The annual meeting of the American Society of Human Genetics kicks off in Orlando this October, <img loading="lazy" decoding="async" class="alignright wp-image-25526 size-medium" src="https://blog-api.23andme.com/wp-content/uploads/2017/06/Logo_with_Register_CMYK-1-300x196.jpg" alt="" width="300" height="196" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/06/Logo_with_Register_CMYK-1-300x196.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2017/06/Logo_with_Register_CMYK-1.jpg 400w" sizes="auto, (max-width: 300px) 100vw, 300px" />packed with five days of seminars, panel discussions, talks, and presentations that are all part of an event that might best be described as the Coachella (or Woodstock if you prefer) of genetics.
This year&#8217;s main event, the “Presidential Symposium,” will be a conversation on global health issues with Microsoft co-founder<a href="https://www.gatesfoundation.org/Who-We-Are/General-Information/Leadership/Executive-Leadership-Team/Bill-Gates"> Bill Gates</a>, who now co-chairs the Bill &amp; Melinda Gates Foundation, and<a href="https://www.nih.gov/about-nih/who-we-are/nih-director/biographical-sketch-francis-s-collins-md-phd"> Francis Collins</a>, the director of the National Institutes of Health.
But highlighting just one of the hundreds of talks during the week risks ignoring dozens of equally arresting subjects that will be part of this yearly event—gene editing, genetic education, and a slew of new genetic research.
Like in past years, 23andMe’s research team and its research will be well represented, but we’ll also be hosting a workshop about our research collaborations and <a href="https://twitter.com/23andmeresearch">live-tweeting from the meeting</a>. We have a few fun surprises while we’re in Orlando.
Here is a list of 23andMe’s involvement at ASHG:
<h5>Educational Event</h5>
GWAS and Beyond: Academic Collaborations with 23andMe
<img loading="lazy" decoding="async" class="alignright wp-image-25740 size-thumbnail" src="http://35.88.189.111/wp-content/uploads/2017/09/©Piter2016-23andMe-AdamAuton-066-150x150.jpg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/09/©Piter2016-23andMe-AdamAuton-066-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2017/09/©Piter2016-23andMe-AdamAuton-066-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2017/09/©Piter2016-23andMe-AdamAuton-066-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2017/09/©Piter2016-23andMe-AdamAuton-066-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2017/09/©Piter2016-23andMe-AdamAuton-066-980x980.jpg 980w" sizes="auto, (max-width: 150px) 100vw, 150px" />
<ul>
<li>Adam Auton, D.Phil. (23andMe): Introduction to 23andMe research and collaborations</li>
<li><a href="http://www.mrc-epid.cam.ac.uk/people/john-perry/">John Perry</a>, Ph.D. (University of Cambridge): Using population genetics to understand the etiology of reproductive health and biological aging</li>
<li><a href="https://web.stanford.edu/~alicesw/">Alice S. Whittemore</a>, Ph.D. and Nilah Monnier Ioannidis, Ph.D. (Stanford University): Collaborations with 23andMe on the genetic basis of cutaneous squamous cell cancer (cSCC)</li>
<li>Time: Oct. 18, 12:30 pm &#8211; 1:45 pm</li>
<li>Location: Lake Eola &#8211; Lobby Level/Hilton Orlando Hotel</li>
</ul>
<h5>Talks</h5>
Large-scale identity-by-descent mapping discovers rare haplotypes of large effect
<img loading="lazy" decoding="async" class="alignright wp-image-25741 size-thumbnail" src="http://35.88.189.111/wp-content/uploads/2017/09/Suyash-Shringapure-150x150.jpg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/09/Suyash-Shringapure-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2017/09/Suyash-Shringapure-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2017/09/Suyash-Shringapure-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2017/09/Suyash-Shringapure-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2017/09/Suyash-Shringapure-980x980.jpg 980w" sizes="auto, (max-width: 150px) 100vw, 150px" />
<ul>
<li>Presenter: Suyash Shringarpure, Ph.D., Senior Statistical Geneticist</li>
<li>Author(s): S. Shringarpure; D. Hinds; V. Vacic; 23andMe Research Team</li>
<li>Time: Oct. 19, 10:15 am – 10:30 am</li>
<li>Location: Room 330A &#8211; Level 3/Convention Center</li>
</ul>
GWAS of canker sores implicates Th-1 pathway and shared genetic architecture with immune-mediated disease
<img loading="lazy" decoding="async" class="alignright wp-image-25500 size-thumbnail" src="http://35.88.189.111/wp-content/uploads/2017/06/FahSathirapongsasuti-Preferred-150x150.jpg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/06/FahSathirapongsasuti-Preferred-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2017/06/FahSathirapongsasuti-Preferred-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2017/06/FahSathirapongsasuti-Preferred-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2017/06/FahSathirapongsasuti-Preferred-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2017/06/FahSathirapongsasuti-Preferred-980x980.jpg 980w" sizes="auto, (max-width: 150px) 100vw, 150px" />
<ul>
<li>Presenter: Fah Sathirapongsasuti, Ph.D., Senior Computational Biologist</li>
<li>Author(s): F. Sathirapongsasuti; S. Pitts; D. Hinds; V. Vacic; R. Gentleman; the 23andMe Research Team</li>
