<img loading="lazy" decoding="async" class="alignright size-medium wp-image-6638" title="freckles_moles" src="https://blog-api.23andme.com/wp-content/uploads/2010/06/freckles_moles-300x199.jpg" alt="" width="300" height="199" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/06/freckles_moles-300x199.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2010/06/freckles_moles.jpg 425w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Melanoma is a rare but deadly form of skin cancer. Known risk factors include pale skin, large numbers of moles (also known as nevi), and prolonged sun exposure. Nevus count has a strong genetic component and researchers have already identified some genetic variants that influence the trait. In a new study published in <a href="http://www.cell.com/AJHG/abstract/S0002-9297(10)00265-X">American Journal of Human Genetics</a>, an international team of scientists led by David Duffy and Grant Montgomery reports a genetic variant newly associated with nevus count and melanoma risk, but with an interesting twist.
When Duffy’s team examined data from about 2,000 adolescents of European ancestry living in Australia, they found that each copy of a T at variant was associated with a significant increase in numbers of “flat” nevi (the most common type of nevus). When they looked at data from the parents of the adolescents, however, they saw no such effect. In fact, the data suggested that the C version of — not the T version — was associated with higher nevus counts in older people. Comparing these results with data from thousands of individuals from the UK confirmed the differing age-dependent effects of .
To investigate whether also influences risk for melanoma, the researchers analyzed data from approximately 3,500 individuals with melanoma and over 5,000 healthy individuals, all of European ancestry. The C version of was associated with 1.15 times higher odds of disease, but when they restricted the analysis based on the location of the melanoma, the association was only significant for melanomas on the trunk (main torso). Each copy of a C led to about 1.3 times higher odds of truncal melanoma.
The mechanisms connecting to melanoma risk are not yet fully understood. While the T version of has been associated with traits typically considered risk factors for melanoma (pale skin, dark hair, and freckling), this study suggests that the T version actually protects against the disease. The observation of age-dependent effects on nevus counts adds more wrinkles to the story. Duffy and his colleagues posit that individuals with a T at are more likely to develop large numbers of moles early in life, but that these moles tend to disappear with age. More research will be needed to determine the relationship between age-dependent patterns of nevus counts and melanoma risk.

23andMe Blog

23andMe Blog Team

Genetic Variant Contributing to Melanoma Risk has Different Effects on Mole Count Depending on Age

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3410" title="istock_000002436798xsmall" src="https://blog-api.23andme.com/wp-content/uploads/2009/04/istock_000002436798xsmall.jpg" alt="" width="279" height="185" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/04/istock_000002436798xsmall.jpg 425w, https://blogcms.23andme.com/wp-content/uploads/2009/04/istock_000002436798xsmall-300x199.jpg 300w" sizes="auto, (max-width: 279px) 100vw, 279px" />
The Genetic Information Nondiscrimination Act, or GINA, is U.S. federal legislation that protects Americans from discrimination (in health insurance and employment decisions) on the basis of genetic information. GINA was signed into law by President George W. Bush on May 21, 2008.
The <a href="http://www.geneticalliance.org/" target="_blank" rel="noopener">Genetic Alliance</a>, the Genetics and Public Policy Center at the Johns Hopkins University, and the National Coalition for Health Professional Education in Genetics have created an online resource to help people better understand the protections GINA provides.   This information is available in English and Spanish at <a href="http://www.ginahelp.org" target="_blank" rel="noopener">www.GINAhelp.org</a>.

Understanding GINA

<img loading="lazy" decoding="async" class="alignright size-full wp-image-6586" title="23andMe_Logo_blog" src="https://blog-api.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog.jpg" alt="" width="222" height="221" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2010/05/23andMe_Logo_blog-271x271.jpg 271w" sizes="auto, (max-width: 222px) 100vw, 222px" />
We recently determined that a number of new 23andMe customer samples were incorrectly processed by our contracted lab. We want to clarify what happened with the sample errors, how it happened and what we&#8217;re doing to prevent it from happening again. Providing each and every one of our customers with accurate data is 23andMe&#8217;s number one priority, and we fully realize the gravity of this incident.
After a full investigation from our contracted laboratory and independent confirmation by 23andMe, we have found that the processing mistake was caused by human error and the incorrect placement of a single 96-well plate used in processing samples.
We are uploading the correct data to impacted customers today, after again independently verifying the new results.
Both our contracted laboratory and 23andMe are adding new procedures to prevent this from happening again. &nbsp; Our contracted laboratory has adjusted the mounting process for these 96-well plates and this new adjustment physically prevents any incorrect manual placement of the plates used at this step of processing. &nbsp; As an additional safeguard, 23andMe will collect data regarding sex for all new customers prior to laboratory processing so an additional quality check can be conducted prior to uploading data.
We are committed to continually improving the quality of our processes. &nbsp;We hope this clarifies what has happened and how we intend to prevent this from happening in the future.

