Already well-known for expanding technological frontiers, Google co-founder Sergey Brin is now pushing the boundaries of personal genomics with a remarkable post on his new personal blog, <a href="http://too.blogspot.com">TOO</a>.
In the post, Brin shares information from his 23andMe account that indicates he is at substantially increased risk for Parkinson&#8217;s Disease. Brin&#8217;s mother, who has already been diagnosed with the disease, has the same genetic mutation.
The mutation in question is in a gene known as LRRK2 on chromosome 12. The single-letter change in the DNA code dramatically increases a person&#8217;s odds of developing Parkinson&#8217;s from one or two in a hundred to as much as eight in 10.
One recent <a href="http://www.thelancet.com/journals/laneur/article/PIIS1474442208701170/abstract" target="_blank" rel="noopener">study</a> found that a person who inherits the mutation has a 28% chance of developing Parkinson&#8217;s by the age of 59, 51% by the age of 69 and 74% by the age of 79.
It&#8217;s sobering to hear this news about someone so closely affiliated with our company (Sergey is married to Anne Wojcicki, one of our co-founders). But we&#8217;re encouraged too, because Sergey&#8217;s post also illustrates the benefit that comes with having access to your genetic information – and the power of sharing it. As Sergey says: 

<blockquote>&#8220;I now have the opportunity to adjust my life to reduce those odds (e.g. there is evidence that exercise may be protective against Parkinson&#8217;s). I also have the opportunity to perform and support research into this disease long before it may affect me. And, regardless of my own health it can help my family members as well as others.&#8221;</blockquote>
There are a number of LRRK2 mutations that substantially increase Parkinson&#8217;s risk. The one Brin has, which is known as G2019S, is most commonly found among people of Ashkenazi Jewish and North African descent. It has occasionally been found in some non-Jewish European populations, but is virtually unknown in East Asia. Any customers who want to know their LRRK2 G2019S status now can find out by using the 23andMe <a href="https://www.23andme.com/you/explorer/">Genome Browser</a> to search for their genotype at the SNP .
Having one or two copies of the A version of this SNP substantially increases a person&#8217;s chances of developing Parkinson&#8217;s Disease. Our upcoming Parkinson&#8217;s Disease entry will offer much more complete information about the significance of having or not having the G2019S mutation. In the coming weeks and months we plan to provide much more information about Parkinson&#8217;s and many other diseases, conditions and traits that are affected by genetics. We hope that like Sergey, you&#8217;ll want to join us on this exploration of the genetic frontier.

A image of double helix showing a variant

23andMe Blog

23andMe Blog Team

Google Co-Founder Blogs About 23andMe Data, Parkinson’s Risk

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1414" title="istock_000001804366xsmall" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/istock_000001804366xsmall.jpg" alt="" width="266" height="265" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/istock_000001804366xsmall.jpg 347w, https://blogcms.23andme.com/wp-content/uploads/2008/09/istock_000001804366xsmall-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2008/09/istock_000001804366xsmall-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/09/istock_000001804366xsmall-271x271.jpg 271w" sizes="auto, (max-width: 266px) 100vw, 266px" />
A special supplement to Nature Reviews Genetics, published online today, details how four countries with emerging economies are building capacity for human genomic variation.  
The study looks at Mexico, India, Thailand, and South Africa and steps scientists there are taking to build capacity for genomics and its applications to healthcare.
Following the completion of the HapMap Project, several consortiums in the developed world have undertaken large-scale genotyping projects. The hope is that these efforts will lead to advances in personalized diagnostics and therapeutics that could one day improve health outcomes.
The authors of the six-part series, all from the McLaughlin-Rotman Centre for Global Health (MRC) in Toronto, conclude that similar initiatives in genomic medicine have great potential to help developing countries by strengthening local research infrastructure and local intellectual property regimes, addressing local health needs and reducing health-care costs.

