<img loading="lazy" decoding="async" class="alignright size-full wp-image-2896" title="442px-reproduction-of-the-1805-rembrandt-peale-painting-of-thomas-jefferson-new-york-historical-society_1" src="https://blog-api.23andme.com/wp-content/uploads/2009/02/442px-reproduction-of-the-1805-rembrandt-peale-painting-of-thomas-jefferson-new-york-historical-society_1.jpg" alt="" width="300" height="406" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/02/442px-reproduction-of-the-1805-rembrandt-peale-painting-of-thomas-jefferson-new-york-historical-society_1.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/02/442px-reproduction-of-the-1805-rembrandt-peale-painting-of-thomas-jefferson-new-york-historical-society_1-222x300.jpg 222w" sizes="auto, (max-width: 300px) 100vw, 300px" />
As we have shown time and again here at the Blog, our DNA can greatly illuminate the lives of our most ancient ancestors.   We&#8217;ve learned how the ancient <a id="em14" title="Phoenicians" href="../2008/10/30/ripples-in-the-mediterranean-tracing-the-genetic-origins-of-the-phoenicians/" target="_blank" rel="noopener noreferrer">Phoenicians</a> left their genetic footprints scattered across the Mediterranean Sea, and seen the DNA signatures of the first <a id="ou4o" title="farmers" href="../2008/12/24/hidden-in-plain-sight-new-genetic-discoveries-shed-light-on-the-spread-of-farming-in-eastern-europe/" target="_blank" rel="noopener noreferrer">farmers</a> sprinkled everywhere from Iraq to Germany to England.   But DNA can also tell us many things about our species&#8217; more recent history as well. Just yesterday we discussed the most recent discoveries regarding the fate of Russia&#8217;s last royal family, the <a id="is69" title="Romanovs" href="https://blog.23andme.com/articles/leaving-no-stone-unturned-dna-analysis-confirms-identities-of-missing-romanovs" target="_blank" rel="noopener noreferrer">Romanovs</a>.   Below we delve deeper into that mystery, as well as two others that reveal how scientists have harnessed the power of DNA to solve some of history&#8217;s seemingly unsolvable mysteries.
<h6> 
Which was Jefferson&#8217;s Son?</h6>
Tales of an affair between our third president, Thomas Jefferson, and his household slave, Sally Hemings, began circulating as soon as the two returned from Paris in 1790.   For her entire life, Hemings served Jefferson and his family at his residence in Virginia.   She bore at least four children throughout her life.   And though the father of Sally&#8217;s children was never divulged, anecdotal evidence, combined with the efforts of a persistent political reporter named James T. Callender, helped spread rumors that the third President of the United States fathered at least one of Hemings&#8217; children.
Two of Hemings&#8217; sons were of particular interest.   The first, Thomas Woodson, was believed to have been conceived while Hemings and Jefferson were living in Paris.   Convincing the public that Woodson was indeed the illegitimate son of Hemings and Jefferson was one of Callender&#8217;s primary goals.
The other child of interest, Eston Hemings, was Sally&#8217;s youngest.   He was born in 1808 and was said to have resembled Thomas Jefferson, and clearly the potential connection was not lost on him: later in his life Eston Hemings moved to Madison, Wisc., and changed his name to Eston Hemings Jefferson.
Yet even with this name change, many of Eston&#8217;s descendants seemed to have no knowledge of their potential ancestry.   And most historians placed more credence on the idea that Woodson was Jefferson&#8217;s son.   In order to discover the true ancestry of both Thomas Woodson and Eston Hemings, researchers turned to DNA.
Geneticists found living males who could document their descent from either Thomas Woodson, Eston Hemings, or Thomas Jefferson along a purely male line. Because the Y chromosome is passed down directly from father to son, the paternal descendant of any of Thomas Jefferson&#8217;s sons would have the same Y chromosome as a descendant of Jefferson himself.
The first thing the geneticists found when they examined the Y chromosomes of all these descendants was that Jefferson himself had a very rare Y chromosome type hardly ever found among people of western European ancestry. Then, when they examined the DNA of Woodson&#8217;s and Hemings&#8217; descendants, they found a perfect match: but only with Eston Hemings&#8217; descendants.   Woodson&#8217;s descendants all had a Y chromosome that is common among West Africans.