Update from 23andMe

<img loading="lazy" decoding="async" class="alignright size-full wp-image-6608" title="Illu_pharynx" src="https://blog-api.23andme.com/wp-content/uploads/2010/06/Illu_pharynx.jpg" alt="" width="325" height="221" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/06/Illu_pharynx.jpg 325w, https://blogcms.23andme.com/wp-content/uploads/2010/06/Illu_pharynx-300x204.jpg 300w" sizes="auto, (max-width: 325px) 100vw, 325px" />
Nasopharyngeal cancer (NPC) arises in the upper part of the throat, behind the nose.
<h6>Rare Condition</h6>
It is rare in most areas of the world–affecting only about 1 in every 100,000 people–but about 25 times more common in southern China, earning it the name &#8220;Cantonese Cancer.&#8221;   NPC rates are also high in southeastern Asia, northern Africa and the Arctic.
<h6>Risk Factors</h6>
Environmental factors play a very large role in NPC.   Smoking increases risk, as does infection with the Epstein-Barr virus.
Diets high in <a href="http://www.cancerhelp.org.uk/type/nasopharyngeal-cancer/about/nasopharyngeal-cancer-risks-and-causes#diet" target="_blank" rel="noopener noreferrer">salt cured food</a>, which are common in many of the areas where increased rates of NPC are seen, have also been shown to increase risk.   These foods can be very high in nitrates and nitrites, which react with protein to form DNA-damaging chemicals.
It&#8217;s also been known for quite some time, however, that genetics contribute to NPC susceptibility.   In 1970s, certain immune markers were associated with increased risk.
<h6>Genetic Associations</h6>
Now a large genome wide association study has revealed three more immune related areas of the genome that are associated with risk for NPC.   These results, published online this week in the journal <a href="https://dx.doi.org/10.1038/ng.601" target="_blank" rel="noopener noreferrer">Nature Genetics</a>, could eventually help develop models for prediction and screening, which in turn would help with early diagnosis.
Researchers from Singapore, China and the United States studied about 5,000 people with NPC and 5,000 controls, as well as more than 250 families, all of southern Chinese descent.
As expected, a strong genetic effect was seen in areas of the genome that encode the previously identified immune markers.   But variants in three other regions were also associated with NPC risk.   Two of these associations were statistically significant. The third SNP did not make the cut off, but was highly suggestive.
The statistically significant genetic associations variants were in the TNFRSF19 and MDS1-EVI1 genes.
<h6>Epstein-Barr Connection</h6>
Previous research has shown that these genes encode proteins that may be involved in the body&#8217;s response to Epstein-Barr virus infection, possibly providing a neat connection between the new findings and a known environmental risk factor for NPC.
The third association was with a variant near the CDKN2A and CDKN2B genes.   This gene cluster is deleted in about 40% of NPC tumors, suggesting that they are crucial for preventing cancerous growth.   Additionally, this same SNP CDKN2A/CDKN2B SNP associated with NPC risk has been <a href="https://blog.23andme.com/2009/07/06/snpwatch-genetic-variants-near-tumor-suppressor-genes-may-increase-risk-for-brain-and-skin-cancer/" target="_blank" rel="noopener noreferrer">linked to glioma</a> in European populations.
All of the genes identified in this study–TNFRSF19, MDS1-EVI1 and CDKN2A/CDKN2B–have previously been shown to be involved in leukemia.   This suggests that there might be common disease mechanisms between that disease and NPC.   Significantly, leukemia is found at higher than average rates in people with NPC.
According to the authors, the next step for research is to investigate the interactions between the genetic susceptibility factors identified by them and others with the environmental risk factors known to influence NPC.