<li>Time: Oct. 19, 11:45 am – 12 pm</li>
<li>Location: Room 220F &#8211; Level2/Convention Center</li>
</ul>
<h5>Posters</h5>
All posters can be found in the Exhibit Hall on Level 1 of the Convention Center
Tipping the scales: Participants make healthy dietary changes in response to direct-to-consumer genetic test results
<img loading="lazy" decoding="async" class="alignright wp-image-25742 size-thumbnail" src="http://35.88.189.111/wp-content/uploads/2017/09/sarah-photo-150x150.jpg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/09/sarah-photo-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2017/09/sarah-photo-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2017/09/sarah-photo-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2017/09/sarah-photo-574x574.jpg 574w" sizes="auto, (max-width: 150px) 100vw, 150px" />
<ul>
<li>Presenter: Sarah Laskey, Ph.D., Health R&amp;D Scientist</li>
<li>Author(s): S.B. Laskey; J.F. Shelton; M. Johnson; C. Wilson; R. Smith; B.L. Koelsch; The 23andMe Research Team</li>
<li>Time: Oct. 18, 3pm &#8211; 4 pm</li>
</ul>
Clonal Hematopoiesis: genetic and phenotypic associations in the general population
<div id="attachment_20934" style="width: 160px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-20934" class="wp-image-20934 size-thumbnail" src="http://35.88.189.111/wp-content/uploads/2014/05/Chao-Square-Photo-150x150.jpeg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-150x150.jpeg 150w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-300x300.jpeg 300w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-768x769.jpeg 768w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-1024x1024.jpeg 1024w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-880x880.jpeg 880w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-1180x1180.jpeg 1180w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-271x271.jpeg 271w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-372x372.jpeg 372w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-574x574.jpeg 574w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-980x980.jpeg 980w" sizes="auto, (max-width: 150px) 100vw, 150px" />Chao Tian</div>
<ul>
<li>Presenter: Chao Tian, Ph.D., Senior Statistical Geneticist</li>
<li>Author(s): C. Tian; P. Fontanillas; J. Tung; D. Hinds; the 23andMe Research Team</li>
<li>Time: Oct. 18, 3 pm – 4 pm</li>
</ul>
Minds, genes, and machines: Performance on online cognitive assessments is correlated with individual characteristics in 23andMe customers
<img loading="lazy" decoding="async" class="wp-image-25743 size-thumbnail alignright" src="https://blog-api.23andme.com/wp-content/uploads/2017/09/OlgaSazonova-preferred-150x150.jpg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/09/OlgaSazonova-preferred-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2017/09/OlgaSazonova-preferred-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2017/09/OlgaSazonova-preferred-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2017/09/OlgaSazonova-preferred-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2017/09/OlgaSazonova-preferred-980x980.jpg 980w" sizes="auto, (max-width: 150px) 100vw, 150px" />
<ul>
<li>Presenter: Olga Sazonova, Ph.D., Senior Computational Biologist</li>
<li>Author(s): O.V. Sazonova; L. Germine; C. Wilson; P. Fontanillas; C.E. Carey; 23andMe Research Team</li>
<li>Time: Oct. 19, 2 pm – 3 pm</li>
</ul>
A web-based initiative to accelerate research on African ancestry in the Americas
<img loading="lazy" decoding="async" class="alignright wp-image-25744 size-thumbnail" src="https://blog-api.23andme.com/wp-content/uploads/2017/09/@PITER-23andMe-MeganMullins-39-copy-150x150.jpg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/09/@PITER-23andMe-MeganMullins-39-copy-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2017/09/@PITER-23andMe-MeganMullins-39-copy-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2017/09/@PITER-23andMe-MeganMullins-39-copy-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2017/09/@PITER-23andMe-MeganMullins-39-copy-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2017/09/@PITER-23andMe-MeganMullins-39-copy-980x980.jpg 980w" sizes="auto, (max-width: 150px) 100vw, 150px" />
<ul>
<li>Presenter: Meghan Moreno, Project Manager</li>
<li>Author(s): M.E. Moreno; K. Bryc; P.K. Penton; R. Rubenstein; L. Vermillion; J.L. Mountain; the 23andMe Research Team</li>
<li>Time: Oct. 20, 12:30 pm – 1:30 pm</li>
</ul>
Human knockouts in the Ashkenazi Jewish population
<img loading="lazy" decoding="async" class="alignright wp-image-25749 size-thumbnail" src="https://blog-api.23andme.com/wp-content/uploads/2017/09/aaron-150x150.jpg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/09/aaron-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2017/09/aaron-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2017/09/aaron-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2017/09/aaron-574x574.jpg 574w" sizes="auto, (max-width: 150px) 100vw, 150px" />
<ul>
<li>Presenter: Aaron Kleinman, Ph.D., Senior Computational Biologist</li>
<li>Author(s): A. Kleinman; O. Sazonova; S. Pitts; V. Vacic; R. Gentleman; the 23andMe Research Team</li>
<li>Time: Oct. 20, 12:30 pm – 1:30 pm</li>
</ul>

