You want to know a little about what it’s like living with lupus, ask a<img loading="lazy" decoding="async" class="alignright size-medium wp-image-22692" src="https://blog-api.23andme.com/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" />
Those are just a few of the bloggers we’ve been following lately who each offer different insight on the day-in and day-out challenges of living with this chronic and incurable condition.
Lupus – systemic lupus erythemotosis – is a hard to diagnose autoimmune disease with a wide range of unpredictable symptoms that mostly impacts women. 
An estimated 5 million people worldwide have been diagnosed with Lupus. Individuals with African American, Latino and Native American ancestry are also at higher odds of getting the condition. While the symptoms can be managed, there currently is no cure. The good news is that in the last 60 years there have been great strides in treating the condition. In the 1950s the prognosis wasn’t good with only half of those surviving five years after their initial diagnosis. Today the survival rate is greater than 90 percent.
While we’ve learned a lot about lupus, we still have a long way to go. We know genetics plays a role, as do environmental and hormonal factors, but the intricate interplay of all those influences, or even why flare-ups are so unpredictable, is little understood.
In May of this year 23andMe and Pfizer joined forces to study the genetics of lupus. Working in collaboration with the<a href="http://www.lupusresearchinstitute.org/"> Lupus Research Institute</a>, we hope to gain a greater understanding of this unpredictable chronic disease and make findings that could lead to new treatments.
As part of the study we plan to recruit 5,000 people with lupus. In just a few months we’ve made huge strides toward that goal, enlisting more than 1,100 participants.
We know from listening to many of those who are living with lupus that one of the most important means of coping with the condition is connecting with others.
And in the spirit of our budding lupus research community, we are highlighting a few of the bloggers that have become beacons of information for those with lupus. So in no particular order here are five of the bloggers we’re reading.
<a href="http://despitelupus.blogspot.com/">Despite Lupus</a> – Since first being diagnosed 14 years ago, blogger and now first-time author (of a book also titled “Despite Lupus”), Sara Gorman has a tried and true strategy for living with lupus by changing expectations and focusing on keeping herself healthy.
<a href="http://undefeateddiva.com/">Undefeated Diva</a> – Blogger Christina Gorgon, the “fiery Latina,” was first diagnosed in 2011. She writes about becoming a mom with lupus. Many of those with lupus, which is difficult to diagnose, can also relate to her story of spending two years enduring a strange assortment of symptoms – joint pain, chest pain, bald spots, and an inability to get out of bed – without knowing what it was that was making her sick.  Her fighting attitude infuses each post.
<a href="http://www.lupuschick.com/">Lupus Chick</a> – Marisa Zeppier-Caruana is the Lupus Chick, and has been featured in several publications including US News &amp; World Report, Glamour and WebMD. Marisa founded the site back in 2002, and also serves on the board of the Florida Chapter of the Lupus Foundation of America. On top of writing about lupus and advocating for those with the condition, Marisa is also the reigning Mrs. New York USA Universal, shooting for title of Mrs. Universe.
<a href="http://www.flowonlupus.com/">Flow On Lupus</a> –  Miz Flow first started showing signs of lupus as a 14 year-old. Now the 30-something blogger is a veteran and survivor, who has weathered a slew of symptoms, that have given her a wealth of knowledge about lupus that she shares on her site.
Molly’s Fund Lupus Blog – This Oregon based non-profit foundation started out of Molly McCabe’s struggle with lupus. Since co-founding the foundation, Molly has also become the face of the organization that offers those with the condition access to support groups in the Oregon area, online support and other resources.
<img loading="lazy" decoding="async" class="aligncenter wp-image-22690 size-larger" src="http://35.88.189.111/wp-content/uploads/2015/07/Lupus-Landing-Page-880x302.jpg" alt="" width="880" height="302" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/07/Lupus-Landing-Page-880x302.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Lupus-Landing-Page-300x103.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Lupus-Landing-Page-768x264.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Lupus-Landing-Page-1024x352.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Lupus-Landing-Page-1180x405.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Lupus-Landing-Page.jpg 1758w" sizes="auto, (max-width: 880px) 100vw, 880px" />

23andMe Blog

23andMe Blog Team

Living With Lupus

We are all unique, and knowing our genotypes at specific places in our genomes may give each of us a better understanding as to why.<img loading="lazy" decoding="async" class="alignright wp-image-18019 size-medium" src="http://35.88.189.111/wp-content/uploads/2013/04/Helix--300x222.jpg" alt="" width="300" height="222" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/04/Helix--300x222.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/04/Helix--768x568.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2013/04/Helix--1024x757.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2013/04/Helix--880x650.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2013/04/Helix--1180x872.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2013/04/Helix-.jpg 1372w" sizes="auto, (max-width: 300px) 100vw, 300px" /> 
with an alphabet made up of just four letters –  A, T, C and G.
Those four letters represent the nucleotide bases – adenine, thymine, cytosine and guanine – that are the building blocks of life. The sequence of A’s, T’s, C’s and G’s run in long stretches of code that instruct the way the human body is built and functions.
In 2003 after ten years and $3 billion, scientists decoded the first sequence of a human genome. Since then costs have dropped for sequencing a genome to as low as $1,000. While very inexpensive in comparison, it would still be prohibitive for most consumers to have their full genome sequenced.
So how is 23andMe able to provide genetic data to so many people at an affordable price in just a matter of weeks?