(The reports are <a href="https://www.nature.com/nrg/journal/v9/n10_supp/index.html" target="_blank" rel="noopener noreferrer">available</a> free of charge from Nature Genetics with registration)

The highlighted initiatives:
<ul>
<li>
<h6><a href="https://dx.doi.org/10.1038/nrg2442" target="_blank" rel="noopener noreferrer">Mexico</a></h6>

Mexico has formed the National Institute of Genomic Medicine (INMEGEN), the first Mexican institute to systematically describe the genomic diversity of the Mexican population. INMEGEN will allow Mexico to focus on the link between genomic variation in the Mexican population, disease susceptibility and drug-response variability.</li>
<li>
<h6><a href="https://dx.doi.org/doi:10.1038/nrg2440" target="_blank" rel="noopener noreferrer">India</a></h6>

The Indian Genome Variation (IGV) database is a collaborative network that will capture essential data about disease predisposition, adverse drug reactions (ADRs) and population migration within India.</li>
<li>
<h6><a href="https://dx.doi.org/10.1038/nrg2443" target="_blank" rel="noopener noreferrer">Thailand</a></h6>

The Thai SNP Discovery Project and the Thai Centre for Excellence in Life Sciences Pharmacogenomics Project will help Thailand understand the genomic diversity of its population and explore the role that this diversity has in drug response and disease susceptibility.</li>
<li>
<h6><a href="https://dx.doi.org/10.1038/nrg2441" target="_blank" rel="noopener noreferrer">South Africa</a></h6>

The South African government is in the early stages of planning a national genomic medicine research program. Public engagement in genomic issues is spear-headed by The Africa Genome Education Institute.</li>
</ul>
“The world has reached a historic moment on the path to genomic medicine — the point where theory is about to be translated into practice,” said the project’s principal investigator, Professor Abdallah Daar, in a statement.
“Benefits of this emerging science cannot be an exclusive luxury reserved for wealthier industrialized countries. Instead, it must be universally advanced by developed and developing countries alike to prevent an increased widening of an already huge difference in global health care quality,” said the project leader.

New Study Looks at Progress and Potential for Genomic Medicine in Developing Nations

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1400" title="bloodclot" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/bloodclot.jpg" alt="" width="303" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/bloodclot.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/09/bloodclot-300x223.jpg 300w" sizes="auto, (max-width: 303px) 100vw, 303px" />
This Monday acting Surgeon General Steven K. Galson issued a Call to Action to reduce the number of people in the United States affected by two serious blood clotting conditions: deep vein thrombosis and pulmonary embolism.
<h6>DVTs &amp; PEs</h6>
Deep vein thrombosis (DVT), sometimes called “<a href="https://www.ncbi.nlm.nih.gov/pubmed/2900413?dopt=Abstract" target="_blank" rel="noopener noreferrer">economy class syndrome</a>” is the formation of a blood clot in a vein deep within the body, usually in the legs. Pulmonary embolism (PE) occurs if the clot breaks free and travels through the circulatory system to the lungs. Together these two conditions affect an estimated 350,000 to 600,000 Americans each year and contribute to at least 100,000 deaths.
&#8220;Deep vein thrombosis and pulmonary embolisms are often &#8216;silent&#8217; conditions – they can occur suddenly and without symptoms,&#8221; Galson said in a statement. &#8220;But we have made a lot of progress in understanding how these disorders develop and how to prevent, diagnose, and treat them. It&#8217;s time to put this knowledge into action.&#8221;
<h6>Factor V Leiden</h6>
Researchers have found that DVT and PE usually develop in response to a triggering event — being hospitalized or confined to bed rest, having major surgery, suffering a trauma, or traveling for several hours &#8212; in people who either have an inherited predisposition to blood clotting disorders or another risk factor.
Having the riskier version of one or both of the SNPs 23andMe reports data for (<a href="http://circ.ahajournals.org/cgi/content/full/107/15/e94" target="_blank" rel="noopener noreferrer">Factor V Leiden</a> and Prothrombin 20210) significantly increases the risk of developing DVT or PE. An estimated 15 to 20 percent of DVT/PE patients have the Factor V Leiden mutation, while 6 percent have the Prothrombin 20210 mutation.
<h6>Risk</h6>
The average risk of DVT/PE in people between the ages of 40 and 59 (anyone can be afflicted, but the risk does increase with age) is 2.5%. But in those people in this age group who inherit a copy of the Factor V Leiden mutation, the risk jumps to 11%. Having one copy of the Prothrombin 20210 mutation raises the risk to 8.8%. In the unlucky few who have one copy of each of these mutations, the risk is a 32%. And in the extremely rare case that someone inherits two copies of both mutations, the risk of DVT/PE is 69%.
(This information applies only to those with European ancestry. Average risk numbers are different for other groups, and the genetic risk factors discussed here are not usually found in people with African or Asian ancestry.)
Other risk factors for DVT and PE include being overweight or obese, cancer and its treatment, pregnancy, and childbirth, use of hormones for birth control or menopause, and smoking.
“We want to increase the awareness and knowledge of these potentially deadly conditions and encourage patients and health care providers to take the steps to prevent them,” Galson said.
For more information:
<ul>
<li>Surgeon General’s Fact Sheet on Deep Vein Thrombosis and Pulmonary Embolism</li>
<li>The Coalition to Prevent Deep-Vein Thrombosis</li>
<li><a href="http://www.ahrq.gov/consumer/bloodclots.htm" target="_blank" rel="noopener noreferrer">Patient</a> and <a href="http://www.ahrq.gov/qual/vtguide/" target="_blank" rel="noopener noreferrer">Provider</a> Guides from the Agency for Healthcare Research and Quality (also available in <a href="http://www.ahrq.gov/consumer/spblclots.htm" target="_blank" rel="noopener noreferrer">Spanish</a>)</li>
</ul>