23andMe Blog

23andMe Blog Team

23andMe At ASHG 2017

Maybe the gap between the Greatest Generation and Generation Z, or the chasm between Baby Boomers and Gen X, isn’t a divide at all; perhaps we just haven’t had the right tools to see the thread that connects us, a thread woven into our very DNA.
October is Family History Month, a time to reflect on where we come from and all those who came before us. 23andMe offers people a different way to learn about themselves and their families, giving families an opportunity to see the DNA they share across generations.
23andMe’s newest tool, GrandTree, allows families to connect deeper across three generations, letting them see the thread that ties grandchildren to their grandparents. 
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2017/10/GrandTree-1024x705.jpg" alt="" class="aligncenter size-large wp-image-25777" width="1024" height="705" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree-1024x705.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree-300x207.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree-768x529.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree-880x606.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree-1180x812.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree.jpg 1188w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />If a grandchild, and a grandparent are 23andMe customers, and they are sharing their 23andMe results with each other, GrandTree allows them to see more than just the percentage of DNA that they share. It also allows customers the chance to trace a trait through generations. Showing if a grandchild got their red hair largely  from one grandparent or another, for instance. If a grandparent or grandchild hasn’t yet tested, 23andMe makes it easy for customers to invite them to sign up.
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2017/10/GrandTree-2-1024x723.jpg" alt="" class="aligncenter size-large wp-image-25776" width="1024" height="723" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree-2-1024x723.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree-2-300x212.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree-2-768x542.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree-2-880x621.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree-2.jpg 1082w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />Looking at DNA offers a unique way to connect across generational lines, and the GrandTree tool is just one of many features  23andMe has to do that. Customers can also use 23andMe’s Share and Compare feature to see what traits and ancestry they share with a brother or sister, or their parents, or children. You can even see the overlapping segments on each chromosome that you share. You can go deeper by using the DNA Relatives tool to do something similar but also compare yourself with a parent, grandparent, child, (or anyone you share with), and see detailed segment data.
Beyond that 23andMe’s Ancestry Composition feature, which highlights the mix of places where your ancestors came from, includes a feature that allows you to compare your DNA to your parents’ — if they are using 23andMe — and see a “split view” of what ancestry came from your mother and what came from your father.
When families use 23andMe together, they connect in a different way, tracing the thread of traits, and ancestry, that links child to parent and grandparent, bridging the gap between each generation.
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2017/10/GrandTree3-1024x751.jpg" alt="" class="aligncenter size-large wp-image-25775" width="1024" height="751" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree3-1024x751.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree3-300x220.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree3-768x563.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree3-880x645.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2017/10/GrandTree3.jpg 1042w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />

