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Diabetics have to be worried about more than just their cholesterol when it comes to the health of their arteries. They also have to watch their blood sugar to help prevent the build up of fatty plaques that can block blood flow.
But new research from the Joslin Diabetes Center and Harvard Medical School shows that high blood sugar may be more dangerous to some diabetics than others.
Dr. Alessandro Doria and colleagues found that a genetic variant on chromosome 9 previously associated with coronary artery disease (CAD) risk in the general population has an even greater effect in diabetics with poor blood sugar control. These results, published online today in the <a href="http://jama.ama-assn.org/cgi/content/short/300/20/2389" target="_blank" rel="noopener noreferrer">Journal of the American Medical Association</a>, could someday help doctors identify people with diabetes who are at higher risk of CAD earlier, allowing them to aggressively target these patients for intervention.
People with diabetes are at least twice as likely as those without to have heart disease. Some studies suggest that middle-aged diabetics have the same high heart attack risk as people without diabetes who have already suffered a heart attack.

The first of two study groups was composed of 322 diabetics with coronary artery disease and 412 without. The researchers found that the risk for CAD was about the same in people with either the AA or AG genotype at rs2383206, even if they had poorly controlled blood sugar.
Having the GG genotype at rs2383206, however, increased the odds of CAD by about two-fold for diabetics with well-controlled blood sugar. And when high blood sugar was thrown into the mix, the odds of CAD for people with two Gs went up higher still — about four times compared to the lowest risk group.
In people with the GG genotype and a long history of high blood sugar, the odds of CAD were increased about seven times compared to diabetics with a history of well-controlled blood sugar.
(The study looked at rs2383206, which is available to 23andMe customers who were genotyped on the second version of our custom chip. But people who were genotyped on the first version can use rs2383207, the SNP we feature in the Health and Traits research report on Heart Attack, as a substitute. The G version is riskier for both SNPs.)
In a separate study group of 475 diabetics who were followed for 10 years, people with the AA or AG genotype at rs2383206 had the same risk of dying in general, or from cardiovascular disease in particular, regardless of their blood sugar. But for people with the GG genotype, the risk of death went up by a factor of two when blood sugar was not under control.
Both groups of diabetics Doria et al. studied were of European ancestry.
“While good glucose control is important for all people with diabetes, testing for this predisposing variant may help doctors identify patients for whom better control is an absolute necessity,” said Doria in a statement. The authors estimate that 30% of diabetics will have two Gs at rs2383206.
The probability of clinically significant CAD is about 30% for type 2 diabetics in general. The authors say this number could shoot up to 60% for diabetics with the GG genotype at rs2383206 and poorly controlled blood sugar.
The authors admit that this is a small study that will need verification. They also note that their findings are at odds with a <a href="https://www.ncbi.nlm.nih.gov/pubmed/18048406?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">previous report</a> that found no difference between the risk conferred by SNPs in the 9p21 chromosomal region (where rs2383206 lies) in diabetic vs. non-diabetic subjects. Due to a number of methodological differences between the two studies, Doria et al say that no direct comparison of the results is possible.

23andMe Blog

23andMe Blog Team

Combination of Genetics and High Blood Sugar May Mean Extra Heart Disease Risk for Diabetics

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For many people, the first and last place they will ever study genetics is high school biology class. So it is crucial that these classes prepare people to deal with the barrage of genetic advancements that are increasingly impacting everyday life.
Unfortunately, many high school biology courses are not doing such a good job of communicating the fundamentals of genetics, according to an analysis by researchers from the American Society for Human Genetics (<a href="http://www.ashg.org/" target="_blank" rel="noopener">ASHG</a>).
For three years now the ASHG, along with several partners, has sponsored the Annual National DNA Day Essay Contest. The contest challenges high school students to examine, question, and reflect on the important concepts of genetics. Shortly before DNA Day 2008, researchers used a selection of these essays from previous years to see where students might be going wrong. Their results were published in the journal <a href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2278104" target="_blank" rel="noopener">Genetics</a>.

