<img loading="lazy" decoding="async" width="290" height="400" class="right size-full wp-image-281" style="float: right;" title="jessejamessmall" src="https://blog-api.23andme.com/wp-content/uploads/2008/06/jessejamessmall.jpg" alt="" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/06/jessejamessmall.jpg 290w, https://blogcms.23andme.com/wp-content/uploads/2008/06/jessejamessmall-218x300.jpg 218w" sizes="auto, (max-width: 290px) 100vw, 290px" />Jesse James

Editor&#8217;s note: This post has been corrected from the original, which gave the incorrect location of Jesse James&#8217; grave. 


One of the most engaging features of 23andMe’s Personal Genome Service is a customer’s ability to trace his or her genetic ancestry using the mitochondrial DNA and the Y-chromosome.
Once customers learn their own ancestry, the Genome Sharing feature allows them to see how they compare with friends and family.
However, the ancestry section of 23andMe also allows customers to see how they compare to well-known individuals. In the maternal and paternal ancestry features, customers can view the haplogroup assignments of such figures as Thomas Jefferson, Genghis Khan and Bono.
<h6>Am I Related to Someone Famous? Sort of.</h6>
But how can anyone know the ancestry of someone like Thomas Jefferson, who has been dead for a few hundred years, or Genghis Khan, who has been dead for close to a thousand?
It turns out there are several ways to find out these well-known figures’ ancestry. The most obvious: Celebrities can sign up for 23andMe’s Personal Genome Service, just like the rest of us! For example, Jimmy Buffett and Warren Buffett have been interested for years in finding out whether their shared surname was an indication of common genetic ancestry. Unfortunately, their genetic profiles show the two are not closely related.
<h6>
 Founding Fathers&#8217; Haplogroups</h6>

But what about people like Thomas Jefferson?
He is no 23andMe customer, but this does not mean that scientists cannot trace his ancestry by other means. Tracing the maternal or paternal ancestry of any deceased individual is usually done by one of two ways: either getting DNA from the physical remains of the individual, or getting DNA from direct descendants of a relevant lineage.
He is no 23andMe customer, but this does not mean that scientists cannot trace his ancestry by other means. Tracing the maternal or paternal ancestry of any deceased individual is usually done by one of two ways: either getting DNA from the physical remains of the individual, or getting DNA from direct descendants of a relevant lineage.
In the cases of Thomas Jefferson and Benjamin Franklin, scientists used DNA from direct descendants of their ancestors. For example, in 1998 scientists inferred Jefferson’s paternal ancestry by analyzing the Y-chromosome of direct descendants of Jefferson’s paternal uncle (Jefferson had no confirmed sons).
<h6>Marie Antoinette and other Royal Haplogroups</h6>
Likewise, in the case of historical royalty such as Tsar Nicholas II of Russia or Marie Antoinette of France, extensive and detailed royal pedigrees make finding direct descendants a breeze.
Likewise, in the case of historical royalty such as Tsar Nicholas II of Russia or Marie Antoinette of France, extensive and detailed royal pedigrees make finding direct descendants a breeze.
In the case of the infamous outlaw Jesse James, a more direct approach was used. It had been widely believed that after James died in 1882, his body was buried at Mt. Olivet Cemetery in Kearney, Missouri. In order to test this hypothesis, scientists exhumed the body, extracting a few teeth. They compared DNA from the teeth to that of the great-grandson and great great-grandson of James’ sister. Scientists found an exact match between the extracted teeth and James’ sister&#8217;s descendants, thus confirming that the body in Mt. Olivet Cemetery was most likely that of Jesse James and establishing his ancestry to boot.