Connecting Generations with 23andMe’s GrandTree

Participants in the 23andMe Parkinson’s disease research initiative have contributed a vast amount of data, that has enabled our researchers and <img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/Brain-Logo-287x300.jpg" alt="" class="alignright size-medium wp-image-22635" width="287" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/06/Brain-Logo-287x300.jpg 287w, https://blogcms.23andme.com/wp-content/uploads/2015/06/Brain-Logo.jpg 438w" sizes="auto, (max-width: 287px) 100vw, 287px" />collaborators to improve our understanding of the genetics of Parkinson’s. But we want to do even more to maximize the use of this data. 
Through ongoing collaborations with The <a href="https://www.michaeljfox.org/">Michael J. Fox Foundation for Parkinson’s Research</a> (MJFF), 23andMe is working with the Parkinson&#8217;s disease community, piloting novel ways to collect and analyze data and advancing genetic research in Parkinson&#8217;s disease.
Part of that work entails supporting a postdoctoral researcher at 23andMe, Karl Heilbron, who is analyzing this extensive data set. We have previously reported on some of <a href="https://blog.23andme.com/23andme-research/parkinsons-research-community-update/">Karl’s work</a>. This summer he presented his findings related to novel traits associated with Parkinson’s disease at first ever Gordon Research Seminar dedicated to the disease. The <a href="https://blog-api.23andme.com/wp-content/uploads/2017/10/Karl.jpg">poster</a> was well received and we were happy when Karl was selected to give an oral presentation on his data.
23andMe also worked with MJFF to invite Parkinson’s researchers from around the world, to submit proposals for collaborations with 23andMe. We contacted more than 12,000 researchers and received a significant number of high quality and innovative proposals. Through an exhaustive review process, we have identified the top four proposals regarding technical feasibility and potential impact. We will feature details of these in upcoming blog posts. 
<div id="attachment_24396" style="width: 209px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-24396" src="https://blog-api.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-199x300.jpg" alt="" class="wp-image-24396 size-medium" width="199" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-199x300.jpg 199w, https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-768x1156.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-680x1024.jpg 680w, https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-585x880.jpg 585w, https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-784x1180.jpg 784w, https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-scaled.jpg 1701w" sizes="auto, (max-width: 199px) 100vw, 199px" />Karl Heilbron</div>
<h5>New data projects</h5>
Off-label drug use survey
In medicine, doctors sometimes prescribe treatment for a condition with a drug that has already been FDA-approved to treat a different disease or symptom. This practice is called ‘off-label’ drug use, and there is little information on how common it is in the treatment of Parkinson’s disease. To find out, researchers here at 23andMe collaborated with MJFF and The Cure for Parkinson’s Trust to create a new off-label drug use survey to address this question.
Although off-label drug use is practiced in medicine, little is known about the safety and effectiveness of drugs in unapproved indications. The survey is not an endorsement of off-label drug use, but instead, an effort to learn more how common it is for the treatment of Parkinson’s. 23andMe encourages individuals with Parkinson’s to talk with their physicians regarding treatment decisions. 
As part of this effort, 23andMe sent an email to participants in the Parkinson’s Disease Research Initiative asking them to take the off-label drug surveys. Respondents were presented with a list of potential off-label medications; exenatide, isradipine, metformin, nicotine patch, nilotinib, and statins, many of which are currently or were recently in clinical trials for Parkinson’s, as well as an “other” free text option. Interpretation of the results is complicated by the fact that many of these drugs are approved for conditions that are also common in those with Parkinson’s, such as type-2 diabetes, high cholesterol, and high blood pressure. We found that 21 of the 1,325 participants (one to two percent), reported that they were prescribed isradipine off-label. None of the other drugs were prescribed off-label to more than a handful of participants if any at all. It’s important to note that we have no information regarding any benefits or side-effects relating to the off-label drugs, or even whether the individuals ever took or are still taking the drugs.&nbsp;&nbsp; &nbsp;
Medical records pilot
Online survey questions continue to be the core of our data collection methods. However, we are always interested in new and different sources of data to add to our research. 
With the recent proliferation of electronic medical record systems, we wanted to determine if these records could be a valuable new source of data for Parkinson’s research. In particular, we’re interested in discovering factors that influence the progression of the disease. A traditional approach to studying this would be to enroll people with Parkinson’s disease in a longitudinal study where they would be asked to complete baseline and periodic (e.g., every three months) follow-up surveys to assess changes in the progression of their Parkinson’s symptoms. 
Many individuals with Parkinson’s disease progress relatively slowly, especially in the early stages. This means that it can be a significant challenge to keep participants engaged in such studies for long enough to see substantial changes in their symptoms. We want to explore whether disease assessments in medical records would allow us to access the same information, but looking backward in time. 
To address this, we recruited approximately 200 participants with Parkinson’s disease who were willing to have us retrieve and analyze their medical records. These participants were assigned to one of two companies that specialize in the retrieving and anonymizing electronic medical records. The companies retrieved and anonymized the records, then mined them for information that we deemed points of interest. So what did we find? &nbsp;&nbsp; 
 &nbsp;&nbsp;
<ul>
<li> Almost all of the participants saw a specialist for management of their Parkinson’s.</li>
<li> The format and content of the medical records were highly variable, as was the number of visits per year.</li>
<li> The most consistently reported data was self-reported data, which can often be more easily recorded by online surveys.</li>
<li> Rating scales for Parkinson’s — the Unified Parkinson Disease Rating Scale (UPDRS) — were rarely and inconsistently included in the records, and, even when present the scores were variably reported. More frequently records had Hoehn and Yahr scores for Parkinson’s, but still insufficient to provide any data on progression. 
</li>
</ul>
In conclusion, the two vendors were able to retrieve records for most of the participants, but the data contained therein were too variable and inconsistent to be of any value for research, especially regarding progression.
Many thanks to all of the 23andMe Parkinson’s disease research initiative participants who contributed to the work!

Update on 23andMe Parkinson’s disease research

Whether we want to be or not, we’re all on a clock — a biological one that ticks off a 24 hour day and regulates our waking and sleep cycle.<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2017/10/iStock-640228980-300x200.jpg" alt="" class="alignright size-medium wp-image-25757" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/10/iStock-640228980-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2017/10/iStock-640228980-768x513.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2017/10/iStock-640228980-1024x683.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2017/10/iStock-640228980-880x587.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2017/10/iStock-640228980-1180x788.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2017/10/iStock-640228980.jpg 1254w" sizes="auto, (max-width: 300px) 100vw, 300px" />
With a nod to the importance of our inner Timex, the Nobel Committee recognized this week the pioneering work of a trio of American scientists —<a href="http://www.bio.brandeis.edu/faculty/hall.html"> Jeffrey C. Hall</a>,<a href="http://www.bio.brandeis.edu/faculty/rosbash.html"> Michael Rosbash</a>, and<a href="https://www.rockefeller.edu/our-scientists/heads-of-laboratories/914-michael-w-young/"> Michael W. Young</a> — that first uncovered the genetic basis of that circadian rhythm.
Studying sleep cycles in fruit flies, the three researchers led teams that identified the key genes that regulate the level of specific proteins that control our active hours and sleep cycles.
“(They) were able to peek inside our biological clock and elucidate its inner workings,”<a href="https://www.nobelprize.org/nobel_prizes/medicine/laureates/2017/press.html"> said</a> Thomas Perlmann, the secretary of the Nobel Committee for Physiology or Medicine. “Their discoveries explain how plants, animals, and humans adapt their biological rhythm so that it is synchronized with the Earth’s revolutions.”