New Genetic Associations Revealed for Nasopharyngeal Carcinoma

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Today, 23andMe received a letter from the  Committee on Energy and Commerce of the  United States House of Representatives asking that, along with Navigenics and Pathway Genomics, we provide information about our genetic testing services. The letter was signed by  Congressmen Henry A. Waxman from California, Chairman of the Committee, Ranking Member Joe Barton from Texas, and the Chairman and Ranking Member of the Subcommittee on Oversight and Investigations, Bart Stupak from Michigan and Michael C. Burgess from Texas.
We look forward to providing information to the Committee and Subcommittee and engaging with them on personal genetic testing, explaining how our services connect people to information about their own bodies, and highlighting the meaningful scientific research we facilitate through our services.
We believe that genetics has a vital role to play in the coming age of personalized medicine, and we view this inquiry as an opportunity to discuss real and important issues that include technology and data quality, scientific rigor, privacy, and accessibility as applied to the rapidly growing body of genetic knowledge.
Through our blog, we will keep you informed of progress on this topic.

Letter from Committee on Energy and Commerce

Aching joints and bones aren&#8217;t always just a normal part of aging, and for some, they are a symptom of Paget&#8217;s disease of bone <a href="http://www.niams.nih.gov/Health_Info/Bone/Pagets/default.asp#b" target="_blank" rel="noopener noreferrer">(PDB)</a>, a condition that affects more than one million people over the age of 45 in the United States.
<h6>More on Paget&#8217;s Disease</h6>
Bone tissue is constantly being recycled.   As old bone is broken down, new bone grows in to replace it.
In PDB, the breakdown process is sped up, so the rate of new bone generation must also increase.   This rapidly grown bone tends to be softer and weaker than normal.   In most people this doesn&#8217;t lead to any symptoms, but for some it can cause bone or joint pain, deformities or fractures.   Tingling or weakness can occur if deformed bones impinge on nerves.
The cause of PDB isn&#8217;t known, but there is thought to be a genetic component to the disease.
<h6>Genetics of Paget&#8217;s</h6>
Between 15% and 40% of people with the disease have an affected mother, father, sibling or child, and mutations in the SQSTM1 gene have been linked to some cases.   To find the remaining genes that predispose a person to PDB, an international team led by researchers at the University of Edinburgh analyzed the DNA of close to 1,200 people with the disease and more than 1,500 controls.   Their results, published online recently in the journal <a href="https://dx.doi.org/10.1038/ng.562" target="_blank" rel="noopener noreferrer">Nature Genetics</a>, identify common variations in three separate regions of the genome contribute to differences in risk of developing the disease.
The strongest genetic association for PDB was seen with in a variant near the   CSF1, which is known to play a critical role in bone cell formation and survival. Another variant associated with PDB is located in a gene region previously   linked to familial PDB. And finally, another variant was found near a gene that encodes a protein called RANK, which is important for bone cell function.   Mutations in this gene cause bone disease in both mice and humans.   It has also been associated with <a href="https://www.nature.com/ng/journal/v41/n1/full/ng.284.html" target="_blank" rel="noopener noreferrer">bone mineral density</a> and fracture risk.
In an interview, the study&#8217;s senior author Stuart Ralston suggested that his team&#8217;s findings could lead to a screening test for PDB.
&#8220;This is important since we know that if treatment is left too late, then irreversible damage to the bones can occur. If we were able to intervene at an early stage with preventative therapy, guided by genetic profiling, this would be a major advance,&#8221; Ralston told the <a href="http://news.bbc.co.uk/2/hi/health/8654795.stm" target="_blank" rel="noopener noreferrer">BBC</a>.
Although the SNPs described in this new study appear to account for a large portion of the genetics of PDB, the authors point out that it is likely that there are other regions of the genome that also contribute to the risk of developing the disease that were not picked up in their analysis.   They suggest that based on their success, further studies are now warranted to identify the rest of the genetic factors associated with the disease.

