<img decoding="async" class="left alignright" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/illuminachip.png" alt="illuminachip.png" />Sometimes our customers ask us about the accuracy of their 23andMe data. How certain are we that they really do have the genotypes we report?
The answer is, very certain. We typically claim that the genotyping technology we use reports the correct call for more than 99.9 percent of the approximately 580,000 single-letter DNA variations we report. Those variations, known as single-nucleotide polymorphisms, or SNPs, are the raw data upon which the 23andMe Personal Genome Service is built.
<h6>Testing Accuracy</h6>
But apparently one of our customers decided to do more than ask. He designed a simple experiment to test the reproducibility of the SNP chips that 23andMe and other companies use to give people access to their genetic data.
Antonio C.B. Oliveira signed himself up for 23andMe and a similar service, then wrote a computer program to compare the genotype calls at the 560,299 SNPs where both companies reported data. He found a grand total of 23 discrepancies, or about 0.004% of the common reported SNPs.
&#8220;This error rate seems to me to be quite acceptable,&#8221; Oliveira concluded on <a href="http://longavista.blogspot.com/">Longa Vista</a>, a blog he established to share his results.
<h6>Another Comparison</h6>
Oliveira is actually the second customer to conduct such an experiment. When Ann Turner compared two datasets for the same person (not herself) back in January, she discovered 35 discrepancies.
And when <a href="http://biology.plosjournals.org/perlserv/?request=get-document&#038;doi=10.1371/journal.pbio.0050254&#038;ct=1">Craig Venter</a> and his colleagues published his full genome last October, they also found the discrepancies between their own sequencing results and two different SNP genotyping platforms to be negligible.
We aren&#8217;t surprised — these results confirm experiments that 23andMe performed before launching our Personal Genomics Service last year. But now 23andMe can say with confidence that independent testing has shown that the Illumina genotyping technology we use is extremely robust.

23andMe Blog

23andMe Blog Team

23andMe Genotyping Technology Aces Independent Tests

<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/05/istock_000002904128xsmall.jpg" alt="istock_000002904128xsmall.jpg" class="right alignright" width="278" height="187" />The amount of sugar in the bloodstream must be tightly controlled. Too much can cause damage to nerves, blood vessels and organs. But too little sugar starves the body, especially the brain, of the energy it needs.
Fasting plasma glucose (FPG) levels are a measure of how well a person’s body can control blood sugar levels, a process that goes awry in diabetes. A report published online today in Science Express finds that FPG levels can be impacted by single-letter variations in genes known to be involved in blood sugar regulation.

<h6>Blood Sugar Levels</h6>
Physicians routinely test their patients&#8217; FPG levels to screen for diabetes and pre-diabetes. A high blood concentration of glucose after 8 to 10 hours of fasting indicates that a person’s ability to regulate blood sugar is impaired. High FPG levels are also associated with coronary heart disease mortality for both diabetic and non-diabetic individuals.
In order to identify genetic variants involved in blood sugar control, Nabila Bouatia-Naji and colleagues carried out a genome-wide association study to find single-nucleotide polymorphisms, or SNPs, correlated with FPG levels.
The most strongly associated SNP in an initial sample of about 650 non-obese French people. The same SNP was correlated with FPG levels in a second sample that included about 3,400 French people, approximately 5,000 Finns and a group of about 860 obese French children.
<h6>Additional Variants</h6>
Two other SNPs that were previously found to be associated with FPG were also found to be significantly associated with FPG levels in this study. The researchers believe that these genes affected by these SNPs affect the threshold level of glucose in the bloodstream, which triggers the secretion of insulin by the pancreas. The higher the threshold, the higher the blood glucose level will rise before insulin starts to regulate it.
“These sequences explain about 5 percent of the normal variation in blood glucose levels between otherwise healthy people,” explained Robert Sladek, one of the study&#8217;s senior authors.
When all three SNPs were considered together to create a score (each person has two copies of each SNP and gets one point for each “low FPG” version, meaning the score can range from 0 to 6), the researchers found that on average people who scored a 5 or 6 had FGP levels 0.24 mmol/l lower than people who scored 0 or 1.
“It’s important to know that a high blood glucose level, even within the normal and non-diabetic range, is a risk factor for early mortality,” said Dr. Philippe Froguel of Imperial College and CNRS. “Epidemiological studies have shown that 80 percent of the risk of cardiovascular disease is related to a blood glucose level just above the average.” The researchers propose that the three SNPs they identified &#8220;are likely to have a non-negligible impact on human health.&#8221;
&nbsp;