Several themes emerged from the authors’ analysis. Most striking were the students’ lack of understanding of the limits to genetic engineering and their belief that single genes always determine traits and diseases.
The researchers attributed students’ misconceptions to “genohype” in media coverage of scientific discoveries, science curriculum standards that lack depth, and even the undergraduate biology education teachers receive.
Students often equated the identification of a disease-associated gene with “curing” a disease through gene replacement. A disturbing number of students thought genetic engineering could be used to “improve” and “design” their offspring, with the goal of having a “perfect” child.
Some students even suggested that genetic engineering would allow scientists to put a gene from one species into another in order to get a specific trait. For example:
“We could eliminate all the premature deaths of people dying around the world from thirst if we genetically modified people to inherit some of the characteristics of the camel, allowing them to go for months at a time without drinking water.”
The rules of the DNA Day Essay contest require teachers to submit the top three essays for each question from their students. The fact that so many essays were from students with serious misunderstandings suggested to the ASHG researchers that the teachers themselves may not be receiving very good undergraduate training in genetics, and that their unchallenged misconceptions are being passed on.
Like many before them, the authors of the ASHG study suggest that partnerships between scientists and educators will be valuable in improving genetics education. They propose shifting instruction from the simple Mendelian view of inheritance to a more nuanced perspective that takes into account multiple genetic and non-genetic contributions to traits and diseases, with a focus on concepts over content. But, they concede, this type of change is impeded by the need for districts and states to demonstrate content knowledge on standardized tests.
“Until significant research is performed by scientists and their educator colleagues that demonstrates which methods adequately teach both content and concepts, schools systems are unlikely to change their methods,” the authors write.
Some resources for genetics education:
<ul>
<li>23andMe&#8217;s own <a href="https://www.23andme.com/gen101/" target="_blank" rel="noopener">Genetics 101</a></li>
<li><a href="http://learn.genetics.utah.edu/" target="_blank" rel="noopener">University of Utah Genetic Science Learning Center</a></li>
<li><a href="http://www.dnalc.org/home.html" target="_blank" rel="noopener">Dolan DNA Learning Center at Cold Spring Harbor</a></li>
</ul>

Student Misconceptions About Genetics

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Not all alcoholics are created equal. People differ in why they drink, how they drink and what effects drinking will have on their health and relationships.
A key biological component of the variability in alcoholism may be in the control of signaling by serotonin, a brain chemical that carries messages between nerve cells and mediates the rewarding effects of alcohol.
Scientists at the University of Virginia have found that a variation in the serotonin transporter gene, which regulates serotonin levels, is associated with drinking intensity. The results, which will appear in the February 2009 issue of Alcoholism: Clinical and Experimental Research, were published online yesterday.

Senevirante et al tested six variations in the serotonin transporter gene for association with drinking intensity in 275 alcoholics seeking treatment – 165 were Caucasian and 110 were Hispanic. Women made up 21.5% of the sample.
In the Caucasian sample only, the researchers found that having one or two copies of a C at rs1042173 led to less intense drinking, defined as number of drinks per drinking day. There was no difference in number of drinks averaged over 90 days. People with the AA genotype drank an average of about 11 drinks per drinking day, while those with the AC or CC genotype drank about eight and a half.
(23andMe customers see their data for rs1042173 using the Browse Raw Data feature)
Previous research has linked a separate variation in the serotonin transporter (5-HTTLPR) with alcohol dependence, but results have been conflicting.
The study’s authors point out that in all cases, the number of drinks people had exceeds the threshold for what is considered heavy drinking (five or more standard drinks per day for men and four or more for women). They also note that their study looked only at alcoholics seeking treatment, who may not be representative of alcoholics in general.
In the future, the researchers say they hope to investigate whether rs1042173 can be used to provide more effective treatment for alcoholism by predicting whether medications that affect the serotonin system will work for an individual.

Genetic Variant Linked to Drinking Intensity in Alcoholics

Yesterday the 23andMe team launched the much-requested user-to-user communication feature, which will allow you to exchange messages directly with your 23andMe connections and other searchable community members. Here&#8217;s how it works:
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To send a message, simply visit a person&#8217;s Member Profile page by searching for them, or clicking their name or picture where it appears in a Community discussion or in your list of connections. If someone else sends you a message you&#8217;ll find it in your Inbox, which can be found under &#8220;Account&#8221; on the left-hand side of the screen. You can reply to messages directly from your 23andMe Inbox.