Genetic Variants Associated with Risk of Paget’s Disease of Bone Identified

<img loading="lazy" decoding="async" class="alignright wp-image-5318 size-medium" title="08D-5313-0" src="http://35.88.189.111/wp-content/uploads/2009/11/arthritishands-300x199.jpg" alt="An image of the hands of an elderly person trying to unscrew a medicine bottle." width="300" height="199" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/11/arthritishands-300x199.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/11/arthritishands.jpg 425w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Rheumatoid arthritis is a common autoimmune disease. An individual&#8217;s own immune system attacks the lining of the joints, causing stiffness and muscle aches. Like other autoimmune diseases, development of rheumatoid arthritis is likely caused by a complex combination of genetic and environmental factors. Research into the genetics of the disease has identified many of the genetic factors. Studies continue to implicate additional variants that may influence risk.
<h6>Genetic Associations</h6>
A pair of such studies published in Nature Genetics found several genetic variants associated with rheumatoid arthritis.
In Japan, a team led by Yuta Kochi and Kazuhiko Yamamoto from the RIKEN Center for Genomic Medicine <a href="https://dx.doi.org/10.1038/ng.583">identified a variant</a>, associated with rheumatoid arthritis risk. The study included over 2,000 Japanese individuals with the disease and 3,400 individuals free of the disease.
The <a href="https://dx.doi.org/10.1038/ng.582">second study</a>, headed by Eli Stahl and Robert Plenge at Brigham and Women&#8217;s Hospital in Boston, confirmed the same association. This second study was done in over 10,000 people of European ancestry with rheumatoid arthritis.
<h6>Immune System</h6>
One of the variants is in an area of the genome associated with a risk for Crohn&#8217;s disease. That region contains a gene called CCR6 that is known to be involved in the immune system.
In follow-up experiments, the RIKEN team demonstrated that the different versions of the variant affect the behavior of CCR6. This provides&nbsp;a potential biological explanation for the variant&#8217;s contribution to rheumatoid arthritis risk.
Stahl and his colleagues also found several other genomic regions associated with rheumatoid arthritis in people with European ancestry, some of which had not yet been linked to autoimmune disease.
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Rheumatoid Arthritis and Immune System