<h6>
How about Genghis Khan?</h6>
He is listed in our famous people sidebar as being a member of Y-chromosome Haplogroup C. But we do not have any information on his direct descendants alive today, nor do we have any preserved remains of his body. However, scientists have examined the Y-chromosomes of many present-day inhabitants of Mongolia (the ancestral home of Genghis Khan).
In doing so, they have found that about 8% of Mongolian males share the exact same DNA pattern in a highly variable part of their Y-chromosomes. Further analysis has revealed that this particular Y-chromosome type, which falls into haplogroup C, originated about 1,000 years ago and that its dispersal across Central Asia corresponds to the boundaries of the Mongol Empire. Historians have long noted Khan’s prolific nature; he is rumored to have fathered more than 40 sons, with some of his descendants also fathering many sons of their own. So it&#8217;s a good bet that we&#8217;re seeing Genghis Khan&#8217;s legacy in the 8% of Mongolian males alive today who have identical Y-chromosome signatures.
There are a number of ways we can determine the haplogroups of well-known figures — both past and present — and displaying information about these individuals adds to the fun of understanding and comparing the genetic ancestry of ourselves, our friends and family, and the rich and famous (or infamous).
Explore the origins of your ancestry at <a href="https://www.23andme.com/dna-ancestry/">23andMe.com</a>.

23andMe Blog

23andMe Blog Team

Haplogroups of the Rich and Famous

Roy King is a clinical psychiatrist at Stanford University. He’s also a scholar who uses genetics and archaeology to figure out how agriculture spread through Anatolia and the Mediterranean region of Europe more than 10,000 years ago.
Now Roy has another genetic puzzle to consider — himself.
With the help of 23andMe, he can now see how his own family tree — which has African American, Native American and Ashkenazi Jewish branches — is reflected in his genome.
Roy recently sat down with some of 23andMe’s scientists to look at his Ancestry Painting. (You can watch video of his conversation with 23andMe’s Matt Crenson below.)


An element of our Personal Genome Service, Ancestry Painting examines the 22 bi-parentally inherited chromosomes one segment at a time and determines for each stretch whether it was most likely inherited from ancestors in Africa, Europe or Asia. Roy’s painting is one of the most colorful our scientists have ever seen — an intricate patchwork of blue, orange and green. The colors indicate which segments of Roy’s DNA he inherited from ancestors in Europe, Asia and Africa respectively.
Though the pattern may look random to the untrained eye, it actually reveals a wealth of information about Roy’s ancestry. It also confirms a lot of what he has discovered in researching his genealogy.

For example, Roy has found records indicating that two 19th-century ancestors on his mother’s side were Native American. The orange stretches in his Ancestry Painting support that account. Native Americans tend to have predominantly orange paintings, with a smattering of blue indicating their descent from Ice Age hunters who lived in Siberia, a part of Asia with some European genetic influence.
According to Roy’s family tree about one-quarter of his ancestry should trace to Europe, because his paternal grandfather was an Ashkenazi Jewish man from New York City.
His other three grandparents were African American.
So why does his Ancestry Painting indicate 51% European ancestry, rather than something closer to 25%?
The reason is that like most African Americans, Roy has some European ancestry from the pre-Civil War era. Roy’s genealogical research suggests, for example, that his great-grandmother may have been the daughter of a white man who raped his great-great-grandmother. Another of Roy’s great-great grandmothers came from New Orleans, where research has shown that the African Americans average about 20% European ancestry.
For an illustration of how a person’s Ancestry Painting and family tree match up, take a look at this illustration of Roy’s pedigree.
Instead of labeling each oval (indicating a female) or square (male) with names and birthdates, we’ve given them colors. Green indicates a person who would typically be considered African American, blue a person of European descent and orange a Native American.
There appears to be more green in Roy’s family tree compared to his Ancestry Painting, due to the presumed presence of European ancestry among some of Roy’s African American ancestors. But other than that, the two illustrations of his ancestry look remarkably similar.

A Beautiful Ancestry Painting

<img decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/cocktail.jpg" alt="cocktail.jpg" class="right alignright">A new study in <a href="https://dx.doi.org/10.1038/ng.151" target="_blank" rel="noopener noreferrer">Nature Genetics</a> shows that the increased risk of developing cancer in the mouth, throat, voice box and esophagus due to drinking is partially offset by the rarer versions of two SNPs associated with alcohol metabolism.
Cancers of the oral cavity, throat (also called the pharynx), voice box (or larynx) and esophagus are collectively known as upper aerodigestive (UAD) cancers. <a href="http://findarticles.com/p/articles/mi_m0CXH/is_3_29/ai_n21041723/pg_1" target="_blank" rel="noopener noreferrer">Alcohol consumption</a> is known to be a significant risk factor for these cancers. Studies have shown that the areas of the body that come into closest contact with ingested alcohol are at highest risk of being affected by cancer.