You&#8217;ll also find occasional messages in your Inbox from the 23andMe Team, letting you know about new features and reminding you to take action on things like pending invitations and account settings.
We are very excited to provide our users with a platform for one-on-one dialogue on the site and are continuously working to improve your experience with our service. If you have any questions or comments, please don&#8217;t hesitate to contact us at help@23andme.com.

23andMe Community Now Includes User-to-User Messaging

You&#8217;ve heard the family legends – or maybe you haven&#8217;t. Now 23andMe has a new ancestry feature that can show you what your genes have to say about where your ancestors originated.
This new feature, called Global Similarity: Advanced, shows you which populations from around the world you are genetically nearest to, giving you a clue as to where in the world your ancestors are likely to have lived over the last half-millennium or so.
<img loading="lazy" decoding="async" class="size-medium wp-image-2005" title="gsa-lillymendel-world" src="https://blog-api.23andme.com/wp-content/uploads/2008/11/gsa-lillymendel-world-293x300.png" alt="Lilly Mendel in Global Similarity: Advanced World view." width="309" height="316" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/11/gsa-lillymendel-world-293x300.png 293w, https://blogcms.23andme.com/wp-content/uploads/2008/11/gsa-lillymendel-world.png 484w" sizes="auto, (max-width: 309px) 100vw, 309px" />Lilly Mendel in Global Similarity: Advanced&#8217;s World view. 
How does it work? Let&#8217;s take 23andMe everywoman Lilly Mendel as an example.   In the image to the right she is shown as a green Google Maps-like cone on a background of colored squares, each of which represents a individual of known ancestry from our reference database.
The closer two people are on the plot, the more similar they are genetically. The genetic similarity is measured over all of Lilly&#8217;s autosomal SNPs, so it reflects the genetic contributions of all of her ancestors (unlike mitochondrial DNA, which is only inherited along the maternal line).
Lilly sits right in the middle of the European reference individuals (yellow squares), far from other reference populations like Native American and Central/South Asian; this means that Lilly&#8217;s ancestors were likely European. Lilly&#8217;s friends and family show up as black cones on the same graphic, so she can see where they each land with respect to the reference individuals and to each other.