<img loading="lazy" decoding="async" class="alignright size-full wp-image-5677" title="alzheimers" src="https://blog-api.23andme.com/wp-content/uploads/2009/12/alzheimers.jpg" alt="" width="350" height="249" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/12/alzheimers.jpg 435w, https://blogcms.23andme.com/wp-content/uploads/2009/12/alzheimers-300x214.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Understanding Alzheimer&#8217;s disease, the most common cause of dementia in people 65 years and older, is of the utmost importance as the population of the United States (and many other nations) becomes increasingly older.
Currently more than five million Americans are thought to have the disease, but by the year 2050 that number is estimated to reach 14 million unless a cure or prevention method is developed.
<h2>APOE</h2>
Until very recently, mutations in only one gene–APOE–had been conclusively associated with the more common late-onset form of Alzheimer&#8217;s (there are others associated with early-onset disease).
In <a href="https://blog.23andme.com/2009/09/08/snpwatch-largest-alzheimers-genetic-studies-to-date-identify-three-new-susceptibility-genes/" target="_blank" rel="noopener">September 2009</a> two groups studying large numbers of people identified variants in three new genes that had small effects on the disease.
Now researchers have pulled together the results of several studies and found variations in two more genes associated with increased risk.   The scientists, whose results appear online today in the <a href="http://jama.ama-assn.org/cgi/content/short/303/18/1832" target="_blank" rel="noopener">Journal of the American Medical Association</a>, suggest that these variants may be important for unraveling the underlying biology of Alzheimer&#8217;s, which will be essential in the quest to find new methods of treatment.
<h2>Other Genes</h2>
Researchers from the CHARGE, GERAD1 and EADI1 Alzheimer&#8217;s research consortia combined data from more than 35,000 people (more than 8,000 with Alzheimer&#8217;s) with European ancestry.   They found a variant near the BIN1 gene was associated with 1.13 times increased odds of Alzheimer&#8217;s.
They also found another variant near the EXOC3L2/BLOC1S3/MARK4 genes was associated with 1.18 times increased odds of Alzheimer&#8217;s.
The BIN1 gene encodes a protein that is highly expressed in the brain and known to be important in processes that are disrupted by the <a href="http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp#plaques" target="_blank" rel="noopener">plaques</a> that form in the brains of people with Alzheimer&#8217;s.   Two of the genes near , BLOC1S3 and MARK4, encode brain proteins that are also involved in processes that are known to be disrupted in Alzheimer&#8217;s disease.   The MARK4 protein in particular is interesting because it interacts with tau, the protein responsible for the tangles seen in the brains of people with Alzheimer&#8217;s .
<h2>Insights into Alzheimer&#8217;s</h2>
Combined analysis of all of individuals studied also provided support for previously identified associations in the CLU and PICALM genes.
Compared to a model that uses only APOE status, age and sex, adding in a person&#8217;s information for the replicated SNPs in the CLU and PICALM genes did not substantially improve risk prediction.   The researchers note that in light of the small effect sizes of these SNPs, this is not unexpected.
&#8220;The value of these associations may lie in the insights they could provide for research into the pathophysiological mechanisms of AD [Alzheimer&#8217;s disease],&#8221; the authors write.
In an accompanying <a href="http://jama.ama-assn.org/cgi/content/full/303/18/1864" target="_blank" rel="noopener">JAMA editorial</a>, Nancy Pedersen of the Karolinska Institute in Stockholm, Sweden, points out that it&#8217;s not surprising that the new variants don&#8217;t add much to risk prediction, writing that this finding &#8220;only verifies the notion that AD is a polygenic disorder; i.e., that potentially tens of thousands of risk alleles, each with a small effect, are important for liability to disease.   What is remarkable is that the single gene APOE is as important as it is for this complex disorder.&#8221;
Pedersen&#8217;s opinion is that researchers should forgo further pursuit of new genetic variants or replications of already identified SNPs, and instead turn their attention to the study of environmental risk and protective factors for Alzheimer&#8217;s disease.   She notes that in identical twins, there is at most a 61% chance that both twins will end up with the disease, indicating that non-genetic factors play an important role.   Further, she points outs that Alzheimer&#8217;s disease that sets in very late in life has been shown to be less heritable, suggesting that environment gets more and more important as people age.
Pedersen ends by noting that right now, the most important thing doctors can do is encourage people to make lifestyle changes, especially those that improve cardiovascular health, that may reduce the risk of dementia or at least postpone it.

Large Study Identifies Two More Genetic Variants Associated with Alzheimer’s Disease