The two SNPs associated with UAD cancers are both located in genes that are part of the alcohol dehydrogenase (ADH) enzyme pathway, a group of proteins that aids the body in metabolizing alcohol. The authors of the study hypothesize that the protective versions of the SNPs they found exert their effect on UAD cancers by changing the carcinogenic effects of alcoholic beverages. These SNPs had no effect among non-drinkers.
Hasibe et al studied six SNPs in ADH pathway genes in a total of 3,876 people with UAD cancers and 5,278 healthy controls, in hopes of finding DNA variants associated with these diseases. This large study group was comprised of three smaller study groups: one group from eastern Europe with 809 patients and 2,586 controls; one group from western Europe with 1,356 patients and 1,407 controls; and a final group from Latin America with 1,711 patients and 1,285 controls.
Both rs1229984 and rs1573496 were significantly associated with UAD cancers in the large study group and each of the smaller study groups individually.
When the researchers broke the patients into groups based on specific cancer type — oral/throat, voice box, and esophagus — they found that both SNPs impacted the risk of developing the subtypes of cancer to different extents (see the chart at the end of this post for details).
About 19 out of every 100,000 people is diagnosed with UAD cancer per year in the United States. Individually, the lifetime risks of developing these cancers are: oral/throat, 1 in 99; voice box, 1 in 274; and esophagus, 1 in 198.
Those who have one or two copies of the T version of rs1229984 were found to have 0.56 times the odds of developing UAD cancer compared to those with two C versions. For those who carry one or two copies of the G version of rs1573496, their odds of developing UAD cancer were 0.68 times those with two C versions. People who carry at least one T at rs1229984 and one G at rs1573496 were found to have 0.45 times the odds of developing UAD cancer compared to people who had no protective versions of either SNP.
The authors say that the exact mechanism by which the protective versions of these two SNPs are working is not clear. It is known that people with one or two copies of the T version of rs1229984 metabolize ethanol up to 100 times faster than people with two copies of the C version. The authors of this study speculate that this faster metabolism may protect tissues by reducing their exposure to the effects of alcohol.
The tables below sum up the results of this study. The “effect” of each SNP is the change in odds for carrying either one or two copies of the protective version.
<img decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/booze2.jpg" alt="booze2.jpg">

Alcohol Metabolism SNPs are Associated with a Decreased Risk for Cancer, but Only in Drinkers

<img decoding="async" class="right alignright" src="https://blog-api.23andme.com/wp-content/uploads/2008/03/beringstrait.png" alt="beringstrait.png" />Just when you thought everything was starting to make sense — new genetic research on the peopling of the Americas throws us a curve.
There has been plenty of research in both <a href="https://blog.23andme.com/2008/03/07/the-amazing-journey-a-new-synthesis-for-the-peopling-of-america/">genetics</a> and <a href="https://blog.23andme.com/2008/05/09/its-all-about-the-seaweed-new-theories-on-the-peopling-of-the-americas/">archaeology</a> recently trying to figure out how the New World was colonized.
Was it by boat or via the frozen wasteland of the Bering Strait? Was it a fast trip down to South America, or did these first inhabitants take a more leisurely stroll? And when did all this happen anyway? 
<h6>New Evidence</h6>
As each new study is published we are learning vital information on the peopling of the Americas. Ideas and theories continue to be retooled as new evidence comes to light.
This will certainly be the case with regards to a paper in the May 2008 issue of <a href="http://www.plosgenetics.org">PLoS Genetics</a>. In this article, researchers from Oxford and Cornell Universities report on a new computer model they have developed to trace prehistoric human migrations across the globe.
Using genetic information from various populations alive today, the authors estimated how those groups may be related to one another. Then they used those relationships to piece together the prehistoric movements of early humans.
<h6>The First Americans</h6>
As expected, their analysis showed a single migration out of Africa that eventually populated Eurasia and the Americas. However, the results for the Peopling of the Americas were more surprising.
The conventional wisdom states that the first inhabitants of the Americas came from Asia in a single wave more than 10,000 years ago. But when the authors compared the genetic data of two Native American groups (one in Colombia and one in the American Southwest) to groups in East Asia, what they found supported a two-wave migration. 
 The Colombian sample of Native Americans was actually more closely related to the East Asian sample than it was to the American Southwest sample. That suggests the two populations come from independent sources — and that there were at least two separate migrations of humans into the New World. Clearly, one of these migrations would have come from East Asia and made its way into South America. However, the data suggest a separate migration, probably from a different part of Asia or Siberia, came at a different time, and this time only made it to North America. This conclusion is significant, as it contradicts current theories on the topic, which argue a more constant flow of migrants from an original source somewhere in Asia. There are still plenty of questions regarding this research, especially with regard to how it compares to the archaeological record and to previous genetic studies. The answers to these questions can only come with additional research, which, thankfully, is always forthcoming on the peopling of the Americas.