Surgeon General Issues Call to Action on VTE: 23andMe Assesses Genetic Risk for Customers

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1344" title="frontshot" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/frontshot.jpg" alt="" width="500" height="330" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/frontshot.jpg 576w, https://blogcms.23andme.com/wp-content/uploads/2008/09/frontshot-300x198.jpg 300w" sizes="auto, (max-width: 500px) 100vw, 500px" />
This is Fashion Week in New York City, a twice-yearly spectacle where designers, models, celebrities, and the merely style-obsessed meet to consider next season&#8217;s top looks. 23andMe managed to lure a few hundred people away from the catwalks Tuesday night to consider the beauty that lies within – DNA.
Our Fashion Week spit party was sort of like a Tupperware party, except instead of buying plastic containers the guests were invited to deposit a saliva sample into one. And instead of taking place at a suburban ranch house designed by Richard Neutra, our spit party went down at the spectacular Manhattan headquarters of IAC/InterActiveCorporation, designed by architect Frank Gehry. The building resembles white curtains billowing in a fresh breeze off the Hudson River. Two gigantic high-resolution video walls line the lobby; the larger one is 118 feet long and 11 feet high.
23andMe team members were on hand to explain the features of our new v2 chip, our new community features. Guests also had the opportunity to purchase our Personal Genome Serviceâ„¢ and produce their saliva samples on the spot (but only if they&#8217;d waited the requisite 30 minutes after consuming an hors d&#8217;oeuvre).
You can see some photos <a href="http://www.zimbio.com/pictures/O2GXwQoazL6/23andMe+Spit+Party" target="_blank" rel="noopener noreferrer">here</a>, or click <a href="https://blog.23andme.com/2008/09/11/23andme-struts-its-stuff-in-nyc-during-fashion-week/#more-1316" target="_self" rel="noopener noreferrer">here</a> for a slide show with more party pics.