The secret lies in a process called “SNP genotyping.”
If you compared two unrelated individuals, you would find that their genetic sequences are about  99.9 percent the same. It is that miniscule variation in their genome that makes all the difference. It’s what makes us each unique.
That small variation is also the key to how 23andMe can efficiently and cost-effectively deliver its service. Scientists have identified the known variation among individuals, specifically locating in the human genome where a single letter differs from one person to the next.
These one-letter variations are called single nucleotide polymorphisms, or SNPs (pronounced “snips”), and they are associated with differences in everything from the color of our eyes, to our risks for certain health conditions, and information about the makeup of our ancestry.
Let’s look at an example of a SNP.
Say a certain percentage of people have  a specific stretch of DNA code that reads ATGCCCGT, but everyone else  has the sequence ATGCACGT along that same stretch.
The nucleotide bases come in pairs, so in this case the difference is between whether a person is CC or AC at this position.<img loading="lazy" decoding="async" class="alignleft size-medium wp-image-22672" src="https://blog-api.23andme.com/wp-content/uploads/2015/07/Image-1-300x119.jpg" alt="Image 1" width="300" height="119" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/07/Image-1-300x119.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Image-1-768x305.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Image-1.jpg 774w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Since these two letters are known to vary among individuals, we would call this position in the sequence a SNP. The difference between two people at a single position – whether you are CC or AC in this case  – is also referred to as the genotype for that SNP. Some of those differences may have no effect, some could be beneficial and some could be deleterious.
The benefit or harm of one version or the other can even change depending on one’s environmental surroundings. 23andMe provides individuals with information on hundreds of thousands of these SNPs.
To do that, 23andMe first has to extract DNA from saliva submitted by a customer. Once the DNA is extracted, it is amplified many times so that there is enough DNA to analyze. The amplified DNA is then cut into smaller pieces and washed over a microarray chip.
This  genotyping chip contains thousands and thousands of tiny probes that are designed to detect specific bits of DNA. Each probe on the chip contains a bit of DNA that matches a genetic variant of interest. Remember the nucleotide bases always come in pairs, an A always pairs with T, while a G pairs with C.   On the microarray chip, when a piece of DNA finds its complementary probe, it will stick to it.
These probes are triggered to glow in a way that indicates which version of each SNP is present in the sample. That fluorescent signal is read by a computer, and the data is then uploaded to the customer’s 23andMe account.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-22673" src="https://blog-api.23andme.com/wp-content/uploads/2015/07/image-2-300x246.jpg" alt="image 2" width="300" height="246" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/07/image-2-300x246.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2015/07/image-2.jpg 566w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Our customers have the ability to view this raw data in a feature called Browse Raw Data.
Our latest genotyping chip, v4, is unlike any of our previous genotyping platforms. Previous genotyping platforms included standard probes included by Illumina, the manufacturer of the chip, as well as additional probes selected by 23andMe.
The v4 chip, consists of a completely custom panel of probes that were hand picked by our researchers. Although our current genotyping chip contains about half a million SNPs (whereas the entire human genome has around 10 million SNPs), we can learn a lot about the human genome simply by looking at these locations where individual genotypes are known to differ. Full genome sequencing provides information on all 3 billion markers in the entire human genome, however it is difficult to predict when full sequencing will be available at an affordable price point for the general public.
<iframe loading="lazy" src="https://www.youtube.com/embed/0gC8RQ7PemM" width="640" height="360" frameborder="0" allowfullscreen="allowfullscreen"></iframe>

What’s Your Type?

I’m sorry to burst your bubble, but you don’t have a gene for being tall, or a gene for caffeine addiction or a gene for intelligence. No one does.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-22682" src="https://blog-api.23andme.com/wp-content/uploads/2015/07/Clare-image-1-300x243.jpg" alt="Clare image 1" width="300" height="243" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/07/Clare-image-1-300x243.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Clare-image-1-768x623.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Clare-image-1-880x714.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2015/07/Clare-image-1.jpg 895w" sizes="auto, (max-width: 300px) 100vw, 300px" />
In an effort to simplify the science, the media sometimes talks about genetics and the influence of genes in these terms.
But there is not a “breast cancer gene,” or a “warrior  gene.”
It’s much more complicated than that. With a few exceptions, everyone has the same genes. But within these genes, there are slight variations – different genotypes – and it’s those small variations that makes us all unique.


So when a customer asks:
“Do I have this gene?”


Technically speaking, the answer is always:
“Yes.” 
The thing is, that’s not really what they are asking. They want to know if they have the genotypes that influence a certain trait. To understand what I mean by genotype, it helps to review a little biology.
Think of your DNA as one long string. A very, very long string that’s crammed into every cell in your body. This string is broken into many segments with each segment serving a different purpose. These segments of DNA are called genes.


Genes provide instructions for your body to produce different proteins. Proteins influence nearly every function of your body. Some proteins effect visible traits like the color of your eyes.  Others prompt biological functions from the ability to lift your arm to intricate cell processes.
With only a few exceptions, everyone has the same genes,  so it’s not the presence or absence of a gene that is variable.* It’s what is within those genes that is different. Each gene contains many positions, and each position is associated with a single genotype. It is the genotypes on a particular gene that make all the difference.
Let’s break this down a bit more.