So even though DNA evidence disproved historians&#8217; suspicion that Sally Hemings&#8217; first son, Thomas Woodson, was fathered by our nation&#8217;s third president, it strongly suggested that her youngest, Eston Hemings, was indeed Jefferson&#8217;s offspring.
<h6>The Case of the Missing Mozart</h6>
On December 6, 1791, famed composer Wolfgang Amadeus Mozart was laid to rest at St. Mark&#8217;s Cemetery in Vienna.   Despite his fame, he was buried in a pauper&#8217;s grave, along with several dozen others. But 10 years later, gravedigger Joseph Rothmayer unearthed Mozart and removed his skull, speculating that there was money to be made from selling the relic.   For the next 200 years, the skull would disappear and and then reappear into the hands of various collectors and Mozart enthusiasts.   Its authenticity could never be verified, so scientists finally turned to DNA to fill in the gaps that other research could not.
In 2005, two independent teams of geneticists analyzed DNA extracted from a tooth in the skull.   They compared this DNA to various members of Mozart&#8217;s family, including his father, grandmother, and niece, who were all buried in the Mozart family tomb.
Both teams arrived at the exact same conclusion: the skull could not have been Mozart&#8217;s.   The DNA extracted from the skull differed too much from that of every family member buried in the Mozart tomb.
<h6>Lost and Found:   The Grand Duchess Anastasia</h6>
On July 16th, 1918, a family of seven, along with their three servants and physician, were murdered outside the small town of Ekaterinburg, Russia.   But this was no ordinary family.   This father was Tsar Nicolas &#8211; the last Romanov Emperor of Russia.   As the Russian Revolution was coming to a head, the imperial family was arrested and held by the Bolshevik rebels.   Then, over a year later, they were held at gunpoint and shot execution style; their bodies were hastily burned and thrown in a shallow grave in the woods outside the town.
Just a few short years after their murder, rumors began circulating that at least one member of the Romanov family had escaped execution.   At exactly the right moment, a young woman emerged in Germany and claimed to be Grand Duchess Anastasia, one of the Tsar&#8217;s daughters.   For the next 60 years, this woman, known as Anna Anderson, stood by her claim that she was Anastasia, and that she had managed to escape the execution in Ekaterinburg.   Her assertions were given extra credence when two amateur historians unearthed a grave site that they claimed contained the remains of the Romanov family, minus the body of Anastasia.   The rumors grew.   Yet the royal houses of Europe, to whom the Romanovs were related, never believed Anderson&#8217;s story. The two sides were in a constant struggle for the truth up to Anderson&#8217;s death in 1984.
<h6>More on the Tsarina</h6>
As with Jefferson and Mozart, researchers finally turned to DNA evidence to test Anderson&#8217;s claim. Scientists retrieved DNA from a tissue sample that had been stored in a hospital after Anderson had a biopsy, and extracted her mitochondrial DNA.   Because mitochondrial DNA is passed down from mother to children, scientists could compare Anderson&#8217;s mtDNA to a living maternal relative of Anastasia.   The relative they chose happened to be Prince Phillip of Great Britain: husband to Queen Elizabeth II and grand-nephew of Nicolas&#8217; wife, Tsarina Alexandra.
Anderson&#8217;s mtDNA did not match that of Prince Phillip, however.   And when new techniques allowed for the extraction of DNA from the burial site in Ekaterinburg, scientists found that Anderson&#8217;s DNA did not match that of the Tsarina or the other children.   To finally close this case, in 2007 archaeologists discovered another grave in Ekaterinburg, near the original, that held more bodies.   Forensic analysis strongly suggested that one of these bodies was the missing Anastasia.
Even though some die-hard fans of Anderson maintain she was always telling the truth, the vast majority of scientists and historians consider her simply a master of deception.   Once again, DNA analysis has been able to prove &#8211; or in this case, disprove &#8211; a seemingly unsolvable mystery.