Genetic Factors Related to Blood Glucose

<img decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/04/siegeofacre1291.jpg" alt="siegeofacre1291.jpg" class="right alignright" />Generally, the DNA in a man&#8217;s Y-chromosome contains information about prehistoric migrations that happened many millennia in the past. But a recent study of men in Lebanon shows that genetics can be a reflection of more recent events as well.
A paper published in the April issue of the American Journal of Human Genetics shows that two major events in the history of religion — the spread of Islam and the Crusades — have left their mark on Lebanon&#8217;s male population.
The authors of the AJHG paper showed that a disproportionate percentage of Muslim men in Lebanon have Y-chromosomes of a type that is common on the Arabian peninsula. Migrants from Arabia brought Islam to Lebanon during the 7th century.
Similarly, a disproportionate number of Lebanese Christian and Druze men have Y-chromosomes similar to those found in western Europe. In fact, the most common Y-chromosome signature in Lebanon is most abundant in France, Spain, northern Italy and the Low Countries. But it is found nowhere else east of Hungary.

The authors of the AJHG paper attribute that remarkable genetic connection to the Crusades, a series of military campaigns by European invaders against Jerusalem and other cities of religious significance in the Near East.
There is also an indication that men from Turkey introduced their genes into the Lebanese population during the time of the Ottoman Empire, which ruled Lebanon from the 16th to 20th centuries.
In most countries, geography is the most significant factor influencing the genetic variability of the population. But in Lebanon, religion accounts for more than three times as much genetic variation as geography.
&#8220;Such structure might arise only when several unusual criteria are met,&#8221; the AJHG paper concludes. &#8220;Migrations based on religion must take place between areas with different representative Y-chromosomal types, and they must establish genetically differentiated communities that remain stable over long time periods. In Lebanon, these conditions appear to have been met for over 1,300 years.&#8221;
&#8220;The Siege of Acre&#8221; by Dominique Louis Papety (1815-1849)

Historical Genetics: Researchers Find Traces of Crusades, Spread of Islam in Lebanon

<div style="width: 435px" class="wp-caption alignright"><img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/03/birthcertificate.jpg" alt="birthcertificate.jpg" class="right" width="425" height="282" />Photo by Nancy Catherine Walker/iStockphoto</div>
If you were adopted, conceived through sperm donation or don’t know your parents for some other reason, 23andMe can give you a glimpse into your genetic legacy. Our service can’t help you locate your biological parents or reveal their medical histories — but it can provide some information about their heritage, and maybe even offer a few hints at some of their traits
Click <a href="https://www.23andme.com/dna-health-ancestry/">here</a> to learn more about what 23andMe&#8217;s Personal Genome Service can and can&#8217;t do with regard to unknown parents:
<h6> 
Ancestry</h6>
23andMe’s Personal Genome Service offers a number of different tools for probing your ancestry. The broadest view comes from the Global Similarity feature, which identifies the native populations around the world you most resemble genetically. It is likely the majority of your ancestors came from the one or two regional populations that are most similar to you.
The <a href="https://www.23andme.com/you/haplogroup/maternal/">Maternal Ancestry</a> feature offers a different vantage point, using one specific part of the genome to <a href="https://www.23andme.com/topics/ancestry/family-tree/">trace a single branch of your family tree</a> back in time and space. The results apply to only one branch — your mother’s all-female lineage — but they trace it all the way back to the origin of the human species about 200,000 years ago. As a result, the Maternal Ancestry feature gives you a very good idea of where your mother’s mother’s mother’s … family came from.
The <a href="https://www.23andme.com/you/haplogroup/paternal/">Paternal Ancestry</a> feature provides similar information, except that it provides information about a person’s all-male ancestral line. Because it analyzes DNA on the Y-chromosome, however, it is only available for men.
Finally, 23andMe recently introduced the Ancestry Painting feature, a new component of our service that could be of great interest to people who are uncertain about their heritage. Ancestry Painting examines each stretch of a person’s DNA and determines which of three continents it most likely came from — Africa, Asia or Europe. Because each person gets a complete set of chromosomes from each parent, the Ancestry Painting feature can tell an adopted person what continent each of his or her parents’ ancestors came from. The daughter of an African-American mother and an Asian-American father, for example, could easily see that signature in her Ancestry Painting.
<h6>Family Relationships</h6>
The data produced by 23andMe&#8217;s Personal Genome Serviceâ„¢ is not a tool to locate unknown parents. But it can be useful for determining the relationships between people. If you suspect another person might be related to you, you could test that theory (as long as that person also signs up for 23andMe and agrees to share profiles). For example, if you and a half-sibling compared yourselves to one another you would find that you share substantial stretches of half-identical DNA. 