Your DNA is made up of nucleotide bases – adenine, cytosine, guanine, and thymine. Your A’s, C’s, G’s and T’s, if you will. You can think of these bases like puzzle pieces. They bind with one another to form your DNA. Your DNA is organized into twenty-three pairs of chromosomes.   These bases together make up your genotype at that position. A genotype is written using the two letters of the two nucleotide bases at a particular position, such as AA or CT.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-22681" src="https://blog-api.23andme.com/wp-content/uploads/2015/07/clare-image-2-300x223.jpg" alt="clare image 2" width="300" height="223" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/07/clare-image-2-300x223.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2015/07/clare-image-2-768x572.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/07/clare-image-2-880x655.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2015/07/clare-image-2.jpg 940w" sizes="auto, (max-width: 300px) 100vw, 300px" />
There are several ways scientists refer to particular points in your DNA.
At 23andMe, we perform genotyping by analyzing single nucleotide polymorphisms (SNPs). It is a location on your DNA where the genotype can vary among people. This means that your genotype at that position may differ from other individuals.
Different genotypes at a particular SNP can indicate something about your physical characteristics, or potential genetic health risk. Genotyping services base interpretations on your genotype for a particular SNP or SNPs, not the presence or absence of a gene.
For example, the type of earwax you have is dependent on a single SNP located on the ABCC11. If your genotype at this SNP is TT, then you have dry earwax. If you have any other genotype at this SNP, then you have wet earwax.
And that’s it! So the next time you wonder if you have a particular gene, you’ll know it’s a bit more complicated than that. It’s all about those base pairs.
___
*There are some conditions caused by gene deletions. 23andMe is not well-suited to detect such genetic changes.
 
**The exception to this are the sex chromosomes.

All About that Base (Pair): The Significance of your Genotypes

Over the last year, three promising new treatments for symptoms of Parkinson’s became available in the United States, but progress has been less hopeful on the development of drugs to modify the progression the disease, according to researchers who spoke at an annual movement disorders conference in San Diego last month.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-22380" src="https://blog-api.23andme.com/wp-content/uploads/2015/03/paul-300x235.jpg" alt="paul" width="300" height="235" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/03/paul-300x235.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2015/03/paul-768x602.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/03/paul-1024x802.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2015/03/paul-880x689.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2015/03/paul-1180x924.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2015/03/paul.jpg 2016w" sizes="auto, (max-width: 300px) 100vw, 300px" />
<a href="https://blog.23andme.com/23andme-research/22378/">23andMe’s Paul Cannon</a>, PhD, who serves as the manager for our <a href="https://www.23andme.com/pd/">Parkinson’s Research Community</a>, was among the thousands of attendees at the massive 19th International Congress of Parkinson’s Disease and Movement Disorders in San Diego. The four-day event attracts scientists, clinicians and medical professionals from around the world, giving them an opportunity to share the latest treatments and the newest research into Parkinson’s disease.


“In terms of treatments for Parkinson’s it was a mixed bag,” said Paul.
While new options for the treatment of symptoms in the form of gels, skin patches, intestinal pumps,<a href="http://www.mdscongress2015.org/Congress-2015/Press/News-Releases/260-Inhaled-Levodopa.htm"> inhalers</a> and even<a href="http://webcache.googleusercontent.com/search?q=cache:WZ8TqAwG5C4J:www.mdscongress2015.org/Congress-2015-Files/pdfs/2015LateBreakingAbstractsPubDoc.pdf+&#038;cd=2&#038;hl=en&#038;ct=clnk&#038;gl=us"> deep brain stimulation</a>, offer Parkinson’s patients new ways for quickly treating certain symptoms, Paul noted that researchers also reported some setbacks in the development of other treatments that many had hoped could slow the progress of the disease. The use of gels, skin patches, pumps and inhalers are used for better delivery of the drugs levodopa and carbidopa, which effectively treat motor function symptoms for Parkinson’s patients. Paul said there is also some interesting clinical studies around non-levodopa drugs such as safinamide and rivastigmine, but there was little new to report around treatment for the progression of the disease.
“In terms of disease modifying therapies it was a much less successful year,” Paul said.