23andMe Blog

23andMe Blog Team

History’s Mysteries:  Finding Answers in our DNA

<img loading="lazy" decoding="async" class="alignright size-full wp-image-2780" title="origin_of_species_title_page" src="https://blog-api.23andme.com/wp-content/uploads/2009/02/origin_of_species_title_page.jpg" alt="" width="174" height="300" />
Biology has changed a lot over the past 150 years. Scientists have discovered entirely new forms of life, deciphered the molecular code of heredity and observed the machinery of life on the smallest dimensions. And through it all, one scientific theory has stood the test of time.
<h6>The Origin of Species</h6>
New discoveries in genomics, medicine, developmental biology, and countless other fields could have derailed the the theory of evolution. But the core principles of evolutionary theory, proposed by Charles Darwin 150 years ago, have remained among the strongest explanations of the natural world ever published.
In honor of Darwin Day 2009, which celebrates the 200th anniversary of Charles Darwin’s birth and the 150th anniversary of the publication of his seminal work, On the Origin of Species, we’d like to take a look at how evolution has itself ‘evolved’ over the decades – how new advances in science and technology have both reinforced Darwin’s original idea and given us insight into the inner workings of the theory that explains so much about the world in which we live.
In 1859, the phrase ‘evolution by natural selection’ was already beginning to make the rounds among the scientific elite in Europe and in America.   This was the year Darwin published On the Origin of Species, and his ideas about how species change over time were causing heated debate among the experts.   
<h6>Theory of Evolution</h6>
But Darwin didn’t invent the idea of ‘evolution’ (that is, the idea that species change over time).   What he brought to the table was an explanation of how species change, a process Darwin called ‘natural selection.’   On his famous journey to the Galapagos Islands 25 years earlier, Darwin had witnessed unique variation in hundreds of species.   
As he pored over his notes for the next two decades, Darwin pieced together the notion that species must adapt to environmental pressures (like changes in climate or a volcanic eruption), in order to survive.   If they did not adapt to these pressures, then they may not survive.   It was natural selection, Darwin argued, that was the basis for the vast differences we see in plant and animal species across the globe.
But there was a lot that Darwin did not know when he published his ideas of evolution.
<h6>Natural Selection</h6>
He did not know, for instance, how changes in a species&#8217; appearance (a longer beak, a bigger shell, or a thicker coat of fur) are passed down from generation to generation.
The idea of discrete units – ‘genes’ that are passed down from parents to children – had not even occurred to Darwin, nor to most of the other scientists of the time.   Even when, in 1866, an Austrian monk named Gregor Mendel reported his ideas on patterns of inheritance in pea plants in the obscure Proceedings of the Natural History Society of BrÃ¼nn, few took notice.
<h6>Genetics</h6>
In fact, the word ‘genetics’ wasn’t coined until 1905, by biologist William Bateson. Bateson, who is sometimes credited with ‘rediscovering’ the lost works of Mendel, helped to usher in a new wave of research and discovery – this time looking at how species differ from each other at the molecular, or genetic, level.   Bateson&#8217;s push for the use of genetics in evolutionary research reached fruition in 1952, when Cambridge scientists James Watson and Francis Crick decoded the structure of DNA.
Soon others discovered how specific genes are passed down from generation to generation, and how changes in our genetic code are connected to changes in species.   As each new genetic discovery allowed us to better understand the natural world at a microsopic level, Darwin&#8217;s theory of evolution by natural selection was continually reinforced.
The evolution of our species, Homo sapiens, forms the basis for virtually everything we can learn from 23andMe&#8217;s <a href="https://23andme.com" target="_blank" rel="noopener">Personal Genome ServiceTM</a>.   The signature of millions of years of evolution is present in every person&#8217;s genome, and often in our physiology, rendering some of us resistant to malaria, others unable to digest milk, and even causing some to have lower risks of cancer or other diseases.   As advances in science and technology continue to bring us more information hidden within our genes, we can be thankful that 150 years ago, an amateur naturalist from Shrewsbury, England, boarded a ship bound for South America and began piecing together the evolutionary story of not just our species but of all life on earth.