The importance of sleep in health is well established, but researchers are still building on the breakthroughs from Hall, Rosbash and Young to learn more.
A few years ago, 23andMe researchers completed a genome wide association study that uncovered 15 genetic variants associated with being a<a href="https://www.nature.com/articles/ncomms10448#results"> morning person</a>. Some of the variants were in newly associated genes, but others were in genes with well-established influence on circadian rhythms, such as PER2. This PER (or “period”) gene was originally identified in the Nobel winners’ work. Despite fruit flies not looking like our closest cousins, circadian rhythm is such an essential trait for living things that basic research in model organisms helps us learn more about human health. (The workhorse, as it were, of genetic research is a small fruit fly called the drosophila, which is also happens to be the name of one of the meeting rooms at 23andMe HQ.) 
Beyond the genetic associations with sleep cycles, our genes also influence how deeply we sleep and whether or not we fidget the night away.
23andMe has two reports, looking at how variants in two genes— BTBD9 and ADA — may influence your ability to drift off into a deep sleep, and how likely you are to move about while you slumber. If you’re a customer you can see your <a href="https://www.23andme.com/topics/wellness/deep-sleep">Deep Sleep report</a> here, and your report on <a href="https://www.23andme.com/topics/wellness/sleep-movement/">Sleep Movement</a> here.
No matter if you are an early riser or a night owl, a deep sleeper or a restless one, the right amount of sleep is important for your health.

Nobel Worthy Sleep Science

By Amick Boone
(Editor&#8217;s note 8/21/202: This post has been slightly edited from when it first published in 2017.) Seven-year-old Shilah Yin likes being different. She even likes it when people describe her hair — a thick frizzy blond mane that juts out at all angles — as looking like the wacky time-traveling scientist Doc Brown’s from Back to the Future. Luckily it’s one of her favorite movies.
<div id="attachment_25723" style="width: 310px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-25723" class="wp-image-25723 size-medium" src="http://35.88.189.111/wp-content/uploads/2017/09/Scalp_hair-uncombable_hair_syndrome-1-300x164.gif" alt="A case of uncombable hair syndrome" width="300" height="164" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/09/Scalp_hair-uncombable_hair_syndrome-1-300x164.gif 300w, https://blogcms.23andme.com/wp-content/uploads/2017/09/Scalp_hair-uncombable_hair_syndrome-1-271x149.gif 271w, https://blogcms.23andme.com/wp-content/uploads/2017/09/Scalp_hair-uncombable_hair_syndrome-1-372x204.gif 372w" sizes="auto, (max-width: 300px) 100vw, 300px" />Source: Cobb HK, Tiu AY. &#8220;A case of uncombable hair syndrome and global developmental delays.&#8221; International Journal of Case Reports and Images 2017;8(2):108–111. doi:10.5348/ijcri-201718-CR-10757</div>
Shilah has something called “uncombable hair syndrome.” It’s a real but rare genetic disorder affecting the hair shaft of the scalp characterized by silvery-blond or sometimes straw-colored hair that stands out from the scalp in a disorderly way and cannot be combed flat.
Stories published in <a href="https://www.today.com/health/uncombable-hair-syndrome-condition-gives-girl-unruly-mane-t114586">Today</a> and <a href="http://www.dailymail.co.uk/femail/article-4735506/Melbourne-schoolgirl-Unbrushable-Hair-Syndrome.html">Daily Mail</a> report that Shilah was born with brown hair, but a strawberry-blond fuzz began to appear when she was about three months old. From then on, it grew straight out from her scalp and became blonder.
Shilah says she’s special and unique, like a unicorn, and her family supports her positive attitude. They document her experience on Instagram to share how special Shilah is and to make others aware of the disorder.
<h2>A Rare Hair Disorder</h2>
Uncontrollable hair syndrome is specific to children, first appearing between three months and 12 years and usually improving or resolving by puberty.
The condition only affects a child’s scalp hair. While the amount of hair remains normal, it often grows slowly. Over time, the hair becomes progressively dry and turns silvery-blond or straw-colored, standing out and growing in different directions.
The first case of uncontrollable hair syndrome was reported in 1912, and in 1973, the syndrome was named &#8220;cheveux incoiffables&#8221; by doctors in France. In the 1980s, it also became known as “spun-glass hair.”
<div style="float: right; text-align: justified; width: 300px; background-color: #eee; padding: 15px; margin-left: 10px;">
<h3>Does 23andMe Test for Uncombable Hair Syndrome?</h3>
23andMe doesn’t report on the genes that cause uncombable hair syndrome, but we do report on genes that influence other hair traits.
23andMe offers customers reports on hair curliness, hair color, <a href="https://www.23andme.com/topics/traits/newborn-hair">newborn hair amount</a>, <a href="https://www.23andme.com/topics/traits/unibrow/">unibrow</a>, and widow’s peak. For men, we report on whether or not you’ve inherited genes that influence back hair, hair loss, or bald spots. <a href="https://www.23andme.com/dna-health-ancestry/">Learn more</a>.
</div>
<h2>How Genetics Contribute to Uncombable Hair Syndrome</h2>
According to the National Institutes of Health, the syndrome is caused by variants in the genes PADI3, TGM3, and TCHH. These three genes code for proteins involved in hair shaft formation. The syndrome appears to be inherited in an <a href="https://medlineplus.gov/ency/article/002052.htm">autosomal recessive</a> fashion, which means that if both parents are carriers, there is a 25 percent chance of their child inheriting both abnormal variants and, consequently, developing the syndrome. There is a 50 percent chance of a child inheriting only one abnormal gene and being a carrier. There is also a 25 percent chance of the child inheriting both normal variants.
These are the variants that researchers know about. Scientists also suspect that some cases of uncombable hair syndrome are caused by other genes that have not yet been identified. These could be inherited, by contrast, in an <a href="https://medlineplus.gov/ency/article/002049.htm">autosomal dominant </a>manner, meaning that having a variant in only one copy of the responsible gene in each cell is enough to cause the condition. When a person with a variant that causes an autosomal dominant condition has children, each child has a 50 percent (1 in 2) chance of inheriting the variant.
Many of these autosomal dominant cases may occur with “reduced penetrance,” which means that not all people with a variant in the responsible gene will have uncombable hair syndrome. With reduced penetrance, a condition may appear to “skip a generation” or may appear to occur for the first time, or only once, in a family.
<h2>Diagnosing Uncombable Hair Syndrome</h2>
People with uncombable hair syndrome often report that no one in their family has had it, and that may well be the case, from what they can see. However, hair shaft abnormalities associated with the syndrome have shown up in unaffected family members when they looked at their hair under a specific type of microscope.
The individual hair strands are either triangular or kidney-shaped in cross-section. The hair strands have a groove along one or two faces. To diagnose uncombable hair syndrome, doctors observe symptoms. They also look under a microscope for these characteristic hair strand qualities.
<h2>Is there Treatment for Uncombable Hair Syndrome?</h2>
Unfortunately, there is no proven treatment for the syndrome. However, the condition usually improves or resolves on its own with the onset of puberty. Gentle hair care is recommended using conditioners and soft brushes. It&#8217;s also recommended to avoid harsh hair treatments, excessive brushing, and blow-drying. Some published studies suggest that <a href="https://en.wikipedia.org/wiki/Biotin">biotin supplements</a> may improve the condition.
Shilah, for her part, loves her unruly hair. She especially likes it when her dad combs and dries. Together, they want to fluff it up as big as it can get.
Learn more about how genetics influences your hair color, curl, thickness, and texture <a href="https://www.23andme.com/topics/traits/hair-texture/">here</a>. 
Amick Boone is a freelance writer who has written about health and life sciences for over a decade.  When she&#8217;s not at her computer, she&#8217;s usually in motion &#8211; doing yoga, riding her bike or traveling.