Peopling of the Americas (Times Two)

<div style="width: 410px" class="wp-caption alignright"><img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/bushsignsgina.jpg" alt="bushsignsgina.jpg" class="right" width="400" height="254" />White House photo by Eric Draper</div>
President Bush has <a href="https://www.reuters.com/article/politicsNews/idUSN2143439320080521">signed</a> GINA, the Genetic Information Nondiscrimination Act, into law.
The legislation, which passed Congress last month after languishing for more than a decade, will make it illegal for employers or health insurers to discriminate on the basis of genetics. Genetic information will still be fair game in life insurance or long-term care coverage, however.
“This is a tremendous victory for every American not born with perfect genes — which means it’s a victory for every single one us,” said Rep. Louise Slaughter , a New York Democrat who first introduced the bill in 1995.
The law will not go into effect immediately. The insurance provisions take effect in about a year, and the employment rules about six months after that. So it remains to be seen how much of an effect GINA will have, especially when you consider that most states already have laws in place prohibiting genetic discrimination.

It’s Official: Bush signs GINA

<img decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/stomach.jpg" alt="stomach.jpg" class="right alignright" />A new study in <a href="https://www.nature.com/ng/index.html">Nature Genetics</a> shows that a version of a SNP in a gene called PSCA is associated with an increased risk in Asians for diffuse-type gastric cancer, a type of stomach cancer.
Gastric cancer, which falls into two main categories — intestinal and diffuse — is the fourth most common type of cancer and second leading cause of cancer death worldwide.
The intestinal type of gastric cancer is typically associated with infection by a type of bacteria called H. pylori, while the diffuse type is not. Previous research suggests that the two types of gastric cancer develop through different pathways and that genetic background is more important for the diffuse type.
<h6>Millennium Genome Project</h6>
The Study Group of Millennium Genome Project for Cancer initially examined more than 85,000 SNPs in 188 diffuse-type gastric cancer patients and 752 healthy controls from Japan to find DNA variations that might be associated with diffuse-type gastric cancer. That research produced a list of 2,880 candidate SNPs that were then examined in an additional 749 patients and 750 controls.
The SNP from that shorter list that was most strongly associated with diffuse-type gastric cancer was rs2976392, in the PSCA gene.
Because the SNPs that are found in genome-wide association studies are often only markers for other SNPs that are actually affecting susceptibility to a disease, the researchers looked at the PSCA gene more closely to find additional SNPs.
PSCA SNP rs2294008 was found to be significantly associated with diffuse-type gastric cancer. Each copy of the T version (which is the most common version in the Japanese population) increased the odds of diffuse-type gastric cancer by 1.67 times.
<h6>Association in Koreans</h6>
The researchers found that rs2294008 was also associated with diffuse-type gastric cancer in a Korean sample of 454 patients and 390 controls. In this population the T version increased the odds of diffuse-type gastric cancer by 1.91 times. In the Korean population, the T version is less common than the C version of SNP rs2294008. 
The researchers think the different versions of rs2294008 might influence the risk for diffuse-type gastric cancer because theory predicts the T and C versions of this SNP should produce slightly different proteins. Laboratory experiments also suggested that when the PSCA gene has the T version of rs2294008, less protein is made from the gene.
More research will be needed to confirm that the T version of rs2294008 is a risk factor for diffuse-type gastric cancer in Asian populations and if so, how it works. Researchers will also need to determine whether this SNP is associated with diffuse-type gastric cancer in other populations.