The Evolution of a Theory:  Darwin and Evolution 150 Year Later

<img loading="lazy" decoding="async" class="alignright size-full wp-image-2521" title="cornflakes" src="https://blog-api.23andme.com/wp-content/uploads/2009/01/cornflakes.jpg" alt="" width="350" height="232" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/01/cornflakes.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/01/cornflakes-300x199.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Pop Quiz: What do women who eat cereal for breakfast each morning have in common?
<ol style="list-style-type: upper-alpha;">
<li>They get a full day&#8217;s supply of 11 essential vitamins and minerals.</li>
<li>They enjoy better <a id="jgop" title="sex lives" href="http://news.scotsman.com/health/Porridge-boosts-your-sex-life.4854146.jp">sex lives</a> than women who don&#8217;t eat cereal for breakfast.</li>
<li>They are more likely to give birth to male children.</li>
<li>They make buying decisions based on the advice of cartoon leprechauns, silly rabbits and mustachioed mariners.</li>
</ol>
Actually, we don&#8217;t know anything about answers A, B and D. But we do know about C. When British scientists announced last year in the <a title="Abstract of Mathews et al (2008)" href="http://journals.royalsociety.org/content/w260687441pp64w5/?p=b72119df2dd049f990eb8b531c3a467c&amp;pi=1" target="_blank" rel="noopener">Proceedings of the Royal Society B</a> that their research suggested <a title="NYT Well Blog Entry" href="http://well.blogs.nytimes.com/2008/04/23/boy-or-girl-the-answer-may-depend-on-moms-eating-habits/" target="_blank" rel="noopener">eating breakfast cereal increases a woman&#8217;s chance of having a male child</a> (among other things), they may have been falling prey to a statistical error that is of constant concern in the kinds of studies that 23andMe uses to provide information about the genetic components of disease risk. This post explains the nature of that misstep, and how we go about avoiding it.
Where did the researchers go wrong? Their research looked at the consumption of 133 different foods by 749 English mothers before and during the course of their pregnancies, and found that among all of these foods, only breakfast cereal was associated strongly with having sons. Nothing wrong with that. The problem arose, a pair of statisticians <a title="Press Release Re: Young et al (2009)" href="http://www.eurekalert.org/pub_releases/2009-01/nios-prn010909.php" target="_blank" rel="noopener">writes in the current online issue</a> of the Proceedings of the Royal Society B, when the original researchers neglected to account properly for the number of opportunities they had had1 to find a significant result.
In statistics, this is called the &#8216;multiple testing&#8217; or &#8216;multiple comparisons&#8217; problem, and it&#8217;s a very important concern for us at 23andMe. It&#8217;s pretty easy to get a feel for what can go wrong: suppose you were to flip a quarter five times, each time noting whether it came up heads. The odds that you would see heads all five times are not good &#8212; they&#8217;re 31 to one, or about 3%. But if you repeated this &#8216;experiment&#8217; 133 times, you would be very likely to see all-heads at least once, and more probably three to five times. So if you see all-heads a few times, it doesn&#8217;t really make sense to regard this outcome as unusual. In fact, it would be very unlikely not to see all heads at least a few times2. It&#8217;s something like the mathematical version of Tom Petty&#8217;s wistful refrain: Even the losers get lucky sometimes.