<h6>
Health and Physical Traits</h6>
Most people make assumptions about some of the genetic variants they have inherited by looking at their parents and grandparents. A family history of heart disease, cancer or diabetes, for example, may indicate that a person has inherited some genetic predisposition for that particular ailment.
Naturally, people who do not know their parents have no idea about any disease-related genetic variants they might have inherited. While 23andMe does reveal some genetic information about genetic variations that have been associated with diseases and conditions, it does not offer a full enough view to establish a family history.
Because genetics is only one among many factors that can influence a person’s health and physical traits (and often only a minor factor!) there is very limited definitive information 23andMe can provide about unknown parents’ physical appearance or medical history. But even at this early stage of research, 23andMe can give you a glimpse at your parents’ DNA simply by showing you your own, along with the results of recent scientific studies that give it context. And over time, we hope to learn much more about how genetic information translates into <a href="https://www.23andme.com/dna-ancestry/">physical traits</a> and health outcomes.

Adoption and 23andMe: Filling Gaps in Your Family Tree

<div style="width: 160px" class="wp-caption alignright"><img loading="lazy" decoding="async" class="right" src="https://blog-api.23andme.com/wp-content/uploads/2008/04/tallshadow2.jpg" alt="tallshadow2.jpg" width="150" height="200" />Photo by Dave2003/istockphoto</div>
Three articles published online this week in the journal <a href="https://www.nature.com/ng/index.html" target="_blank" rel="noopener noreferrer">Nature Genetics</a> report a bumper crop of SNPs associated with human height.
Unlike other physical characteristics such as obesity that are caused by a mix of genetic and environmental factors, 90% of normal variation in human height is due to DNA alone. But unraveling the details of the genetics has been difficult.
Last year, two large studies (<a href="https://www.ncbi.nlm.nih.gov/pubmed/17767157?ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">here</a> and <a href="https://www.ncbi.nlm.nih.gov/pubmed/18193045?ordinalpos=2&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">here</a>) looked for SNPs associated with height. Only two convincing candidates were found. Both of them accounted for only about a half-centimeter difference in height.
<h6>New Studies</h6>
The three new studies (<a href="https://dx.doi.org/10.1038/ng.121" target="_blank" rel="noopener noreferrer">here</a>, <a href="https://dx.doi.org/10.1038/ng.125" target="_blank" rel="noopener noreferrer">here</a>, and <a href="https://dx.doi.org/10.1038/ng.122" target="_blank" rel="noopener noreferrer">here</a>) were able to find more SNPs associated with height. The studies were successful by using extremely large sample sizes. Two of the studies had more than 30,000 participants and the third study looked at more than 15,000 people. Large sample sizes increase the chance that SNPs with small effects will be found.
Like the previously found height SNPs, the new SNPs each individually account for only a fraction of a centimeter in height difference.
The authors of all three papers note that statistical analyses of their data indicate that many more small effect SNPs are waiting to be found. Even bigger sample sizes may be necessary to detect these SNPs.
Many of the SNPs associated with height are in genes with well-documented functions in processes such as cell division, cell-to-cell signaling, and gene regulation.
<h6>New Associations</h6>
Other SNPs, however, are in genes about which little is known.
“There may be more than a hundred genes which affect our height,&#8221; said Mike Weedon, lead author of one of the papers. &#8220;Many of which will work in surprising or unpredicted ways.”
“The challenge now for us is to understand how they influence growth in the body. This could open up new avenues for treating a range of diseases,” said Weedon.
Want to know how you stack up?
23andMe users can see their data for 46 distinct height-related SNPs in the Genome Explorer (now called Browse Raw Data) (in some cases we substitute a SNP from the three new studies with an equivalent one that is included on our chip).
We’ve used the data in each paper to calculate the approximate effect in centimeters for each SNP. The effect shown is the increase in height (in cm) that each copy of the &#8220;tall&#8221; version of the SNP would give a person compared to someone who had two &#8220;short&#8221; versions. At this point, these findings apply only to people of European ancestry.
<img decoding="async" class="left" src="https://blog-api.23andme.com/wp-content/uploads/2008/04/picture-5.png" alt="picture-5.png" />
 