Probably the most notable setback in the drug development pipeline was the news around the<a href="http://jama.jamanetwork.com/article.aspx?articleid=2108890"> halt of a late stage study of creatinine</a>, an amino acid that researchers thought could help protect nerve cells in Parkinson’s patients. But the study was stopped because interim data showed the treatment didn’t help patients any differently than those treated with a placebo. Another disappointment was around the<a href="http://www.thelancet.com/journals/laneur/article/PIIS1474-4422%2815%2900144-1/abstract"> failure of the drug pioglitazone</a>. In Paul’s assessment of the study for pioglitazone, there was some indication from biomarkers that the drug could still hold benefits if used at a different doses.
But in his time at the conference Paul said there were several presentations that indicate there are also some studies currently in the drug development pipeline. He singled out three that are either in phase three development or about to start – studies into the drugs<a href="https://clinicaltrials.gov/ct2/show/NCT02168842"> isradipine</a>,<a href="https://www.michaeljfox.org/foundation/grant-detail.php?grant_id=403"> inosine</a> and<a href="https://www.michaeljfox.org/foundation/grant-detail.php?grant_id=1124"> exanatide</a>.
Others therapies to pay attention to, according to Paul, are two in early development that target alpha-synuclein – an antibody from the drug company Prothena, and a vaccine from Affiris.
If you’ve paid much attention to research into Parkinson’s you’ll know that a lot of focus has been on the role alpha-synuclein plays not just in Parkinson’s but also other neurodegenerative disorders. Alpha-synuclein is a protein that is primarily found in brain tissue. In Parkinson’s patients this protein clumps together in the brain. Warren Olanow, an MD and professor of neuroscience at Mount Sinai, discussed some of theories on the best therapeutic approaches to deal with this from using antibody based treatments to systems of either blocking the clumping or reducing the gene expression of alpha-synuclein.


Working at 23andMe, where our researchers have done several genome wide association studies that helped uncover new genetic associations with Parkinson’s, Paul said he was struck by some of the information presented by Andy Singleton, of the National Institutes of Health. Although studies indicate that as much as 30 percent of the risk for the most common type of Parkinson’s is genetic, the genetic variants found so far account for only about five percent of that risk. Even though genome wide association studies were used to discover 28 known variants associated with Parkinson’s disease, Singleton favors the use of whole genome sequencing as a better approach to find the remaining genetic variants. (23andMe is working on a multi-year study with Genentech to sequence 3,000 Parkinson’s patients to learn about the genetic underpinnings of the disease.)


In another promising presentation, the researcher Haydeh Payami, PhD at UC Berkeley and a joint faculty member at the<a href="http://hudsonalpha.org/research/faculty-and-projects/faculty-profiles"> HudsonAlpha Institute</a>, reported on a nice example of gene environment interaction, Paul said. Looking at caffeine consumption and genetic risk, Payami’s research found that drinking coffee in general can reduce one’s risk for Parkinson’s by 30 percent. But for individuals with certain genotypes in two genes – GRIN2A and MAPK10 – caffeine consumption did little to reduce their risk for Parkinson’s. Yet when Payami looked at the 7 percent of individuals who had the less common genotypes in both of those genes coffee consumption was “highly protective.”


“In summary whilst lack of progress in the clinic is disappointing, continued insights into the underlying disease mechanisms from genetics and other routes of investigation, gives hope that we will see an increasing number of rationally targeted therapies being tested in well designed studies,” Paul said of what he learned at the conference. “Resources such as 23andMe Parkinson’s Research Community are a key part of this on-going research effort.”
<img loading="lazy" decoding="async" class="aligncenter wp-image-22634 size-large" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/Parkinsons-Research-Community-640x238.jpg" alt="Parkinson's Research Community" width="640" height="238" />

Research Update on Parkinson’s Disease

The amazing <a href="http://www.yourgeneticgenealogist.com/p/about-me.html">CeCe Moore</a>, a genetic genealogist and 23andMe Ancestry Ambassador, has done it again, solving a family<img loading="lazy" decoding="async" class="alignright size-full wp-image-12939" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/CeCephoto.jpg" alt="CeCephoto" width="114" height="162" /> mystery and helping a woman connect with her biological mother for the first time.
“DNA,” Moore told the Orange County Register, “was the only way to solve this.”
<a href="https://www.ocregister.com/articles/tovo-670236-kayla-baby.html">The story</a>, which appeared in the Orange County Register, generated a lot of questions and some strong reactions. CeCe and her team had helped Kayla Tovo, a 27 year-old mother and US Army veteran, solve the mystery of her birth.
Kayla was just a few hours old when a janitor found her wrapped in a towel in a milk crate left in the back of an Alpha Beta grocery store.
Her story could have ended in tragedy if not for being adopted by a wonderful loving mother and growing up in a supportive home. But after having children of her own, and a brush with death in Afghanistan, Kayla decided to try in earnest to find the woman who abandoned her. She wanted to know why. A friend connected her to CeCe. Kayla then tested with 23andMe and found a first cousin once removed, providing her the pivotal lead to connect her to her biological family.


“I received questions from all over social media on this story,” CeCe told us. “(Kayla) was lucky, and some have complained they don&#8217;t have matches that close.”


But as the database grows, so too does the possibility for new and closer matches, she said.


“New matches are coming in all the time and the newer ones are more likely to respond and share family tree information than the older matches,” CeCe said.
Check out Kayla’s <a href="https://www.ocregister.com/articles/tovo-670236-kayla-baby.html">story</a>.

More Than Just Luck

Anne Wojcicki, 23andMe&#8217;s CEO and co-founder, spoke recently with Kai Ryssdal, the host and senior editor at 
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-22084" src="https://blog-api.23andme.com/wp-content/uploads/2015/01/Anne_Color_-Seated-250x300.jpg" alt="Anne_Color_ Seated" 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" />Marketplace, about the company, genetics, and the future of health care.