At 23andMe, the genetic association studies underlying our Health and Traits reports are saddled with the mother of all multiple testing problems. The basic idea behind these studies is pretty simple. They look at single-letter DNA variations known as SNPs in, say, 1,000 people who have a disease. Then they look at those same SNPs in another 1,000 people who are similar to the first thousand in as many ways as possible, except that they do not have that disease. If researchers were to look at a SNP and find, for example, that 80% of the people with the disease have the AA version, and only 30% without the disease do, then they&#8217;d be justified in suspecting that they&#8217;d found something significant.
But here&#8217;s the rub. These studies don&#8217;t look at just one SNP; they typically look at half a million to a million. A million is a lot more than 133; if association studies didn&#8217;t correct for multiple testing, every one of them would be expected to find tens of thousands of falsely associated SNPs mixed in with the really associated ones. That would not do.
Fortunately, there are many ways to correct for the multiple testing problem, ranging from dead-simple to math-degree-required. The top genetics journals will accept an association study only if the analysis has corrected for multiple testing using a standard method. Since we at 23andMe will consider a paper for use in Health and Traits only if it has come from a top journal (with some exceptions), we usually don&#8217;t have to worry about whether the studies we rely on are statistically sound. And, we go a step further by insisting that any finding used in Health and Traits must have been replicated by at least two independent groups of researchers. This policy helps to guard both against possible failure of multiple testing correction and unintended error on the part of the researchers conducting the study.
So how did the breakfast cereal-boy baby study make it into print? That remains a bit of a mystery to this reporter-slash-scientist. But anyone who is dreaming of having their own baby boy will just have to rely on alternative types of <a id="s-js" title="lucky charms" href="http://pregnancy.about.com/od/boyorgirl/a/chooseaboy.htm">lucky charms</a>.
<hr />
<ol>
<li> The original paper looked at the womens&#8217; diets before pregnancy and both in early and later pregancy, and tested each food in each time interval, so they appear to have conducted 399 (133*3) separate tests. They only report a significant association between consumption of breakfast cereal and bearing sons for the &#8216;before pregnancy&#8217; and &#8216;later pregnancy&#8217; time periods, so it is unclear whether they also tested the &#8216;early pregnancy&#8217; time period. If they only tested &#8216;before&#8217; and &#8216;later&#8217;, which seems odd, then that would mean they conducted 266 separate tests. Either number of tests, 266 or 399, suffices to cast serious doubts on the soundness of their result.</li>
<li>How unlikely? We want to know: what is the chance that in 133 5-coin-flip &#8216;experiments&#8217;, we never see all-heads? Well, per experiment, given a fair coin, the probability of getting five heads in five coin-flips is 1/32 (= (1/2)^5), about 3.1%. Therefore, the probability of not seeing all-heads is one minus the chance of seeing all-heads, or 31/32, about 96.9%. This is exactly the same as the chance of seeing at least one tail in five flips. The chance, then, that you see at least one tail in each of 133 flips is (31/32)^133, which is 1.47%. If you doubled the number of experiments to 266, the chance of never seeing all-heads (ie, seeing at least one tail in each experiment) is (31/32)^266, or 0.021%. This fits with your intuition: as the number of experiments goes up, the chance of never seeing an all-heads outcome goes down, because you have increased the number of opportunities in which to see this outcome. 
</li>
</ol>