World view shows our entire reference database at once. But Global Similarity: Advanced also lets you look at about a dozen further views, corresponding to different groupings of the world&#8217;s people. Lilly and her family are likely to be especially interested in the four European views, including Europe overall, and separate Northern, Southern, and Eastern European views.
<div id="attachment_2006" style="width: 310px" class="wp-caption alignleft"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-2006" class="wp-image-2006 size-medium" title="gsa-lillymendel-northerneurope" src="http://35.88.189.111/wp-content/uploads/2008/11/gsa-lillymendel-northerneurope-300x169.png" alt="" width="300" height="169" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/11/gsa-lillymendel-northerneurope-300x169.png 300w, https://blogcms.23andme.com/wp-content/uploads/2008/11/gsa-lillymendel-northerneurope.png 429w" sizes="auto, (max-width: 300px) 100vw, 300px" />Lilly Mendel in Northern European view.</div>
Here&#8217;s an image of Lilly and the rest of the Mendel family in the Northern European view. The same reference individuals from World view are labeled here with their countries of origin so we can get a closer look at the Mendels&#8217; ancestry.
The Mendels tend to fall closest to German and French reference individuals, suggesting that their ancestry is quite probably Northern European, and probably a mix of a number of European peoples.
Satisfyingly, one of 23andMe&#8217;s science team was born and raised in Dublin, and he falls right in the middle of the Irish cluster of reference individuals. Another 23andMe&#8217;er has one Eastern Asian parent and one European parent; she shows up about halfway between Europe and East Asia in World view. On the plot it looks like she&#8217;s closest to Central Asian populations, but it&#8217;s really saying that she&#8217;s roughly equidistant from Europe and Asia.
If the arrangement of the clusters of people looks a bit like that of a geographic map to you, 1) congratulations on staying awake in class, and 2) this isn&#8217;t an accident. As we&#8217;ve written recently in the Blog (<a href="https://blog.23andme.com/2008/08/13/a-different-kind-of-gene-mapping-comparing-genetic-and-geographic-structure-in-europe/">here</a> and <a href="https://blog.23andme.com/2008/09/03/a-different-kind-of-gene-mapping-comparing-genetic-and-geographic-structure-in-europe-the-return/">here</a>), geneticists are learning that genetic distance corresponds rather closely with geographic distance &#8212; or at least   it did until transoceanic ships and airplanes came on the scene. You can use your knowledge of geography to help interpret your results. For instance, our reference database currently doesn&#8217;t have any individuals of Korean ancestry. If you or a friend has Korean ancestry, it shouldn&#8217;t be a big surprise to find that person situated in the empty space between the Japanese and Chinese reference individuals, just as Korea is on a geographic map.
We&#8217;ve developed an animated Tour that both helps explain Global Similarity: Advanced and roughly documents the peopling of the Earth, beginning with the origin of modern humans in Africa about 200,000 years ago and their spread around the globe. Try clicking &#8220;Take a Tour&#8221; as you begin to explore the feature to start the animation. (And if you like that, be sure to give our fun and more detailed new video <a href="https://www.23andme.com/gen101/prehistory/prologue/">Human Prehistory: Prologue</a> a try.)
The idea underlying Global Similarity: Advanced is simple enough. We calculate the genetic distances between all pairs of individuals that you&#8217;d like on the plot, again based on all the autosomal SNPs. In general, these points are arranged in some high-dimensional space, so you can&#8217;t readily picture them in two dimensions. We coax them down into two dimensions, like so: you lay all the individuals out in a plane, and move them around until the distances between each pair of points in the plane are as close as possible to the corresponding genetic distances. Once you find this optimal two-dimensional arrangement of the points, you&#8217;re done. There do arise some interesting technical issues when the rubber hits the road, and these are discussed in the feature&#8217;s white paper.
The reference database the feature is based on includes more than 1,200 individuals drawn from the CEPH-HGDP project, whose SNP genotyping 23andMe funded and made publicly available, and from Illumina&#8217;s iControlDB. This dataset does a great job at covering the breadth of human genetic diversity. Still, there are many peoples that we look forward to adding to the database to round it out, and in the near future we will be asking our customers if they wish to become part of this ancestry reference. As they say, watch this space.
Try out Global Similarity: Advanced for yourself or, if you don&#8217;t have an account yet, via one of our <a href="https://www.23andme.com/user/signup/">free demo accounts</a>. Let us know what you think of the feature at <a href="mailto:help@23andme.com">help@23andme.com</a>, or better yet, in the 23andMe Community!

The Debut of a New Ancestry Feature

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Recent genetic discoveries have taught researchers a lot about type 2 diabetes and identified particular genetic variants that can influence a person&#8217;s risk of developing the condition.
But two studies published this week in the New England Journal of Medicine conclude that genetic information still pales in comparison to factors like body weight, smoking, cholesterol levels, and other medical diagnostics when it comes to predicting who will develop the condition.
The papers are a reminder that although personal genomics promises to become a valuable supplement to preventive medicine, the information it provides shouldn&#8217;t be considered a replacement for regular check-ups and a healthy lifestyle. And though genetics certainly plays a role, diet, exercise and other environmental factors have a substantially greater impact on whether a person will develop type 2 diabetes.