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Large Studies Find SNPs with Small Effects on Height

It was not very long ago — at least in evolutionary terms — that humans first ventured beyond the continent of their species’ birth. But once people did begin migrating out of Africa about 50,000 years ago to populate the lands we now call the Middle East, Asia, Europe and the Americas, the transformation of the species, and the planet, was swift.


Now, 2,000 generations later, 23andMe is launching a new feature that can help you see the traces of those ancient voyages in your chromosomes. As populations became separated over the millennia, small genetic differences developed that can still be used as signatures of geographic ancestry.
<h6>Coloring our Ancestry</h6>
Ancestry Painting looks at those signatures in the 22 numbered chromosomes (that is, all but X and Y) to infer where in the world the ancestors who passed you each stretch of DNA were most likely to have lived — Africa, Asia or Europe.

Ancestry Paintings essentially give you a snapshot of where your ancestors lived before the beginning of the colonial era about 500 years ago. That’s because the massive migrations that have occurred since then have blurred many of the genetic boundaries that had developed over the millennia. For example, most Americans trace their ancestry not to the continent where they live but to Africa, Asia, Europe or a combination of those places.
The best way to understand Ancestry Paintings is to take a look at some.
For example, this is the painting of a woman who has three grandparents from Germany and one from Norway:

Her painting is nearly uniformly navy blue, an indication that all of her chromosomes come from European ancestors. There are a few brief stretches of orange (meaning Asian ancestry), but in light of the overall pattern it is more likely that the orange stretches are statistical &#8220;noise&#8221; than indicators of true Asian descent.

<h6>African American Ancestry Painting</h6>

Now suppose that woman had a child with an African man. Because each person has 22 pairs of numbered chromosomes — one from each parent — Ancestry Paintings depict both in a single band. So the child of a mother with fully European ancestry and a father with fully African ancestry would have a painting consisting of 22 half-navy and half-green stripes.
It’s in subsequent generations that things really get interesting.
For example, this is the painting for a man who identifies himself as African American:
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/03/african-american-faq.png" alt="Ancestry Painting of African American Man" class="alignright" width="390" height="325" />
Genetic studies show that most African Americans have at least some European ancestry, and that finding is borne out by this man’s Ancestry Painting.
In fact, all the chromosomes are at least half blue, suggesting that this person has one parent of fully European ancestry. The solid blue color in some stretches indicates at least partial European ancestry for the other parent, whereas the stretches that are half blue and half green indicate African descent from one parent and European from the other. The overall fraction of each type of ancestry — African, Asian and European — is tabulated in the legend in the upper right of the display.
Log into your 23andMe account to find many more examples of paintings from individuals from around the world, along with descriptions of the events in human history underlying each and more detailed information about how to interpret them.