Amick Boone

Understanding Uncombable Hair Syndrome

We all hunger for identity. It gives us a sense of belonging. But increasingly, traditional categories fall short. We are all more than just white or black, Latino or Asian. We need a better way to define ourselves. <img loading="lazy" decoding="async" class="alignright size-medium wp-image-25713" src="https://blog-api.23andme.com/wp-content/uploads/2017/09/media-2-300x300.png" alt="" width="300" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/09/media-2-300x300.png 300w, https://blogcms.23andme.com/wp-content/uploads/2017/09/media-2-150x150.png 150w, https://blogcms.23andme.com/wp-content/uploads/2017/09/media-2-271x271.png 271w, https://blogcms.23andme.com/wp-content/uploads/2017/09/media-2-372x372.png 372w, https://blogcms.23andme.com/wp-content/uploads/2017/09/media-2.png 377w" sizes="auto, (max-width: 300px) 100vw, 300px" /> 

<h2>Self Exploration</h2>
At the core of the <a href="https://www.23andme.com/" target="_blank" rel="noopener">23andMe</a> experience is self-exploration, giving people a chance to peer into their DNA to find that subtle, sometimes surprising, and even uncomfortable mix in their identity: A Lebanese man with deep Arab roots learning he has <a href="https://youtu.be/0ueSiDXce2E">Ashkenazi Jewish ancestry</a>, an African American woman of deep faith learning that her <a href="https://youtu.be/iMk-ZdBLcEE">religious heritage</a> is more mixed than she imagined, a proud son of the South meeting and reconciling with his <a href="https://www.youtube.com/watch?v=akc6tbW8aOg&amp;list=PLFvkfbvHpp1lQ8bqNZaO629ePXdH7qSPx&amp;index=2&amp;pbjreload=10">African American cousin</a>, and a successful young woman, <a href="https://youtu.be/PLazxh2pBdQ">Angelina</a>, who described herself as African American discovering she has Native American and Latino ancestry.
For years, we’ve heard from customers who have shared their stories of self-exploration. Over the summer, we began to explore some of these in short videos. We delve into this new notion of self-identity, finding people who learn about their own surprising mixed ethnicity.
<h2>New Campaign</h2>
Elegantly assembled by Emmy Award-winning filmmakers Jeremy Levine and Landon Van Soest of Transient Pictures, this campaign is more than just a company embracing a message of diversity. It offers people the tools to look into their DNA to help them redefine themselves and change how they look at the world.
<img loading="lazy" decoding="async" class="aligncenter wp-image-25712 size-full" src="http://35.88.189.111/wp-content/uploads/2017/09/Stories.001.jpg" alt="" width="1024" height="768" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/09/Stories.001.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2017/09/Stories.001-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2017/09/Stories.001-768x576.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2017/09/Stories.001-880x660.jpg 880w" sizes="auto, (max-width: 1024px) 100vw, 1024px" />