Both studies looked at one-letter DNA variations known as single-nucleotide polymorphisms (SNPs) that have been linked to diabetes. The 23andMe Personal Genome Serviceâ„¢ provides information on nine diabetes-associated SNPs.
One study used data from the legendary <a href="http://www.framinghamheartstudy.org/">Framingham Heart Study</a>, which has followed three generations of participants over a period of 60 years, to show that inheriting a greater number of high-risk diabetes genes does increase a person&#8217;s chances of developing the condition. But when added to traditional measures of diabetes risk such as family history, body-mass index, fasting plasma glucose level, and blood pressure, a person&#8217;s genotype at the 18 SNPs studied did not significantly improve the researchers&#8217; ability to predict which of the 2,377 study participants became diabetic over a period of 28 years.
The other study, which looked at 16 SNPs in 16,061 Swedish and 2,770 Finnish subjects who had been followed for an average of 23.5 years, produced a similar result. The authors concluded that &#8220;common genetic variants associated with the risk of diabetes had a small effect on the ability to predict the future development of type 2 diabetes.&#8221;
However, because the physiological risk factors typically develop later in life (though they are becoming distressingly common in younger populations) the authors of the Framingham-based study suggest genetic information could be useful in motivating young people who have inherited a high diabetes risk to control their weight and take other preventive measures.
And research is bound to produce more knowledge about the genetic roots of diabetes. So in the not-too-distant future, a person&#8217;s genotype is likely to provide substantial predictive information beyond what is available from family history and physiology.

Diabetes Risk and Genetics

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About 4,600 years ago, in northern Germany, a small village buried 13 of its residents.
<h6>Violent Death</h6>
The deceased ranged in age from less than a year to nearly 60 years old and were buried in pairs or small groups. And virtually all of them had suffered violent, probably painful deaths.
Because the majority of the deceased were women or children, the archaeologists who discovered their remains have argued that these victims were likely the unfortunate casualties of a violent raid by a neighboring village – a common occurrence during this period.
Research on the skeletal remains of the deceased, as well as the grave goods with which they were buried, have revealed much about the lifestyle and culture of these early Europeans.
<h6>Using Genetics to Find Relationships</h6>
But many questions — especially about the relationships between the buried individuals themselves — were left unanswered.   So, a team of scientists from Germany and the United Kingdom decided to use the DNA preserved in these skeletal remains to discover what relationships — if any — existed between these 13 individuals.   The results of this study are reported in this week’s <a id="c_vf" title="Proceedings of the National Academy of Sciences" href="https://www.pnas.org/content/early/2008/11/17/0807592105.abstract" target="_blank" rel="noopener noreferrer">Proceedings of the National Academy of Sciences</a>.
Specifically, the scientists were interested in whether the individuals buried closest to each other were also close relatives.   The 13 victims were found in four separate graves.
Each contained at least one adult, along with anywhere from one to three children.   As a result, some scientists have speculated that each grave might represent a separate family killed in the attack.     D
NA analysis, they argue, would allow them to fill the gaps surrounding the identities of the deceased.
Scientists extracted DNA from the teeth of all 13 individuals.   They focused on the mitochondrial DNA (mtDNA), which is passed down from mother to child, the Y-chromosome, which is passed down from father to son, and small segments of the remaining chromosomes, which are passed down from both parents to their children.
<h6>A Family That Died Together</h6>
Even though ancient DNA is notoriously difficult to work with, the authors were able to extract usable DNA from nine of the 13 individuals.
The results from one of the four burials, Grave 99, were especially intriguing.   The grave contained the remains of an adult male, an adult female, and two male children.   DNA analysis revealed that the adult female had the same mtDNA type as the two male children (K1b).   Analysis also revealed that the adult male had the same Y-chromosome DNA type as the two male children (R1a).
Due to the ways that mtDNA and Y-chromosome DNA are passed from one generation to the next, these results suggest that the two adults in Grave 99 were husband and wife, and that the two male children were their offspring.   Indeed, the authors had originally hypothesized some sort of connection between these four individuals, because while the two adults adhere to normal burial patterns for the time period (lying toe-to-toe facing south), the two children face north, toward their parents.
The notion of these four individuals being buried together, as a family, raises many questions on the origins of the nuclear family in ancient times.   Even the authors admit that “our image of past family life and structure is still dominated by 19th century ideals, and reconstruction of prehistoric families even now adhere to these orthodox schemes.”
Indeed, there has been little evidence to precisely date the origins of the nuclear family, and this example hardly closes the book on how and when such a social unit developed.   However, it does show that using ancient DNA can be quite useful in determining ancient biological relationships.   Indeed, the results from Grave 99 reveal how important the nuclear family must have been to these villagers; that they chose to bury these four victims not as individuals but as a social unit, huddled together in a single grave.