It&#8217;s a good overview of some of what we&#8217;ve been doing lately here at 23andMe.
Anne takes time to explain some of 23andMe&#8217;s core mission about helping people access and benefit from their genetic information, as well as explain how this information will become increasingly important in the future.


Genetic information is already changing health care, but it is also changing drug development and discovery. 23andMe recently announced the creation of its new therapeautics group, lead by renowned scientist Richard Scheller, Ph.D. Anne talked a little bit about this effort and how it aligns with 23andMe&#8217;s overall mission.


It&#8217;s worth taking a few minutes to listen to the piece.

The Future of Health Care

While 23andMe can inform you about your ancestry, that information doesn’t define you, as has been so eloquently written about by Jesmyn Ward <a href="https://www.newyorker.com/tech/elements/innovation-cracking-the-dna-code" target="_blank" rel="noopener noreferrer">in the New Yorker</a>, and by Simone Kitchens in <a href="http://www.glamour.com/inspired/2015/02/what-are-you-how-to-answer-identity-questions" target="_blank" rel="noopener noreferrer">her story</a> that first <img loading="lazy" decoding="async" class="alignright wp-image-22626 size-large" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/0315-GL-AABY06-01-copy-e1435353553605-452x768.jpg" alt="At Home in the WorldIn my apartment, with a favorite photo of me and my mom.Rachel Comey dress. See GLAMOUR Shopper for more information." width="452" height="768" />appeared in Glamour. Both Jesmyn and Simone write about being multiracial and the difficulty of navigating not just how their mixed race influences how others perceive them, but how they perceive themselves. In his new book <a href="http://www.penguinrandomhouse.com/books/219260/loving-day-by-mat-johnson/" target="_blank" rel="noopener noreferrer">Loving Day</a>, the writer <a href="http://www.esquire.com/entertainment/books/interviews/a35341/mat-johnson-interview-mixed-race-in-america/" target="_blank" rel="noopener noreferrer">Mat Johnson</a> covers some of the same territory. How people think about race, and the commonly accepted notions about what it means, are changing. Probably at the forefront of that transformation are people like these three writers who are of mixed ancestry. More and more people are walking this path. In the United States nearly 7 percent of adult Americans have a multiracial background, according to a <a href="http://www.pewsocialtrends.org/2015/06/11/multiracial-in-america/" target="_blank" rel="noopener noreferrer">new report</a> by the Pew Research Center. Many other people simply do not know of their own mixed ancestry. Reconciling what it means to be mixed is complicated, and that process is elegantly captured in Simone’s piece, which we’re republishing here. Take a look. 



By Simone Kitchens
This is what I look like to you:
I&#8217;m brown.
Various shades of brown. Dark brown curly hair, darker brown eyes, skin a tan sort of brown. You might think I&#8217;m black or part black, but most people have trouble pinpointing my race. I do too.
I&#8217;ve gotten the &#8220;What are you?&#8221; question about once a week for the past 20 years, ever since I heard it for the first time in the girls&#8217; bathroom in sixth grade. I was looking in the mirror when a girl at the sink yelled over, &#8220;Are you mixed?&#8221; She was black. She came closer to get a better look. &#8220;What are you?&#8221; she asked. A group of girls, her friends, studied me as well.
&#8220;I don&#8217;t know,&#8221; I said.
The girl went back to drying off her hands and said, &#8220;You&#8217;re half-black.&#8221; She was matter-of-fact, as if she were filling me in on something I wasn&#8217;t aware of. From that moment on, I&#8217;ve known myself as a half-black person.
But &#8220;half-black&#8221; has never felt like the whole story.
I grew up with my mom, who was adopted and didn&#8217;t know her background. I look like her; she&#8217;s brownish too. I always had my mom for reference, and while I didn&#8217;t know my dad, I didn&#8217;t think a lot about why I look the way I do. Still, as a brown girl in Oklahoma, there were times when I noticed I was the only nonwhite person at a roller-skating rink or food court.
Some mixed people feel they&#8217;ve lived a black experience in America. President Obama, who is mixed-race, once said:
&#8220;I self-identify as African American–that&#8217;s how I&#8217;m treated and that&#8217;s how I&#8217;m viewed. I&#8217;m proud of it.&#8221;

In many ways, I identify. At times I&#8217;ve also gotten the feeling that people are assuming something about me, trying to place me. I get it–skin tone isn&#8217;t an easy thing to sort out. (And if anyone should understand skin tone, it&#8217;s me: I&#8217;m a beauty editor. I&#8217;ve worked on stories about how hard it is for women of color to find their true foundation shade, a frustration I&#8217;ve experienced firsthand.)
When it comes to people&#8217;s curiosity, this awareness of my skin tone, I&#8217;ve heard it all. The conversation usually goes like this:


&#8220;Where are you from?&#8221;


&#8220;Oklahoma.&#8221;
&#8220;No, but where are your parents from?&#8221; People seem unsatisfied when I say my parents are also from Oklahoma; perhaps they&#8217;re expecting something more &#8220;exotic.&#8221;
By the time I was in my twenties, my response to the question took on a &#8220;Sorry, can&#8217;t help you&#8221; tone. A friend joked that when a group of people looked at me for a little too long, they were playing Guess Her Race. What I never admitted was that I was playing the same game. My biggest insecurity was that I didn&#8217;t have the answer.