New Feature: Ancestry Painting

<img decoding="async" class="right alignright" src="https://blog-api.23andme.com/wp-content/uploads/2008/03/beringstrait.png" alt="beringstrait.png" />People who study the spread of humans to the Americas can agree on one thing — the first migrants crossed from Asia by way of a land bridge connecting Siberia and Alaska.
Just about everything else is subject to debate: who the people were, where they originated, when they migrated, how numerous they were and what they did once they crossed into the Americas.
Finally, a solution to the decades-old dispute may be at hand. That&#8217;s because genetic analyses are beginning to converge on a scenario that fits in with all the archaeological, linguistic, climatological and ecological data relevant to the issue — and also seems to make sense.
<h6> 
Rapid Migration</h6>
In this month&#8217;s issue of the American Journal of Human Genetics, researchers from Brazil and California argue that the present-day pattern of genetic diversity among Native Americans suggests a rapid southward migration along the Pacific coast that began about 18,000 years ago and took only a few thousand years to reach the tip of South America.
It was only later, the researchers claim, that people made their way inland in pursuit of large game animals such as woolly mammoth. The traditional view is that these mammoth hunters, who appear in the archaeological record about 13,000 years ago, were the first Americans.
This is not the first time a migration down the Pacific coast has been proposed. But the researchers were able to show by comparing the mitochondrial DNA of 86 Native Americans that all five of the major genetic branches in the New World trace back to an ancestral population of a few thousand people that began expanding rapidly around 18,000 years ago.
<h6>Coastal Route</h6>
At that time — not long after the peak of the Ice Age — glaciers thousands of feet thick blocked the land route from Alaska into the heart of North America. But the coast was clear. Recent research indicates the Pacific rim of North America was relatively ice-free by about 19,000 years ago.
The DNA evidence also offers information about the ancestral Asian populations that gave rise to the first Americans. The researchers compared the Native American DNA samples to their closest known relatives in Asia. It also found that the Asian and American lines appear to have split about 5,000 years before the rapid population expansion on the American side.
That suggests a long period of isolation. This was probably in the region that is now around (and underneath) the Bering Strait, before the first people flooded into the New World.
<h6>Native American Diversity</h6>
Two recent papers in the open-access journal Public Library of Science One suggest a similar scenario, albeit with slightly different dates. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0001596">One study</a>, published last month by University of Florida researchers, analyzed mitochondrial DNA donated by 77 Native Americans. That study found that the overall pattern of diversity was most consistent with a population that has experienced two episodes of rapid growth. The first was about 40,000 years ago, and period of growth happened about 15,000 years ago.
<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0000829">A second study</a>, published last year by a global team of researchers, found that all of the major genetic branches of Native Americans appear to have started diversifying about 14,000 years ago. This was after being isolated for a long period of time.
The beauty of these genetic studies is their ability to explain the vexing archaeological evidence for the migration of people into the Americas. There are signs of humans living in Siberia, far from the major population centers of the time, as early as 30,000 years ago. And there is evidence of people at the Monte Verde archaeological site in southern Chile as early as 14,500 years ago.
Yet there are no archaeological sites intermediate between those two very distant locations in time and space. The genetic evidence suggest two reasons why. First, a small number of people migrating very quickly down the Pacific coast wouldn&#8217;t have left many artifacts behind. And second, if the migration happened shortly after the peak of the Ice Age, as the genetic evidence suggests, then the coastline it followed is now well offshore. Sea level has risen 120 feet since then.

The Amazing Journey: A New Synthesis for the Peopling of America

It’s a question we’re getting used to: “Why are you called 23andMe?”
Many of you know the answer by now: our name refers to the 23 pairs of chromosomes usually found in humans.
But a question you may not know the answer to is “Why do humans have 23 pairs of chromosomes? Why not 13? Or 27?”
Well, it would take a while to trace the history of each of our chromosomes. But the tale of how we got down to 23 pairs from the 24 of the common ancestor we share with chimpanzees, our closest relatives in the animal kingdom, is pretty straightforward — and pretty cool.