Exploring Ancient DNA Insights

This guest post is by Brenna Henn, a Stanford University&#8217;s Department of Anthropology doctoral student and a 23andMe consultant. Brenna studies human evolution using genetic information. Her interests include the origin of modern humans, migration patterns among African groups, and genetic models of demography.
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One of the reasons genetics is such a powerful tool for telling us about the past is that mutations that accumulate over the generations can be used as a clock, allowing scientists to calculate when different events occurred in the prehistoric past.
By counting the number of mutations differentiating one person from another, we can determine when in the past they shared a common ancestor. Each mutation is like a genetic tick of the clock, equivalent to a certain period of time. But figuring out how frequently mutations occur, and thus how long each tick of the genetic clock takes, is a major enterprise.
In a new paper appearing this month in <a href="https://dx.doi.org/10.1093/molbev/msn244" target="_blank" rel="noopener">Molecular Biology and Evolution</a>, scientists from 23andMe propose that the genetic clock may have started running faster after the Ice Age ended about 15,000 years ago. If so, they may have resolved a discrepancy that has perplexed researchers for a number of years.

DNA mutation rates are estimated in two different ways. Geneticists can either count the number of mutations that occur in one generation (the changes between parents and their children), or they can count the number of differences between human and chimpanzee DNA and calculate a mutation rate based on the number of years since the two species diverged &#8212; about 6 million years.
It turns out that mitochondrial DNA mutation rates measured by these two methods described differ almost 10-fold. This difference is seen not only in humans, but also in species such as birds and fish. The discrepancy hints at the possibility that what we are measuring might be more complicated than we previously thought.
Working with Marcus Feldman of Stanford University, 23andMe scientists set out to find a new way of estimating the human DNA mutation rate by comparing the genetic diversity of lineages derived from the first human inhabitants of various continents and islands with archaeological finds that give precise information about when those colonists arrived (such as Polynesia).
We focused our studies on mitochondrial DNA data because there are a large number of mitochondrial sequences available in databases and the mutation rate of this DNA is known to be higher than in the autosomal DNA found in the 23 pairs of chromosomes,
What we found was surprising. Younger lineages (i.e. groups of people that have more recent common ancestors) had higher rates of mutation than older lineages, meaning that the molecular clock is not constant for human mtDNA: it slows down as lineages get older.
But why?
In our study the estimated mutation rates dropped off quickly around the end of the Ice Age &#8212; 15,000-20,000 years ago &#8212; suggesting that population history may play an important role in explaining the reduction in genetic diversity, and thus the changing pace of the DNA clock.
Prior to 20,000 years ago, humans lived in small hunter-gatherer groups that likely experienced boom and bust cycles: periodic climatic shifts or food shortages probably caused frequent and sudden population collapses. When populations decrease in size, or “bottleneck,” some genetic lineages are lost, which decreases the genetic diversity of the population. Since mutation rates are calculated using genetic diversity, the mutation rate estimates from these older lineages are slower.
After the climate warmed about 15,000 years ago and humans subsequently invented agriculture, populations grew dramatically. This resulted in more stable genetic diversity and faster mutation rate estimates.
More research needs to be done before we can determine whether population history or other factors, such as natural selection changing mutation rates, are primarily responsible for the human molecular clock slowdown. For example, we could simulate genetic diversity changes when a population size decreases and see if this matches the empirical mutation rate estimates.
Using our new data, which trace the slowdown in mutation rate back in time, scientists can identify the number that is most appropriate to use for studies of particular population events.
To date, the timing of most population events in human evolutionary genetics was estimated has used a rate close to the slower one we see for older lineages, before the end of the Ice Age. So our understanding of the genetic history of early human evolution shouldn’t change very much. But the timing of the splits between mitochondrial lineages associated with relatively recent events, such as agricultural expansions, may need revision. Using our newly calibrated mitochondrial mutation rates, researchers will be better able to correlate genetic, archaeological and linguistic data, leading to a more accurate understanding of human prehistory.