<h6>
Checking the Box–or Not</h6>

When I applied for college in 2002, I had to state my race. On the application there were six options, and I was instructed to choose one: Caucasian, African American, Hispanic, Native American, Asian, or Other. I identified with a few of these, but not fully enough that I felt I could legitimately tick only one, so I checked &#8220;Other,&#8221; then wrote &#8220;See essay&#8221; next to it. I wrote honestly about how it felt not to know, and then to have to choose an option as faceless as &#8220;Other.&#8221; For better or for worse, my identity could not be contained in a box.
I finally met my dad and his side of the family a few years later. In them I found a loving group of people–siblings, aunts, uncles, cousins–who embraced me. I also found out more about my ancestry. It turns out his side of the family is part German and part Native American, though if you saw my dad walking down the street, you&#8217;d probably think, White guy. I was so happy to connect and learn more about myself and my family, but I still couldn&#8217;t relate it to the tone of my skin.
Then I moved to New York City, a place where everyone on the subway looks like they&#8217;re from somewhere else. I still got the question, but now people took the liberty of telling me what they thought I was: &#8220;You look Egyptian&#8230; Brazilian&#8230; Dominican&#8230;.&#8221;
&#8220;I&#8217;m not sure,&#8221; I&#8217;d say with a smile. This was the way I lived my life–I&#8217;d become seemingly comfortable with the unknown.
And then the impossible happened. A year ago, after a lifetime of near misses, my mother met her birth mother. Here, I thought, was the missing link to what I was, and maybe, finally, an answer. My maternal grandmother, I discovered, is Irish and part Native American. But, frustratingly, there were few clues about my mom&#8217;s birth father, my grandfather–a man who doesn&#8217;t look that brown in the one black-and-white photo I&#8217;ve seen. I still didn&#8217;t feel any closer to understanding why I&#8217;m this color.

<h5>
Time to Turn to Science</h5>

Then, last spring, I learned that Henry Louis Gates Jr., Ph.D., would be speaking in New York, and I knew I had to hear him. With his PBS show, Finding Your Roots, this pioneer in ancestry research has helped many celebrities trace their backgrounds. He&#8217;s also a proponent of genetic testing kits like 23andMe, now easily available online.
At the end of the lecture, I introduced myself to Gates and mentioned that I was from Oklahoma. His response:
&#8220;I was going to say you look Native American.&#8221;
My heart sank.
Here I was in this room, with a lot of other black people, and didn&#8217;t look black to Henry Louis Gates Jr., one of our nation&#8217;s foremost experts on race. I ordered a 23andMe kit the next day. I had to know.
The kit costs $99 and is simple to use. You spit (a good amount) into a plastic vial, close it up, and send it off. It takes about three weeks to get your ancestry reports. The wait felt like an eternity.
When the email arrived, I was with two of my best friends, Rightor and Elizabeth. I held up my phone, pointing to the message that would reveal my race, my identity, my everything.
They went silent.


When I&#8217;d dispatched my kit, it had never occurred to me that I might not be ready to receive this information. Now I realized: I didn&#8217;t want to open the email–not yet. Suddenly, certainty didn&#8217;t seem so exciting.
Rightor whispered, &#8220;I do still hope you&#8217;re part black. You&#8217;re our half-black friend.&#8221;
We all laughed. I&#8217;d gotten used to being the brown friend among white friends. Now this message had the power to change my idea of myself.
I had taken the test last June, in a time we could call pre-Ferguson, pre-Eric Garner, two tragedies that drastically shifted the conversation around race in our country. Now, as the email waited in my inbox, I watched what felt like injustice on repeat. I kept asking myself, Where do I fit in?
When I went to the Millions March NYC protest in December, I stood shoulder to shoulder with blacks, whites, Asians, Hispanics. Still, I wondered: What am I, here in this crowd? One of the oppressed? An empathizer? An outsider?
I realized that while I&#8217;d been searching for the answer to what I was, I&#8217;d also been looking for affirmation of the black part of me. I wanted to belong to that group because I did identify myself in that way. But what if technically, genetically, I didn&#8217;t belong? I was scared to find out.
The test results sat in my inbox for months. Then, one day, it hit me: I could know or not know. Live my life being safe, like I&#8217;ve always done, or take this leap. I was searching for answers, but did I actually want to hear them? I hadn&#8217;t been ready before; now all of a sudden, for some reason, I was.
My hands shaking, I opened the message. A map of the world popped up, indicating I had roots all over. Almost every continent was highlighted in a bright color.
The cold, hard science, the letter told me, was this: I was 67.8 percent European and just 2.9 percent West African; about a third of my DNA was labeled &#8220;unassigned.&#8221;
I had a moment of feeling, What the f&#8211;k? I&#8217;d waited 30 years only to find out that a good chunk of me was still a mystery, even to a genetic-testing company?
I read further. As it happens, DNA that traces from multiple continents is labeled &#8220;unassigned.&#8221; I also learned that Native American DNA is hard to test for, since there are few reference populations available to provide samples. (The Native American sample pool used for my analysis is smaller than the European samples.) With a good portion of my genetic makeup still unknown (mostly the not-white portion, it seemed), I went to bed feeling hollow.
When I started this process, my initial excitement had been clouded by a thought: More actual facts about my history might close off the possibility that I could be black, Brazilian, Dominican, fill in the blank.
All my life there&#8217;s been a chance that I could be a lot of things, and I&#8217;ve embraced that. Feeling unattached to groups and hard to categorize had become the most defining part of me. Not having a fixed identity had become my identity.
The day after I opened the email, I went through my morning, still feeling disappointed. As I crossed the street, a black man passed me on the left. At the same time a white woman came toward me on my right. For the first time in my life, it flipped for me: Before, I wasn&#8217;t sure which one would have thought I was part of their culture, what they would have called me. But in that moment, I saw parts of myself in both of them–I could identify with each one and, for that matter, whomever I wanted.