A few million years ago after the final evolutionary split between man and chimp, two chromosomes fused. In humans, two chromosomes came together end to end, creating our chromosome 2.
The fusion of two chromosomes wasn’t particularly unusual — throughout evolution chromosomes have been breaking apart and joining together in new combinations. Many of our chromosomes can be shown to be rearranged versions of chromosomes found in other animals.
Scientists can “paint” chromosomes using fluorescent probes that detect specific DNA sequences. When they paint the DNA of a human cell with probes that detect human chromosome 2 sequences, they see one pair, as expected. But if the same probes are used in a chimp cell, two pairs of chromosomes light up, showing us chromosomes 2’s parents.
<img loading="lazy" decoding="async" class="aligncenter wp-image-110 size-full" src="http://35.88.189.111/wp-content/uploads/2008/02/chr2_orang_human.jpg" alt="" width="484" height="275" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/02/chr2_orang_human.jpg 484w, https://blogcms.23andme.com/wp-content/uploads/2008/02/chr2_orang_human-300x170.jpg 300w" sizes="auto, (max-width: 484px) 100vw, 484px" /> 
Chromosome 2 painting in a human cell, right, and an orangutan cell, left (which has 24 chromosomes like a chimp). Stefan Mueller, Department Biologie II der Ludwig-Maximilians-Universitie Muenchen.
Check out <a href="https://www.23andme.com/gen101/genes/" target="_blank" rel="noopener noreferrer">Genetics 101</a> for more info on chromosomes and the numbers found in other species.

How’d We Get 23?

<img decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/02/coldguy.jpg" alt="coldguy.jpg" class="right alignright" />Modern lifestyles are often blamed for diseases such as obesity, <a href="https://www.23andme.com/topics/health-predispositions/fh/">high cholesterol</a>, heart disease and diabetes. But from an evolutionary standpoint those ailments may have roots in changes that occurred tens of thousands of years ago, when humans first left balmy Africa for more northerly climes.
Climate is already known to be partially responsible for the variations seen in body shape and size among humans. It&#8217;s no accident that Arctic Inuit tend to be short and squat while East African Maasai are long and lean.
<h6>Genetic Adaptations</h6>
Researchers at the University of Chicago recently hypothesized that climate might also have influenced genetic differences in metabolism.
“As some populations migrated out of Africa to much cooler climates, there would have been pressure to adapt to their new settings by boosting the processes that produce and retain heat,” said Anna Di Rienzo, a professor of genetics at the university.
A study published by Rienzo and her colleagues in today&#8217;s PLoS Genetics shows that genetic adaptations to colder climates do seem to affect susceptibility to many common metabolism-related disorders.

<h6>The Study</h6>
The scientists tested their idea by looking at SNPs in metabolism genes in 54 populations from around the world. They found that as a group, variations in these genes are correlated with climate measures such as temperature, humidity, and UV exposure.
Some of the variations that increased in frequency as people moved farther out of Africa have turned out to be harmful in the modern world. For example, the protein made by the FABP2 gene helps the body transport, absorb, and metabolize fats. A version of a SNP in this gene that is more prevalent in populations at higher latitudes causes the protein to bind fats more tightly. It has also been associated with increased insulin resistance, higher cholesterol and triglyceride levels, and more abdominal fat.
<h6>Adaptations for Colder Climates</h6>
But adaptations to colder weather that took place thousands of years ago don’t necessarily doom a population to a higher risk for disease today. A version of a SNP in the PON1 gene (which encodes a protein involved in dilation of blood vessels) is more common in populations from cooler regions. That version is associated with decreased risk for coronary artery disease, stroke, and heart attack.
According to the study’s authors, whether a variation increases or decreases risk for metabolic disorders will depend on exactly how the variation helped people deal with their new environment. For example, a variation in the LEPR gene probably helped early humans generate more body heat. Today this variant is associated with lower BMI. But the variation in the FABP2 gene discussed above, probably helped people stay warm by increasing BMI.
<img decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/02/climatpic22.jpg" alt="climatpic22.jpg" class="alignright" align="bottom" /> 
The frequencies of the two different versions of SNP rs662 in the PON1 gene are shown as a pie chart for each of the tested populations against a background map showing summer surface solar radiation. (From Hancock et al. (2008) Adaptations to climate in candidate genes for common metabolic disorders. PLoS Genet 4(2): e32. doi:10.1371/journal.pgen.0040032.g001)

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