[minislides]
Photos by Monica De Armond

23andMe Struts its Stuff in NYC During Fashion Week

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1326" title="beer" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/beer.jpg" alt="" width="279" height="207" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/beer.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/09/beer-300x223.jpg 300w" sizes="auto, (max-width: 279px) 100vw, 279px" />
Just four simple ingredients &#8212; water, malt, hops, and yeast — go into making beer, a delicious and intoxicating brew that has been enjoyed for the past 6000 years.
The yeast not only ferments sugars into alcohol, but also affects the appearance, aroma and taste of a beer. It’s not surprising then that each brewery maintains it own unique yeast strains. These strains, however, can be broken down into two main types: ale yeasts and lager yeasts.
It’s been known for some time that lager yeast is a genetic mix of yeast species S. cerevisiae (the same species ale yeasts hail from) and another species, S. bayanus. But the results of a new Stanford study that will be published online Thursday in <a href="http://www.genome.org/cgi/doi/10.1101/gr.076075.108" target="_blank" rel="noopener noreferrer">Genome Research</a> are the first to show that this mixing of DNA actually happened twice during the history of lager, and that the strain of S. cerevisiae involved was an ale yeast both times.
“We were excited to find this connection, because it makes so much sense,” said Gavin Sherlock,one of the study&#8217;s authors, in a statement. “The same breweries were used for both ale and lager, so it was really gratifying.”
Lager beers are brewed at much cooler temperatures than ales (52-58 ° F vs. 64-70 ° F), a tradition that dates back to Bavarian brewers who stored their beer in icy caves in the Alps during the summer months.
“It’s possible that the ale strain provides a certain flavor profile, while the second strain conferred the ability to ferment at cooler temperatures,” said Barbara Dunn, the other study author, referring to the hybridization events that created lager yeasts.

“Mixing them together is a nice way for the yeast to double its genetic options.”
When the researchers looked at yeast descended from the two groups of lager yeast, they saw further variation between strains.
“The fact that lager yeasts isolated from different breweries each seem to have a unique genomic make-up may indicate that the yeasts are adapting to the conditions specific to each brewery,” explained Dunn.
“Our discovery that unique genomic structures may be characteristic of each brewery and/or beer type could lead to insights on how to directly control flavor and aroma in beer.”
That’s the kind of science we can all raise a glass to.

BEER! Now that we have your attention, a little science…

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1282" title="amish" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/amish.jpg" alt="" width="276" height="205" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/amish.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/09/amish-300x223.jpg 300w" sizes="auto, (max-width: 276px) 100vw, 276px" />
A good diet and plenty of exercise are important for maintaining a healthy weight, but they’re not the whole story. Studies have shown that there’s a substantial genetic component to body mass index. Research published today in <a href="http://archinte.ama-assn.org/cgi/content/short/168/16/1791" target="_blank" rel="noopener noreferrer">Archives of Internal Medicine </a>demonstrates, however, that in people with a genetic predisposition for obesity, DNA is not necessarily destiny.
Scientists studying about 700 Old Order Amish men and women in Pennsylvania found that SNPs in a gene called FTO were associated with being obese or overweight. These associations, however, applied only to people with low physical activity levels. In people categorized as highly active for their age and sex, their FTO variants didn’t make a difference.
The high and low activity groups differed by about 900 kcal/day in their energy expenditures &#8212; the equivalent of three or four extra hours of moderately intensive physical activity like brisk walking, house cleaning, or gardening. While this might seem like a lot of activity, the authors point out that it’s typical for the lifestyle of the Old Order Amish, who farm without the aid of modern machinery.
Additional research is needed to determine the lower bound of how much exercise is really needed to negate the effect of an FTO-related genetic predisposition to weight gain. And then comes the hard part — figuring out exactly how the FTO gene influences weight and why physical activity seems to modulate its effect.