23andMe Customers Share Their Stories of Discovery

In a first-of-its-kind study, researchers at 23andMe found a link between the susceptibility for some of the most common infectious diseases and dozens of specific variants in genes involved in the body’s frontline immune response system.<img loading="lazy" decoding="async" class="alignright size-medium wp-image-25703" src="https://blog-api.23andme.com/wp-content/uploads/2017/09/iStock-174861783-300x200.jpg" alt="" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2017/09/iStock-174861783-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2017/09/iStock-174861783-768x513.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2017/09/iStock-174861783-1024x684.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2017/09/iStock-174861783-880x588.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2017/09/iStock-174861783-1180x788.jpg 1180w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Published today in the journal <a href="https://www.nature.com/articles/s41467-017-00257-5">Nature Communication</a>, the research is unique. Up until now, very few genome-wide association studies (GWAS) have looked specifically at common and non-life threatening infectious diseases. Most have focused on more serious maladies such as HIV, hepatitis, and malaria.
“While these are not as serious as HIV or malaria, they are the most common infections suffered by people and they have a profound impact on human health,” said lead author Chao Tian, Ph.D., a Senior Statistical Geneticist at 23andMe.
<div id="attachment_20934" style="width: 310px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-20934" class="wp-image-20934 size-medium" src="https://blog-api.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-300x300.jpeg" alt="" width="300" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-300x300.jpeg 300w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-150x150.jpeg 150w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-768x769.jpeg 768w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-1024x1024.jpeg 1024w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-880x880.jpeg 880w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-1180x1180.jpeg 1180w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-271x271.jpeg 271w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-372x372.jpeg 372w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-574x574.jpeg 574w, https://blogcms.23andme.com/wp-content/uploads/2014/05/Chao-Square-Photo-980x980.jpeg 980w" sizes="auto, (max-width: 300px) 100vw, 300px" />Chao Tian, PhD, a Senior Statistical Geneticist at 23andMe, who is the lead author of the paper.</div>
<h6>Health History</h6>
For this study, Chao and a team of researchers at 23andMe looked at data from more than 200,000 23andMe customers who consented to participate in research and who completed surveys on their health history.
By looking at their history of infections and infection-associated procedures, as well as running GWAS  on those conditions, the researchers were able to identify relationships between host genes and common infections.
The conditions that they found associations for include chickenpox, shingles, cold sores, mononucleosis, mumps, hepatitis B, strep throat, <a href="https://blog.23andme.com/articles/study-on-pneumonia">pneumonia</a>, yeast infections, urinary tract infections, tonsillectomy and childhood ear infections, to name a few.
<h6>Associations</h6>
In all, more than 50 genetic variants were found that were associated with 23 common infectious diseases. The study also revealed important roles of specific amino acid mutations at the antigen-binding site of human leukocyte antigen (HLA) genes. The HLA genes are the hundreds of genes on chromosome 6 that regulate the body&#8217;s immune system.
Each individual’s HLA response is expressed slightly differently as it discerns whether something is an invading pathogen, like a virus or bacteria. That difference can have an impact on an individual’s susceptibility to infectious diseases.
<h6>Different HLA Regions</h6>
The study found that the associations map to different HLA regions. These differences depend on whether the infectious disease is caused by a virus, as with shingles, or if it was induced from bacteria, as with <a href="https://blog.23andme.com/articles/study-on-pneumonia">pneumonia</a>.
Previous research  has found associations between HLA systems and some individual diseases. Among those studies was one <a href="http://stm.sciencemag.org/content/9/389/eaai8708">published in May</a> by researchers at Vanderbilt University Medical Center (VUMC) and the University of Arizona College of Pharmacy.
The study used electronic health records and genetic information from about 28,000 people. By combing this information the study found associations between HLA regions and certain autoimmune diseases such as type 1 diabetes and rheumatoid arthritis. However, there have been very few studies of this type, and this new research from 23andMe is the first to look at common infections.
Read the full paper in Nature Communications <a href="https://www.nature.com/articles/s41467-017-00257-5">here</a>.

Study Finds Genetic Links for Vulnerability to Common Infectious Diseases

A new survey found that most Americans are interested in using DNA testing to understand more about their health and ancestry, but the national survey also revealed a need for better education around the science of genetics.
Commissioned by 23andMe, the survey found that people had a strong interest in genetics, but that interest was out ahead of their understanding of the science. Many people still struggle with basic genetic concepts, according to the survey. This gap in genetic literacy follows similar findings around the need for improved <a href="http://www.pewinternet.org/2015/09/10/what-the-public-knows-and-does-not-know-about-science/">science literacy in the United States</a>.
Thao Do, PhD, 23andMe Education and Academia Program Manager, sees that gap between interest in genetics and knowledge about genetics as an opportunity, for engaging with people on the science.
“It presents an opportunity to educate people in fun and interesting ways,” said Thao.
Genetic testing itself offers people an engaging way not just to learn more about their health and ancestry, but also the science behind their results.
The survey offered some striking contrasts between people expressing a strong desire to tap into potential insights obtained by genetic testing, while at the same time illustrating that they did not fully understand the science behind the tests. For example, nearly three-fourths of those surveyed (74 percent) said they were interested in testing, but about the same percentage of people (75 percent) didn’t know that humans have 23 pairs of chromosomes.
But most most Americans, about 77 percent, know that genetics plays a role in the risk for certain diseases, and about 90 percent of respondents knew that DNA testing could inform them about their ancestry. The vast majority of Americans, 94 percent, said that whether it is information about their health, or ancestry, or traits, that they feel they have a right to at-home DNA testing to directly access this type of genetic information.
23andMe partnered with Kelton Global to generate the 23andMe DNA Survey, which was conducted between July 5th, 2017 and July 12th, 2017 among 1,000 nationally representative Americans ages 18+, using an e-mail invitation and an online survey, with a margin of error of +/- 3.1%.
<img loading="lazy" decoding="async" class="aligncenter size-full wp-image-25728" src="https://blog-api.23andme.com/wp-content/uploads/2017/09/Survey-Infographic-facts-fix.jpg" alt="" width="2667" height="9140" />

