 
“It didn’t occur to me that I was at risk because I didn’t have a mother or sister or aunt with it,” she said. “I didn’t understand the genetic component.”
&nbsp;
It was a shock for Ann Mellinger too. 
&nbsp;
Ann, a CEO, and mother in New York didn’t have information about her biological father’s family health history. 

&nbsp;
“Most people who test positive for the BRCA1 mutation have a family history of breast and ovarian cancer, but I was aware of no cases in our family,” she said. “Knowledge is power, and in my case, the information I gained could quite possibly have saved my life.”
&nbsp;
Now, more than four years later, with our third FDA authorization we can again offer a BRCA report to customers covering the selected BRCA1/BRCA2 variants. It’s the first time the Agency has authorized a direct-to-consumer genetic test for cancer risk without a prescription. 
&nbsp;
This is a major milestone for 23andMe. But more importantly, a significant step forward for consumers who want direct and affordable access to their health information. Over the last four years, it has kept me up at night knowing that we have customers with one of these risk variants but have been unable to tell them. I can sleep better knowing that soon, if our customers choose to, they can view this information. We know from our own data that this information can be incredibly meaningful for customers and, in some cases, could even save lives. 
<footer class="footnotes">References:</footer>
<footer class="footnotes">
<a id="f1" href="#a1">[1]</a><a href="https://jamanetwork.com/searchresults?author=Mary-Claire+King&amp;q=Mary-Claire+King" target="_blank" rel="noopener noreferrer">King, M</a> et al. (2014). &#8220;<a href="https://jamanetwork.com/journals/jama/fullarticle/1902783">Population-Based Screening for BRCA1 and BRCA2</a>&#8221; JAMA. 2014;312(11):1091-1092. doi:10.1001/jama.2014.12483 <a href=" https://jamanetwork.com/journals/jama/fullarticle/1902783"></a></footer>
<footer class="footnotes">
<a id="f2" href="#a2">[2]</a>Ibid.</footer>
<footer class="footnotes">
<a id="f3" href="#a3">[3]</a>Statistics come from internal data of 23andMe customers. 23andMe’s research team is working on a manuscript focusing on this data.</footer>
<footer class="footnotes">
<a id="f4" href="#a4">[4]</a><a href="https://peerj.com/articles/8/" target="_blank" rel="noopener noreferrer">Francke, U</a> et al. (2013). &#8220;<a href="https://jamanetwork.com/journals/jama/fullarticle/1902783">Dealing with the unexpected: consumer responses to direct-access BRCA mutation testing</a>&#8221; PeerJ 2013. </footer>

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