Solution to Mutation Rate Discrepancy

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Because their ancestors often were slaves during the 18th and 19th centuries, and therefore usually lacked birth or death certificates, it is very difficult for African American genealogists to trace their ancestors further than a few generations.
Even when they can trace their ancestry to the slavery era, it is virtually impossible to find exactly where their ancestors originated because slave ships did not keep passenger lists of the people they captured from Africa.
As a consequence, many have been turning to genetics as a tool to help trace their African ancestry. But how reliably can genetics trace a person&#8217;s ancestry back to a specific African location or ethnic group?
Using genetics this way is quite complex; even the most advanced analysis can&#8217;t provide all the answers.

Relying on genetic data for genealogical purposes can be problematic, especially if your expectations are too great.
For example, Henry Louis Gates, Jr., the Director of the W.E.B. Du Bois Institute for African and African American Research at Harvard, had his Y-chromosome genotyped by two different companies. The first told him that his ancestors likely traced back to Nubia or Egypt, while the second test more accurately placed his paternal ancestry in Europe.
As an African American, Gates believes that the first company may have simply &#8216;told him what he wanted to hear&#8217;: that all of his ancestry traced back to Africa. But, as is often the case, one&#8217;s genetic ancestry can be more complex than meets the eye.
One problem is that genetic analyses predominantly trace deep ancestry. Because genetic information does not change significantly within one or two generations, genetics generally shows where a person’s ancestors lived thousands of years ago. This is hardly useful to genealogists who are looking for information about ancestors who lived only a few hundred years ago.
That isn&#8217;t to say we can’t learn anything useful about the deep ancestry of many African Americans — in fact, studies of genetic ancestry have yielded much information about prehistoric population movements across the continent. For example, there are clear genetic ‘footprints’ in modern Africans – and African Americans – indicating massive expansions of Bantu-speaking peoples from West Africa into the eastern and southern part of the continent over 4,000 years ago. This has helped archaeologists understand the extent to which not only the Bantu culture and language, but the people themselves, spread throughout the continent.
Most African Americans have the signature of this Bantu migration in their genes because they are descended from populations that were affected by it. But many, including Gates, have the genetic signature of another widespread group: Europeans. Indeed, European ancestry is not uncommon among African Americans, whose ancestors can include white slave owners who fathered children with their slaves.
The use of genetic data can be useful in confirming anecdotal evidence of a non-African ancestor in an African American&#8217;s family tree.
Many African American genealogists want greater detail and resolution from their genetic information, even a link to a specific nation or tribe. But in many cases this is simply not possible. The population history of Africa — especially sub-Saharan Africa — is older and more genetically complex than that of any other region of the world. Homo sapiens evolved in East Africa more than 150,000 years ago, and has been living throughout Africa continuously since that time.
There have been countless migrations, dispersals, and expansions of African peoples to all parts of the continent — in addition to the Bantu expansions. As a result, the genetic diversity of present-day Africans is incredibly complex.
In many cases, scientists are unable to associate a specific genetic classification with a specific tribe or ethnic group. There are of course a few exceptions — isolated hunter-gather groups like the !Kung of the Kalahari Desert and the Pygmies of the Central African Rainforest have lower levels of genetic diversity as a result of their relative isolation. But in West Africa, where the majority of slaves were captured, there is significant genetic diversity both within countries and within tribal or ethnic affiliations.
The high level of diversity means that scientists have a difficult time pinpointing where a particular person&#8217;s genetic roots trace beyond a more general geographical region (i.e. West Africa). For example, the paternal haplogroup E3a, found in more than half of African American men, is just as common in Africa itself &#8211; and spread throughout the continent. So, for an African American male who&#8217;s paternal ancestry falls within the E3a haplogroup, it could be virtually impossible to narrow down the place of origin of his African ancestors.
Still, when traditional tools are unavailable or incomplete genetics can reveal useful genealogical information, whether a person&#8217;s roots trace back to Africa, Europe, or someplace else entirely.

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