Cereal Killer: The Tragic Tale of a Fatal Statistical Flaw

By Joyce Tung and Amy Kiefer
<img loading="lazy" decoding="async" class="alignright size-full wp-image-2445" title="istock_000002575226xsmall" src="https://blog-api.23andme.com/wp-content/uploads/2008/12/istock_000002575226xsmall.jpg" alt="" width="282" height="426" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/12/istock_000002575226xsmall.jpg 282w, https://blogcms.23andme.com/wp-content/uploads/2008/12/istock_000002575226xsmall-199x300.jpg 199w" sizes="auto, (max-width: 282px) 100vw, 282px" />
It&#8217;s been an exciting seven months since we launched <a href="https://www.23andme.com/research/" target="_blank" rel="noopener">23andWe</a>, the arm of 23andMe that gives people an unprecedented opportunity to collaborate with us on cutting-edge genetic research. Since May, the amount of data we’ve collected has grown at a fast and furious pace. For those of us who are used to the difficult and painfully slow accumulation of data in academic research projects, this information explosion has been nothing short of amazing.
From our first baby steps with “Ten Things About You” in May, to our three latest surveys – &#8220;Health Habits,&#8221; &#8220;Where Are You From?&#8221; and &#8220;What Do You Do?&#8221; – 23andWe has undergone some serious evolution. Almost every month, we have published more surveys and developed more features to help make the survey-taking experience simpler, more interesting, and more rewarding. We want to make it easy for our customers to provide truthful, good quality data, as that is the first and most important step towards doing high quality research. A big thank you to all our survey takers–we pledge to constantly work on improving this feature so we can keep you coming back for more.
We’re starting to look at genetic associations with the traits we ask about in our surveys, and we expect to have some exciting ones to report soon. But we’ve already learned some interesting things just by looking at the survey responses themselves. For example, while a few sources suggest that a higher percentage of men are left-handed than women, our data so far suggest that once you control for age this is not the case. It seems like our society is becoming more accepting of us female lefties! We’ve also seen that handedness does indeed significantly correlate with footedness. That is, left-handers are more likely to be left-footed, and right-handers are more likely to be right-footed. Similarly, handedness significantly correlates with ocular dominance, as left-handers are more likely to be left-eye dominant, and right-handers are more likely to be right-eye dominant.
And proving mom right once and for all, we&#8217;ve found that a sweet tooth does lead to more cavities. After controlling for sex and age, you&#8217;re more likely to report having many cavities (as opposed to few or none) if you reach for either something sweet or something sweet and salty when it&#8217;s time for a snack.
How is this kind of information going to usher in the era of personalized medicine? Handedness may seem like a relatively trivial trait, but it is correlated with risk for learning disability, schizophrenia, exceptional mathematical talent and other relevant traits. Understanding the biological underpinnings of what makes us choose one hand over the other for all our most delicate tasks may help us better understand the basis for these other complex traits.
As 23andWe matures we plan to start focusing more directly on health-related traits. Look for surveys in the very near future that ask about various medical conditions whose genetics is not yet understood. By combining the information customers provide in their survey responses with data from our custom chip, we can look throughout the genome for DNA variations linked to many different traits. This method can help us find genes that no one thought would be involved with a particular condition. For example, genome-wide studies on age-related macular degeneration (a leading cause of blindness) recently surprised researchers by identifying associations with genes that make components of the innate immune system. This gave scientists a whole new pathway in which to search for treatments.
We can’t guarantee that we’ll find something useful or interesting with every analysis that we do; science is a game you have to play a lot of times in order to win. But we can guarantee that we will strive to do the best research and that we will share our findings with the scientific community. By contributing to the body of knowledge on human genetics, we believe we can help bring the dream of personalized medicine a few steps closer to reality.
And all we need you to do is take some surveys.

Joyce Tung

23andWe: The First Annual Update

This is a repeat of a post we ran back in September. While you&#8217;re sitting around the table with your loved ones, don&#8217;t forget that it&#8217;s National Family History Day!
<img loading="lazy" decoding="async" class="alignright size-full wp-image-2086" title="thanksgiving" src="https://blog-api.23andme.com/wp-content/uploads/2008/11/thanksgiving.jpg" alt="" width="325" height="215" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/11/thanksgiving.jpg 325w, https://blogcms.23andme.com/wp-content/uploads/2008/11/thanksgiving-300x198.jpg 300w" sizes="auto, (max-width: 325px) 100vw, 325px" />
I’m a bad patient.
Every time I go to a doctor she asks, “Do you have a family history of any diseases?”
I’m ashamed to say that my answer is always “I don’t think so.”
Your family health history is a powerful tool for your doctor; it can help him or her make vital screening and treatment decisions. Yet a recent survey (Porter Novelli Healthstyles 2004) found that although 96% of Americans recognize the importance of their family history, only 33% have ever tried to gather and organize this data for themselves.
23andMe helps people see what their DNA might have to say about a host of common and not-so common diseases and conditions; but we don’t want anyone to think that purchasing our Personal Genome Serviceâ„¢ is a substitute for a detailed family health history.