I flashed back to the Millions March, to all the faces on the New York City subway, to that sixth-grade girl looking in the bathroom mirror. What I had been seeing were just skin tones. I&#8217;d spent so much time trying to understand my own color, but as it turned out, there was something empowering about the fact that I didn&#8217;t have to take ownership of any particular race. I realized: I could be what I was by being who I was. My search led me to my father&#8217;s family, whom I adore, and to my mother&#8217;s family, whom I&#8217;m getting to know–and, most important, to myself. The daughter I am, the sister I am, the friend I am.
This is who I am. No email could ever change that.
The next time someone asks what I am, my response will be ready:
&#8220;I&#8217;m Simone. What are you?&#8221;


Simone Kitchens, Glamour&#8217;s deputy beauty editor, lives in Brooklyn.

Simone Kitchens

I’m Simone

A new study involving participants in <a href="https://www.23andme.com/pd/" target="_blank" rel="noopener noreferrer">23andMe’s Parkinson’s Disease Community,</a> offers hope for the future of telemedicine and the ability of clinicians to quickly and accurately assess and recruit patients for research and clinical trials. 
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-22634" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/Parkinsons-Research-Community-300x112.jpg" alt="Parkinson's Research Community" width="300" height="112" />


This is particularly good news for patients far removed from medical research hubs or who have a debilitating condition, like Parkinson’s, that can make travel difficult if not impossible.
Lead author of the paper, <a href="https://www.urmc.rochester.edu/people/26764214-e-ray-dorsey/researchers" target="_blank" rel="noopener noreferrer">Ray Dorsey at University of Rochester</a>, said he has always been optimistic regarding the effectiveness of telemedicine and self-assessment, but he was pleasantly surprised by how well it worked in this study.


While studies have looked at “remote assessment” for clinical evaluations or probed the ability of people to self-assess their symptoms using such tools as 23andMe’s self-reported data, <a href="http://dhj.sagepub.com/content/1/2055207615592998" target="_blank" rel="noopener noreferrer">this study</a>, published in the journal Digital Health, looks at both. 
23andMe has the world’s largest cohort of genotyped Parkinson’s patients and depends in part on self-assessment in collecting data for research.
Although it was a small study, the work offers a glimpse at how these two important processes – self-assessment and remote assessment – could work together to streamline recruitment for research, making it more affordable, faster and less onerous on participants. More than three-quarters of participants in this study completed a post-assessment survey, and 87 percent said they would be more or much more willing to participate in future clinical trials if they could do it remotely.
<img loading="lazy" decoding="async" class="alignright wp-image-22641 size-medium" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/@PITER-23andMe-EmilyDrabant-19-200x300.jpg" alt="@PITER-23andMe-EmilyDrabant-19" width="200" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/06/@PITER-23andMe-EmilyDrabant-19-200x300.jpg 200w, https://blogcms.23andme.com/wp-content/uploads/2015/06/@PITER-23andMe-EmilyDrabant-19-768x1152.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/06/@PITER-23andMe-EmilyDrabant-19-683x1024.jpg 683w, https://blogcms.23andme.com/wp-content/uploads/2015/06/@PITER-23andMe-EmilyDrabant-19-587x880.jpg 587w, https://blogcms.23andme.com/wp-content/uploads/2015/06/@PITER-23andMe-EmilyDrabant-19-787x1180.jpg 787w, https://blogcms.23andme.com/wp-content/uploads/2015/06/@PITER-23andMe-EmilyDrabant-19-scaled.jpg 1707w" sizes="auto, (max-width: 200px) 100vw, 200px" />
“This approach lays the foundation for larger scale, broader scope studies that can target genetic sub-populations of different disorders and foster partnerships between consumer genetics companies, pharmaceutical firms, academic institutions, and patient communities,” according to the paper.
Co-author Emily Drabant Conley, PhD, director of 23andMe’s business development, said this study offers a test case for some of the work 23andMe has already been doing in certain disease communities. Emily, who spent several years working directly with the Parkinson’s community, said she’s most excited by how this approach could be applied to other conditions being studied by 23andMe researchers.
“This study extends these disruptive models for clinical research,” Emily said. “It lays the foundation for expanding participation in clinical research by leveraging genotype data for patient selection and remote assessment to make participation more convenient.”