It’s Not Genes or Environment, It’s Genes AND Environment

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1261" title="samaritans" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/samaritans.jpg" alt="" width="350" height="186" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/09/samaritans.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/09/samaritans-300x159.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Upon hearing the name &#8220;Samaritans,&#8221; many people are immediately reminded of the famous passage from the Gospel of Luke (10: 25-37), the so called ‘Good Samaritan’ parable. Jesus tells of a Levite (a Jew) who is beaten and left on the side of the road. None who pass by the injured man stop to help, save a Samaritan. This parable was originally meant to highlight the fact that, even when two groups of people disapprove of each other (as did the Jews and the Samaritans), a single person from one group can still show kindness towards a member of the other.
<h2>Who Are The Samaritans?</h2>
Many people who know this parable or the term ‘Good Samaritan’ are unaware of who the Samaritans really are. In actuality, the Samaritans are a unique people whose history can be traced to Biblical times.
They are not considered ethnically Jewish or Arab, despite the fact that Samaritans have lived in close proximity to both groups for thousands of years. Though they used to be numerous, there are now only about 700 Samaritans left, divided between two towns near Tel Aviv and Jerusalem. They rarely marry non-Samaritans, and their religious practices are distinct from all Jewish sects.
Their ability to remain both (seemingly) genetically and culturally isolated in one of the most diverse regions on Earth has piqued the interest of both geneticists and historians, who have spent years trying to understand this unique group of people tucked away in the Levantine desert.
<h2>The Origins of the Samaritans</h2>
The origins of the Samaritans have always been clouded in uncertainty.
The traditional view is that, when the Jews were captured by the Assyrians in 721 BC as part of the infamous Babylonian Captivity, the Assyrians then repopulated Israel with people from the land of Samaria to the east. Then, when the Jews finally returned from exile 200 years later, they found these Samaritans already living in their ancestral homeland. As can be expected, tensions between the Samaritans and the Jews quickly escalated and would persist for the next several hundred years.
<h2>New Insights</h2>
However, recent archaeological findings, coupled with a deeper examination of religious texts, have led researchers to propose that the Samaritans were Jews themselves.
(Learn more about your ancestry and trace your family tree with 23andMe&#8217;s <a class="waffle-rich-text-link" href="https://www.23andme.com/dna-ancestry/">DNA Ancestry service</a>, or sign-up for a <a class="waffle-rich-text-link" href="https://www.23andme.com/membership/">membership</a> for advanced ancestry reports and features.)
Specifically, researchers argue that during the Babylonian Captivity, not all Jews were rounded up by the Assyrians. Some stayed behind, possibly marrying other Assyrian exiles who themselves had been relocated. This would make sense given that, even though Samaritans are not considered Jews, they share many of the same ancient Hebrew rituals.
While these rituals have evolved for hundreds of years among most Jewish sects, they remain unchanged among the isolated Samaritans, even to this day. This also fits well with the historical animosity of Jews toward Samaritans because of their association with non-Jews.
<h2>The Genetics of Samaritans</h2>
But what do the genetic data reveal about the Samaritans&#8217; origins? Luckily, there have been many genetic studies of the Samaritans, both to uncover their origins and to understand how they have survived so many generations of isolation.
One such study by Peidong Shen and colleagues in the Journal Human Mutation has used both mitochondrial DNA and Y-chromosome DNA of modern-day Samaritans to discover their origins and genetic relationship to Near Eastern Jews. Their results are fascinating.
The mitochondrial DNA results, which show maternal history (i.e. your mother’s mother’s mother, etc.), reveal no major difference between the Samaritans, Jews, or Palestinians in the Levant who were also sampled. These three groups have relatively similar maternal genetic histories.
<h2>Insights from the Y-Chromosome</h2>
However, the story of the Y-chromosome, which shows paternal history (i.e. your father’s father’s father) is quite different. Indeed, not only are the Y-chromosomes of the Jews and Samaritans more similar to each other than either is to the Palestinians&#8217;, the Y-chromosomes of the Samaritans show striking similarities to a very specific Y-chromosome most often associated with Jewish men. Although the Samaritan type is slightly different from the Jewish type, it is clear that the two share a common ancestor, probably within the last few thousand years.
As a result, Shen and colleagues argue that the traditional hypothesis, that the Samaritans were transported into the Levant by the Assyrians and have no Jewish heritage, is largely incorrect. Rather, these Samaritan lineages are remnants of those few Jews who did not go into exile when the Assyrians conquered the northern kingdom of Israel in 721 BC. Those who remained in the Levant may have take non-Jewish wives, which would account for the genetic admixture on the female side. But according to the authors the Y-chromosome clearly shows that the Samaritans and the Jews share common ancestry dating to at least 2,500 years ago.
The similarity between the Y chromosomes of Samaritans and Jews illustrates that groups considered quite distinct today can actually have relatively recent genetic connections. Indeed, we are all connected to each other in some way through our shared genes, shared ancestry, and shared history. The research into the origin of the Samaritans is just one example of this connection.
<h2>Learn More</h2>
Explore more about 23andMe&#8217;s ancestry reports <a href="https://www.23andme.com/ancestry-composition-guide/">here, or </a> find out if your <a href="https://www.23andme.com/test-info/genetic-health/">genetics</a> might Increase your risk for any health conditions with 23andMe.