23andMe Asks About DNA

Researchers at 23andMe and Genentech have identified 17 new genetic variants associated with <img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/Brain-Logo-287x300.jpg" alt="" class="alignright wp-image-22635 size-medium" width="287" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/06/Brain-Logo-287x300.jpg 287w, https://blogcms.23andme.com/wp-content/uploads/2015/06/Brain-Logo.jpg 438w" sizes="auto, (max-width: 287px) 100vw, 287px" /><a href="http://www.23andme.com/topics/health-predispositions/parkinsons-disease/">Parkinson’s disease</a>. The findings almost doubling the total number of known risk variants for the condition. They gives scientist hints at potential new targets for drugs to treat the disease.
The work is part of a multi-year collaboration between the two companies begun in early 2015 aimed at identifying new therapeutic targets for Parkinson’s.
<h6>Research on Parkinson&#8217;s Disease</h6>
“We are incredibly excited by these findings and their potential to lead to breakthroughs in therapeutic research and treatment for Parkinson’s disease,” said Anne Wojcicki, 23andMe’s co-founder and CEO. “The 23andMe Parkinson’s community is powered by our customers who are motivated to make a difference and see the Parkinson&#8217;s research advance.   The community is unlike any other, and it is an incredible asset for researchers to make breakthrough discoveries. These findings are a testament to both the power of the 23andMe Parkinson’s community and the company’s novel research model.”
Published in the journal <a href="https://www.nature.com/ng/journal/vaop/ncurrent/full/ng.3955.html?foxtrotcallback=true">Nature Genetics</a>, the study is the largest meta-analysis of Parkinson’s disease to date, using data from more than 425,000 individuals.
<h6>Large Study Size</h6>
More than 370,000 of those individuals were 23andMe customers who consented to participate in research. About 10,000 of them have Parkinson’s disease and are part of 23andMe’s Parkinson’s Research community, which is now the largest Parkinson’s disease community for genetic research in the world. The researchers also used data from individuals that are part of<a href="http://www.pdgene.org/citing"> PDGene</a>, a clearinghouse for Parkinson’s related research data that also includes data from 23andMe.
In addition to identifying the 17 new risk genetic variants associated with Parkinson’s, the study confirmed many variants already known to be associated with Parkinson’s. A neurology-centric strategy was used to identify candidate genes linked to variants associated with Parkinson’s. These genes are involved in lysosomal and autophagy biology, sometimes referred to as the body’s recycling and trash collection centers. This vital process involves first a sweep of the cells by autophagosomes, which collect damaged material. Then that material is transferred to lysosomes, which either break down the material or recycle it into new structures.
<h6>Hints Concerning the Development and Progression of Parkinson&#8217;s</h6>
More recent research suggest that beyond its important recycling function, autophagy and lysosomal biology may also play important roles in<a href="https://www.quantamagazine.org/lysosomes-gene-regulation-signaling/"> regulating cell function</a>. Last year the Japanese researcher<a href="https://www.theguardian.com/science/2016/oct/03/yoshinori-ohsumi-wins-nobel-prize-in-medicine"> Yoshinori Ohsumi</a> won a Nobel Prize for his work looking at autophagy and its role in certain diseases like Parkinson’s. (Here’s more on <a href="https://www.quantamagazine.org/lysosomes-gene-regulation-signaling/">autophagy and lysosomal biology</a>.)
Mounting evidence suggests that this process of clearing out damaged cellular material may be impaired in patients with Parkinson’s, and that this may contribute to the development and progression of the disease. Parkinson’s disease, which affects an estimated six million people worldwide, is characterized by loss of nerve cells in various parts of the body, including dopaminergic neurons in the brainstem, an area important for the regulation of movement. The loss of neurons is associated with accumulation of insoluble abnormal forms of the protein alpha-synuclein, which make up the Lewy body deposits characteristic of Parkinson’s. These abnormal proteins are believed to impair nerve cell function and survival.
Not all candidate genes make good therapeutic targets. Most drugs are small chemical molecules. The term <a href="https://commonfund.nih.gov/idg/overview">“druggable genome,”</a> is often used to include those genes that make proteins whose function can be changed by the binding of drug-like small molecules.
A number of the candidate genes identified in this study — such as STK39 and ITPKB — fall into this category. They may therefore represent new targets for the discovery and development of novel treatments for Parkinson’s.

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