Associations in Asians for type of stomach cancer

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-231" src="http://35.88.189.111/wp-content/uploads/2008/05/istock_000005569535xsmall-300x225.jpg" alt="" width="300" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/05/istock_000005569535xsmall-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/05/istock_000005569535xsmall.jpg 400w" sizes="auto, (max-width: 300px) 100vw, 300px" />One of the most exciting aspects of archaeology is how new research can alter previously held notions about prehistoric events.
One of the most hotly debated events is the peopling of the Americas. Theories on the timing and specifics of the arrival of the first Americans are continuously modified as new evidence from fossil, paleoclimatic, and genetic records is examined.
<h2>First to the New World</h2>
A study in last month’s <a href="https://blog.23andme.com/2008/03/07/the-amazing-journey-a-new-synthesis-for-the-peopling-of-america/">American Journal of Human Genetics</a> argued for an ancient and fast migration of prehistoric humans across the Bering Strait and down the Pacific Coast based on a genetic analysis of present-day Native Americans. That study was provocative because it significantly pushed back the arrival date of humans to the New World to 18,000 years ago from the previous estimate of 13,000 years.
Now, results from a new study in this week’s Science further bolster that theory, using the prevalence of preserved seaweed as an indicator.
Anthropologists at Vanderbilt University excavated a South American archaeological site, Monte Verde II. In southern Chile, Monte Verde II is midway between the Pacific Coast and the Andes mountains. It dates to approximately 14,600 years ago, making it one of the oldest archaeological sites in the New World. The age of Monte Verde II, combined with its extreme southern location, lends additional support to the hypothesis of an early arrival of humans into South America.
<h2>Seaweed</h2>
The sheer abundance of preserved seaweed in various huts at Monte Verde II lends additional support for the initial migration occurring down the Pacific Coast rather than further inland. Seaweed is an incredibly fragile material and does not preserve well. However, remains of seaweed are found all over Monte Verde II. The authors think the seaweed was probably used extensively for food and medicinal purposes, which still continues in present-day coastal communities.
The presence of some foods from inland areas indicates that the inhabitants of Monte Verde also traveled inland at some point during the year or else mingled with other communities that did so.
So, how do these findings help us to understand the earliest inhabitants of the Americas? Most importantly, this study supports the idea that the first Americans traveled down the length of the Americas via the Pacific Coast. However, it also shows that there seems to be some relationship between coastal communities, such as Monte Verde, and those more inland groups.
In fact, the authors of this study use this possible relationship to propose a slight variation on the theme of a coastal migration route, saying that the first inhabitants may have taken a slower journey down the coast, spreading out in the interior along the way. Although this hypothesis needs additional support, it is clear that the debate on the people of the Americas is far from over.