The Genetic History of the Samaritans

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1249" title="mappinghumanhistory" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/mappinghumanhistory.jpg" alt="" width="199" height="300" />
For more than a century anthropologists have studied the multitude of cultures and ethnicities that exist across the globe, delving deep into the various ways that populations develop their own unique identities.
With the development of genetic anthropology over the last 15 years, scientists have begun to examine whether these cultural identities align with a population’s genetics. How do we as humans differ genetically from one another, and how have these differences arisen throughout our species&#8217; history?
<h6>Discovering the Past Through Our Genes</h6>
This fascinating question is tackled by Steve Olson in Mapping Human History: Discovering the Past through our Genes.
Olson is well suited to explain the complex genetic history of our species. He has worked for the National Academy of Sciences, the White House Office of Science and Technology Policy, and written several books and articles for general audiences on human genetics.
While researching this book he interviewed a large number of anthropological geneticists. He uses his experience in science communication – as well as those interviews – to tell the story of Homo sapiens, beginning in Africa and touching on nearly every major geographical region in the world.

<h6>Starting in Africa</h6>
Olson starts his exploration of our species’ genetic history where it began, in Africa. He begins by describing some of the most isolated and interesting ethnic groups – the so-called Bushmen of southwest Africa and the Kalahari Desert. This well known group of hunter-gatherers has interested anthropologists and geneticists alike for many decades. The Bushmen are relatively isolated, maintaining a hunter-gatherer lifestyle even as many populations around them have taken on new lifestyles. They also speak languages that are famous for their ‘click’ sounds. Belonging to the Khoisan language family, these languages are believed to be some of the most ancient still spoken among humans.
Olson uses examples such as the Bushmen to delve deeper into the science of genetic ancestry. He clearly explains how scientists use DNA to trace both maternal and paternal ancestry, similar to what we at 23andMe do as part of our Personal Genome Service.
<h6>Prehistoric Migrations</h6>
After spending time discussing Africa Olson moves on, tracking our species’ prehistoric movements into the Near East, Asia, Europe, and even the Americas. He also spends time discussing some of the most interesting genetic questions about our species, such as the origins and migrations of the Jews throughout history, and how changes in languages can sometimes be connected to genetic changes.
The final portion of Mapping Human History investigates more closely the cultural and ethnic issues that have arisen over the past ten years because of studies that examine the genetic ancestry of specific populations. Some Native American groups, for example, protest studies such as these because they conflict with their own tribes’ creation stories.
However, Olson argues this research should actually be applauded, because &#8220;the study of genetics has now revealed that we are all linked…. We are members of a single human family, the products of genetic necessity and chance.&#8221;
<h6>Our Genetic Past</h6>
Mapping Human History is, overall, a good foray into our species’ genetic past and how genetics studies can reveal many things – both about how we are different, and how we are the same. Olson peppers his arguments with engaging anecdotes, such as the story of a female researcher in South Africa with mixed heritage, or how the peopling of Hawaii led to such unique genetic diversity among its current inhabitants. These anecdotes would be welcome for any general reader, making the concepts Olson discusses more real and accessible to a general audience.
There are many books that deal with genetic ancestry, and this one does cover many of the same topics as countless others.
But what distinguishes Mapping Human History is its focus on genetic versus cultural and ethnic divisions in our societies. This alternative angle may prove interesting to general audiences with non-science backgrounds, as Olson brings in issues such as race relations and cultural and ethnic diversity that are relevant to many people.
This text would prove an appealing read for 23andMe customers looking to put their own genetic information into a global context. In addition, it would be well-suited for anyone interested in how our species has evolved and expanded over the last few hundred thousand years, and how these past migrations have shaped the ethnic and cultural identities that exist today across the globe.
Mapping Human History: Discovering the Past through our Genes 
Steve Olson 
2002 
New York: Hougton Mifflin Company

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