For example, the effect of the SNPs 23andMe reports on for breast cancer pales in comparison to that of mutations in the well-known BRCA1 and BRCA2 genes, which run in families and can increase a woman’s breast cancer risk three- to seven-fold (23andMe does not report data on these mutations). So even if your 23andMe data says that you have average or even below-average risk for breast cancer, a strong family history of the disease indicates the strong possibility of a genetic mutation that trumps the information we have gleaned from your SNPs.
In other cases, your family health history might dovetail with your 23andMe data, giving a fuller picture of, and perhaps increasing, your predicted risk for a certain disease. For example, a report published just last week in the <a href="https://www.ncbi.nlm.nih.gov/pubmed/18780872?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">Journal of the National Cancer Institute</a> showed that a SNP recently associated with lung cancer (customers can see their data in Health and Traits) has a significantly larger effect in people where three or more first-degree relatives have been diagnosed than in people who develop a sporadic case of the disease.
The bottom line: It is very helpful to be aware of your family health history and share it with your medical provider. Here are a few resources to help you get you started:
<ul>
<li>The U.S. Surgeon General’s Family History Initiative 
For the past four years the Surgeon General has designated Thanksgiving, a time when families naturally gather together, as National Family History Day. You can use the online tool “My Health Portrait” to help guide you in collecting your own family’s health history. (Also available in Chinese, Polish, Spanish, French and Portuguese from the Brigham and Women’s Hospital National Family Health Initiative Website.)</li>
</ul>
<ul>
<li>The Genetic Alliance 
Links to sites that can help with collecting a family health history, including resources for family reunion organizers who want to incorporate this into their next gathering.</li>
</ul>
Mom, get ready for some questions.

Thanksgiving is National Family History Day

<img loading="lazy" decoding="async" class="alignright size-full wp-image-2073" title="studentdna" src="https://blog-api.23andme.com/wp-content/uploads/2008/11/studentdna.jpg" alt="" width="350" height="233" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/11/studentdna.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/11/studentdna-300x200.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
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

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:
<img loading="lazy" decoding="async" class="alignnone size-full wp-image-2025" title="u2u_blog_1120083" src="https://blog-api.23andme.com/wp-content/uploads/2008/11/u2u_blog_1120083.gif" alt="" width="607" height="213">
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

When 23andMe launched last November, we set out to make genetics accessible to everyone — not just the experts. &nbsp; So we created a series of education videos called <a id="vzgt" title="“Genetics 101.”" href="https://www.23andme.com/gen101/" target="_blank" rel="noopener noreferrer">Genetics 101.</a>
These videos educated viewers on the basics of genetics: &nbsp; What is a gene, what is a SNP, how genes are inherited from generation to generation, and a host of other useful topics.
But understanding your genetic code is only part of what the <a id="f.ep" title="23andMe Personal Genome ServiceTM" href="https://23andme.com/" target="_blank" rel="noopener noreferrer">23andMe Personal Genome ServiceTM</a> offers its customers. &nbsp;