<img loading="lazy" decoding="async" class="alignright size-full wp-image-6513" title="joanna_africa4" src="https://blog-api.23andme.com/wp-content/uploads/2010/05/joanna_africa4.jpg" alt="" width="357" height="246" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/05/joanna_africa4.jpg 357w, https://blogcms.23andme.com/wp-content/uploads/2010/05/joanna_africa4-300x207.jpg 300w" sizes="auto, (max-width: 357px) 100vw, 357px" />The author during her time as a Peace Corps volunteer in Kenya.
As a Peace Corps volunteer teaching in Kenya 25 years ago, I was fascinated by the cultural, linguistic, and physical differences among the people of eastern Africa. One of our Kenyan trainers took us to a &#8220;boma&#8221; where his tall, cattle-herding Maasai-speaking family lived.   Once I began working, I lived with a Luo-speaking fellow teacher who emphasized the cultural differences, for instance in circumcision practices, between the Luo and other ethnic groups.   Later I taught Bantu-speaking children of farmers and fishermen along the coast of Kenya. Physical features hinted at ethnic identity and, even within the village where I taught, skin color ranged from quite light to relatively dark.   At the time I saw patterns, but understood little of the history behind those patterns.
Upon returning to the United States, I was fortunate to join the lab of geneticist Luca Cavalli-Sforza, who was studying the genetics of people across Africa. At that time, relatively little was known about human genetic diversity, in particular for Africa. I leaped at the opportunity to compare the hidden dimension of genetic diversity with the linguistic and cultural variation that I had observed in Kenya. In the 25 years since then, the study of diversity in Africa has blossomed. Thanks to advances in DNA technology, researchers have begun to augment information about the cultural and linguistic variation with information about how Africans differ at the genetic level. Online last week in the <a href="https://dx.doi.org/10.1073/pnas.1002563107" target="_blank" rel="noopener">Proceedings of the National Academy of Sciences</a>, authors Laura Scheinfeldt, Sameer Soi and Sarah Tishkoff pulled together recent discoveries about the population history of Africa based on languages, artifacts and DNA. Their paper paints the prehistory of the continent in broad strokes, beginning over 100,000 years ago.
(This paper is one of many to come out of In Light of Evolution IV: The Human Condition Sackler Colloquium presented by the National Academy of Sciences in December 2009.   Links to other papers from this series can be found <a href="https://www.pnas.org/content/early/recent" target="_blank" rel="noopener">here</a> (after this week they should be here.).   Podcasts of presentations from the colloquium can be found here.)
As these authors note, the genetic data indicating that our species originated in Africa has accrued significantly and convincingly. And we now know that today&#8217;s African populations began forming over 50,000 years ago. From among those early populations, a relatively small group of individuals migrated out of Africa to populate Eurasia and Oceania. Within Africa, meanwhile, technological innovation (such as the use of more refined stone tools, and later, iron tools) and the development of today&#8217;s language families paralleled the formation of today&#8217;s ethnic groups.   The combination of archaeological, linguistic and genetic data has revealed that some populations remained relatively isolated from one another for tens of thousands of years, but that interactions between groups, especially within the last 5,000 years, have also shaped the genetic diversity of the continent. For instance, the DNA is very clear in revealing the interactions between migrating agriculturalists and pastoralists and the hunter/gatherers who they encountered.
As a result of the rich prehistory outlined in this paper, today&#8217;s Africans can trace their ancestry to central and southern Africa, where a few click-speaking <a href="http://ngm.nationalgeographic.com/ngm/0102/feature6/" target="_blank" rel="noopener">Khoe-San peoples</a> continue to subsist through hunting and gathering; to northern Africa, where migrations of <a href="http://www.azawan.com/" target="_blank" rel="noopener">Afro-Asiatic speakers</a> from the Middle East to the western coast have been taking place for 14,000 years; to the Sahel region near the equator, where Nilo-Saharan (including Luo) and Afro-Asiatic speakers have traveled back and forth from eastern Sudan to <a href="http://earthshots.usgs.gov/LakeChad/LakeChad" target="_blank" rel="noopener">Lake Chad</a> for at least 10,000 years; or to western Africa, where the innovations of agriculture and iron age technology supported the migration of Bantu-speaking peoples to all corners of Sub-Saharan Africa within the last 4,000 years.   And, of course, many Africans trace ancestry to multiple corners of Africa and to other continents as well.
As one of the authors, geneticist Sarah Tishkoff, noted when I spoke with her recently, &#8220;The strength of this paper is the deep integration of the genetics, linguistics, and archaeology.&#8221; With this synthesis of 25 years of research in mind, I see the diversity that I observed in Kenya in a continental context. The Maasai-speaking Peace Corps trainer undoubtedly had ancestors 4,000 years ago who lived further north in eastern Africa, and may now have distant cousins whose ancestors migrated to southern Africa with their cattle 2,000 years ago.   My fellow teacher who spoke Luo inherited her language, cultural traditions and some DNA from her eastern African Nilo-Saharan ancestors, but, according to this PNAS article, probably also traced quite a bit of ancestry to Bantu-speakers of western Africa. My Bantu-speaking students were descendants of migrants from western Africa, but Arab slavery within the last several hundred years may explain some of the lightness of their skin color.   Understanding the prehistory of the people I worked with has led me to appreciate, more than ever, the opportunity I had as a Peace Corps volunteer to know such a diverse set of people.
23andMe has supported several initiatives that are contributing to the understanding of genetic diversity within Africa.   In fact, 23andMe provided funding for one of the studies (<a href="https://www.ncbi.nlm.nih.gov/pubmed/18292342" target="_blank" rel="noopener">Li et al, 2008</a>) reviewed in this paper, knowing that the study would enable 23andMe to provide richer interpretations of customers&#8217; data. I am looking forward to further discoveries that strengthen our understanding of where we, as a species and as individuals, have come from.

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