It’s All About the Seaweed: New Theories on the Peopling of the Americas

Editor&#8217;s Note: This post does not reflect our current product offering. 23andMe&#8217;s ancestry product looks at the autosomes (chromosomes 1-22), the sex chromosomes (XY), and mitochondrial DNA (mtDNA). For more information about how results are different for men and women go here.
One of the most exciting parts of 23andMe’s <img decoding="async" class="right alignright" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/gus.jpg" alt="gus.jpg">
<h6>Paternal vs. Maternal</h6>
At present, 23andMe customers can trace two branches of their genetic family tree — one that follows the all-female line on the maternal side (through mitochondrial DNA) and another the all-male line on the paternal side (through the Y chromosome).
Not all DNA is created equal, however: males have both mitochondrial DNA AND a Y chromosome, so they can trace both their maternal and paternal ancestry. Females, who have mitochondrial DNA but no Y chromosome, can trace only their maternal ancestry.
So how can females discover their paternal history? One solution is to ‘borrow’ the Y chromosome of her most immediate paternal ancestor — her father. A female can have her father send his own DNA sample to 23andMe, then examine his Y chromosome as a way of understanding his paternal ancestry and her own.
<h6>Discovering Paternal Ancestry</h6>
But what if a woman&#8217;s father can&#8217;t or won&#8217;t share his DNA? By sharing 23andMe accounts with the right male relative, a woman can still discover both her maternal and paternal ancestry.
So whose DNA can a female customer use, besides her father&#8217;s? It could be anyone who shares his Y chromosome — her brother, paternal uncle (father’s brother), or even paternal grandfather (father’s father). The chart below illustrates some of the possibilities in one woman&#8217;s family tree; male relatives who share her father&#8217;s Y chromosome are depicted in blue.
You may look at the chart and ask: Why not her son’s Y? After all, he&#8217;s a male relative, too. But even though a mother shares 50% of her genes with each of her children, only fathers pass Y chromosomes to their sons. So any examination of her son’s Y chromosome would yield not her father&#8217;s paternal history, but her husband&#8217;s.
<img decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/erinpaternal33.png" alt="erinpaternal33.png"> 
The woman whose family tree is shown here (&#8220;Me&#8221;) could determine her paternal ancestry using the Y chromosomes of males who are colored blue.

Whose Y to Use? Paternal Ancestry for Ladies

<img decoding="async" class="right alignright" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/feetscale.jpg" alt="feetscale.jpg" />The Atkins diet, the South Beach diet, the Grapefruit diet, the Cabbage Soup diet — we know all these fad diets have their limits, because ultimately, the only way to lose weight is to eat fewer calories and burn more.
But have you ever thought about what controls your appetite? What if your body didn’t tell you to stop eating when you’d consumed enough calories?
You&#8217;d gain weight, that&#8217;s what. It&#8217;s long been known that mutations in a gene called MC4R cause mice to become bigger and fatter than their regular counterparts.
It&#8217;s thought that eating a lot causes the body to turn on MC4R, which in turn tells the mice to stop eating by making them feel full. There are also rare variations that disrupt the human MC4R protein and cause children to eat too much, leading to severe childhood obesity.
Interesting, you say, but does this apply to the general population too? Research published online Sunday in the journal <a href="https://www.nature.com/ng/index.html" target="_blank" rel="noopener noreferrer">Nature Genetics</a> suggests that the answer is yes.

A large study of over 77,000 Europeans by <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.140.html" target="_blank" rel="noopener noreferrer">Loos et al.</a> found a SNP near the MC4R gene, rs17782313, that was strongly associated with body mass index (BMI), a measure of obesity. (To calculate your own BMI, go to: http://www.nhlbisupport.com/bmi/bmicalc.htm) They found that each copy of the C version of rs17782313 was associated with an increase of 0.22 BMI units in adults (for a person of my height, 5 ft 3 in, that’s a little over a pound). In children, they found that this SNP had an even larger effect. Unlike the rare changes in MC4R that cause severe childhood obesity, 30 to 50% of the population has at least one copy of the C allele of rs17782313.
A second paper by <a href="https://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.156.html" target="_blank" rel="noopener noreferrer">Chambers et al.</a>, also published online Sunday in Nature Genetics, studied more than 14,000 Indian Asians and Europeans and found that a different SNP near MC4R, rs12970134, is associated with waist circumference. Each copy of the A version is associated with a 0.88 cm (0.3 in) increase in waist circumference. That means that on average, the waists of people with two copies of the A version of rs12970134 are 0.6 inches larger than the waists of people with two copies of the other version of the SNP. Talk about pinching an inch!
Fortunately for most of us, genes are only one player in our risk for obesity, as our behavior and environment can still play a large role in maintaining a healthy weight.
Calculating your BMI: You can calculate your own BMI using the following formula: multiply your weight in pounds by 0.454 to get your weight in kilograms. Then multiply your height in inches by .0254 to get your height in meters and square the result. Divide your weight in kilograms by your height in meters squared to get your BMI. A BMI less than 18.5 is considered underweight, between 18.5 and 24.9 normal, between 25 and 29.9 overweight, and above 30, obese.

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