<h6>Learning</h6>
We also want our customers to understand their genetics in the context of human evolution: &nbsp; How did our species evolve, how did we come to populate the globe, and how can we account for the diversity of peoples living today on our planet?
Those questions are the basis for a new series of videos, dubbed Human Prehistory 101. Using the same creative team as with Genetics 101 (led by chief illustrator <a href="http://arianakilloran.typepad.com/ariana_killoran/" target="_blank" rel="noopener noreferrer">Ariana Killoran</a>), we developed a series of videos that tell the human story, from the birth of our species to present day. &nbsp; The first installment, the Prologue, was released last week on 23andMe’s website.
<h6>The Human Story</h6>
The <a href="https://www.23andme.com/gen101/prehistory/prologue/" target="_self" rel="noopener noreferrer">Prologue</a> sets the stage for the human story, beginning with our closest living relatives, the chimpanzee. &nbsp; We then see how the earliest humans lived in Africa nearly 200,000 years ago, and follow some of our fossil ancestors such as Homo erectus – who ventured into Asia long before we did. &nbsp; We also learn that our evolutionary cousins, the Neanderthals, were not so very different from early humans; they cared for their sick and even buried their dead.
This installment will soon be followed by others, each tackling a key chapter in the evolution of our species. &nbsp; Future videos will explain how and when humans ventured out of Africa for the first time, how they survived the Last Ice Age, and how they came to populate so many parts of the world. So be sure to stay tuned for more Human Prehistory 101!

Human Prehistory 101:  The Newest Video Series from 23andMe!

23andMe is always looking for ways not just to give our customers more data, but to help them better understand their genetic information and what it means for them. This week, we&#8217;re introducing a new way to look at Health and Traits data that does just that by pinpointing for each person the particular topics they are likely to find most important. We expect this new approach to become especially valuable as the amount of information provided by our Personal Genome Service continues to grow.
This is what the new view looks like:
<img loading="lazy" decoding="async" class="aligncenter size-full wp-image-1583" title="hntdash" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/hntdash.png" alt="" width="500" height="408" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/10/hntdash.png 500w, https://blogcms.23andme.com/wp-content/uploads/2008/10/hntdash-300x245.png 300w" sizes="auto, (max-width: 500px) 100vw, 500px" />

The Clinical Reports page (above) shows topics containing information that is both supported by solid scientific evidence and has the potential to make a real difference in terms of your disease risk or odds of having a particular trait. There are four different sections within Clinical Reports:
<ul>
<li>Disease Risks shows you the currently covered health conditions for which your risk is most elevated.</li>
<li>Carrier Status tells you whether you have one or more of the disease-causing mutations we cover.</li>
<li>Traits tells you what your genes indicate with regard to a number of physical attributes, from earwax consistency to malaria resistance.</li>
<li>New and Recently Updated is just that – a list of our newest and most recently updated Health and Traits topics.</li>
</ul>
The second page of the dashboard contains a list of Research Reports. These contain information that either has not yet been scientifically validated or has been. However they don&#8217;t have a substantial influence on your odds of having a disease or trait. On the left side of the list there are colored dots that indicate what effect, if any, your data have on your genetic risk of disease.
Here&#8217;s what the Research Reports page looks like:
<img loading="lazy" decoding="async" class="aligncenter size-full wp-image-1584" title="researchrptsdash" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/researchrptsdash.png" alt="" width="499" height="274" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/10/researchrptsdash.png 499w, https://blogcms.23andme.com/wp-content/uploads/2008/10/researchrptsdash-300x165.png 300w, https://blogcms.23andme.com/wp-content/uploads/2008/10/researchrptsdash-271x149.png 271w, https://blogcms.23andme.com/wp-content/uploads/2008/10/researchrptsdash-372x204.png 372w" sizes="auto, (max-width: 499px) 100vw, 499px" />
The new Health and Traits dashboard isn&#8217;t intended to give you all of your information on a single page. You still need to look at the individual reports to see what they contain. But as the number of diseases, conditions and traits we cover continues to grow, we hope it will help our customers find the ones that are of greatest interest to them!

23andMe and You — Page 12

History’s Mysteries: Finding Answers in our DNA

The Evolution of a Theory: Darwin and Evolution 150 Year Later

Cereal Killer: The Tragic Tale of a Fatal Statistical Flaw

23andWe: The First Annual Update

Thanksgiving is National Family History Day

Student Misconceptions About Genetics

23andMe Community Now Includes User-to-User Messaging

Human Prehistory 101: The Newest Video Series from 23andMe!

A New Way to View Your Data

Stay in the know.