Virtual doctor’s visit and genetic testing for Parkinson’s disease

Consider the cow, and this humble herbivore’s contribution to the human story.<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/dairy-cow-300x200.jpg" alt="dairy cow" class="alignright size-medium wp-image-22620" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/06/dairy-cow-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2015/06/dairy-cow-768x511.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/06/dairy-cow.jpg 849w" sizes="auto, (max-width: 300px) 100vw, 300px" />


We’re not just talking burgers and ice cream, archeological evidence suggests that cows were likely first domesticated from aurochs (extinct wild oxen) as long as 11,000 years ago when farmers used their milk to <a href="https://www.npr.org/sections/thesalt/2012/12/27/168144785/an-evolutionary-whodunit-how-did-humans-develop-lactose-tolerance" target="_blank" rel="noopener noreferrer">make cheese</a> and yogurt.
Nutrient-rich with plenty of vitamin D for the sun-starved in Northern Europe, milk was a kind of superfood of the Bronze Age.
But <a href="https://www.nature.com/news/dna-data-explosion-lights-up-the-bronze-age-1.17723" target="_blank" rel="noopener noreferrer">new research</a> suggests that it took a long time before Europeans could actually benefit from this potent potable.
Looking at DNA samples from the remains for more than 100 individuals who lived in Eurasia from 3,000 to 5,000 years ago, researchers in Norway found that it took a surprisingly long time before Europeans could tolerate milk.
The study looked at much more than whether those early Europeans could tolerate dairy, and focused more broadly on a wide variety of physical and physiological traits including hair thickness, height and skin color.
But the DNA samples indicate that those early Europeans were mostly lactose intolerant, suggesting that even though they had domesticated cows at the time they were unable to digest raw milk as adults. The exception appears to be among the Yamnaya, a group of people who migrated into Northern Europe from an area near the Altai Mountains in what is now central Russia. Researchers speculate that natural selection favored this trait, giving those with it a rich source of nutrition that could sustained them during times of famine when harvests failed. 
 
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/milk-287x300.jpg" alt="Glass of milk isolated on white. Vector illustration" class="alignright size-medium wp-image-22621" width="287" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/06/milk-287x300.jpg 287w, https://blogcms.23andme.com/wp-content/uploads/2015/06/milk-768x802.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2015/06/milk-980x1024.jpg 980w, https://blogcms.23andme.com/wp-content/uploads/2015/06/milk-843x880.jpg 843w, https://blogcms.23andme.com/wp-content/uploads/2015/06/milk-1130x1180.jpg 1130w" sizes="auto, (max-width: 287px) 100vw, 287px" />

<h5>
Intolerant, even today 
</h5>

Most people are actually lactose intolerant as adults. Only about <a href="https://www.sciencedirect.com/science/article/pii/S0958694611002536" target="_blank" rel="noopener noreferrer">35 percent of people worldwide</a> can digest lactose beyond the age of about seven or eight.
The numbers tell a deeper story when demographically divided. While the majority of people of European ancestry <a href="https://www.nature.com/news/archaeology-the-milk-revolution-1.13471" target="_blank" rel="noopener noreferrer">can tolerate milk</a> into adulthood, only a small minority of people of Asian ancestry can. Among 23andMe customers who consented to research only about 16 percent of those of European ancestry reported that they were <a href="https://www.23andme.com/topics/wellness/lactose-intolerance/">lactose intolerant</a> compared to about 85 percent of people of Asian ancestry.

<h5>
So what gives? 
</h5>

There are a number of <a href="https://www.npr.org/sections/thesalt/2012/12/27/168144785/an-evolutionary-whodunit-how-did-humans-develop-lactose-tolerance" target="_blank" rel="noopener noreferrer">theories</a> about why there are differences among people of different ancestry, and a recent study of ancient Northern European DNA suggests the ability to digest dairy is a relatively new phenomena.
Drinking milk is a problem for most adults. It contains high amounts of a sugar named lactose. As children, we all produce lactase, an enzyme that allows us to break up lactose in our mother&#8217;s milk. As we grow older lactase levels go down, making it harder for adults to breakdown the lactose sugars and causing gastrointestinal &#8220;discomfort.&#8221;
In populations with domesticated cattle, however, there may have been an evolutionary incentive to being able to drink milk as adults and several populations – including populations in Northern Europe – developed genetic variants that enabled adults to continue to breakdown lactose into adulthood. This genetic variant offered a likely evolutionary advantage because milk is nutrient rich, plentiful, and cleaner than many sources of water. In times of famine it offered an alternative source of food for those who could tolerate it.


In the book 10,000 Year Explosion: How Civilization Accelerated Human Evolution, anthropologists Gregory Cochran and Henry Harpending called humans with this variant “<a href="https://westhunt.wordpress.com/2012/10/23/mampires/" target="_blank" rel="noopener noreferrer">mampires</a>,” because it allowed people to feed on the milk of other animals. It’s a clever term, but maybe with a little darker connotations than necessary. As the anthropologist <a href="http://johnhawks.net/weblog/reviews/accel/question-on-selection-and-lactase-2014.html" target="_blank" rel="noopener noreferrer">John Hawkes noted</a> in his blog, milk from domesticated animals is a much more efficient use of farm animals than raising them for meat. In places in Europe, Arabia and in parts of Africa where cold or arid climates made consistent yields from farming grain difficult, milk was a good alternative source of nutrition.

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