<img loading="lazy" decoding="async" class="alignright size-full wp-image-1035" title="Peacock" src="https://blog-api.23andme.com/wp-content/uploads/2008/08/istock_000000236820xsmall-300x225.jpg" alt="" width="300" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/08/istock_000000236820xsmall-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/08/istock_000000236820xsmall.jpg 400w" sizes="auto, (max-width: 300px) 100vw, 300px" />
An animal&#8217;s ability to survive often depends on how well it can avoid predators.   Many species of fish, birds, and mammals have evolved ingenious methods of staying hidden from predators by blending into the background in one form or another.   But what about animals that do the opposite?   How and why would such attention-grabbing features as a lion’s mane, a male deer’s antlers, or a peacock’s tail evolve?   As it turns out, these traits can be explained by something called sexual selection.   Sexual selection is an aspect of evolutionary theory developed by Charles Darwin in the 19th century after he began to notice many traits that were exaggerated, especially among the male members of the species.   Darwin reasoned that within a species, there must be a &#8220;struggle between the individuals of one sex, generally the males, for the possession of the other sex.&#8221;   So in the same way that women may prefer men with broad shoulders, female peacocks prefer their male counterparts to have ornate feathers — the larger the better. Evolutionary biologists have understood the concept of sexual selection for years, but there has been much debate over how this process occurs at the genetic level.   For example, male and female lions have basically the same set of genes. So how are these genes modified such that male lions develop a mane while females do not?   The answer, as it turns out, is surprisingly simple.
 In this week’s issue of Cell, molecular biologists tackled the question of how sexual selection works by examining the genetics of fruit flies. Male fruit flies have evolved a unique coloring pattern on their abdomens that apparently attracts females in the same way that a peacock’s feathers do.   Females lack the markings, yet they have basically the same genome males do. So how is it that the same basic genome (aside from sex chromosomes) can lead males and females to develop different physical traits? According to University of Wisonsin-Madison biologist Sean Carroll, &#8220;The flies did not need new genes … they just changed how males and females use a common set of genes.&#8221; Carroll and his team discovered that while both male and female fruit flies have the genes necessary to create the abdominal coloring pattern, it is only the males who have that gene switched on.   In female fruit flies, this gene lies dormant. “With this particular trait, it evolved by exploiting (genetic) information that was already there to make male bodies different from female bodies,’ explains Carroll. So how does the genetics of a coloring pattern on fruit fly abdomens apply to sexual selection in other species?   According to Carroll and his colleagues, the same genetic mechanisms that are at play in the fruit fly also operate in a multitude of other animals — including lions, deer, peacocks, and even humans.   This study, in showing the genetic means for how sexual selection may operate, illustrates the ingenuity of evolution — how a seemingly simple genetic switch can create such beautiful and elaborate features in the male members of thousands of the world’s species.

23andMe Blog

23andMe Blog Team

Is That a Peacock Feather under your Coat … Or are You Just Happy to See Me?

<img loading="lazy" decoding="async" class="alignnone size-medium wp-image-1011" title="cigarettes2" src="https://blog-api.23andme.com/wp-content/uploads/2008/08/cigarettes2-300x225.jpg" alt="" width="300" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/08/cigarettes2-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/08/cigarettes2.jpg 640w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Tobacco use is the leading cause of preventable deaths in the United States – every year it kills nearly 440,000 Americans.
While about 70 percent of the 45 million Americans who currently smoke have said they want to quit, the Centers for Disease Control and Prevention estimates that only about 10 percent of them will succeed, due in large part to the addictive qualities of the active ingredient in tobacco, nicotine.
Researchers have been looking at the genetic basis of nicotine dependence, characterized by tolerance to the drug and the presence of withdrawal symptoms in its absence, with the long-term goals of better assessing a person’s risk for addiction and potentially developing targeted treatments.
Last year, Laura Bierut and her colleagues at the Washington University School of Medicine <a href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&amp;pubmedid=17135278" target="_blank" rel="noopener noreferrer">identified</a> a single variant in a nicotine receptor that increases a person’s risk of developing nicotine dependence. A later study indicated the same SNP can actually reduce the risk of developing cocaine dependence. And now a study published this month by Bierut and her colleagues shows that the variant also influences how much pleasure a first-time smoker will experience from the first puff of a cigarette.

&#8220;The type of variant you have at this particular receptor – the alpha-5 nicotinic receptor – may actually predict whether or not you will do well on nicotine replacement therapy,&#8221; Bierut said in a statement at the time.
The version of SNP that can increase the risk for nicotine addiction is found at <a href="https://www.ncbi.nlm.nih.gov/pubmed/18519524?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">appreciable levels</a> only in European populations. People with two copies of the less common A version of the SNP are twice as likely to develop nicotine dependence when exposed to smoking than people with two copies of the more common G version.
A new study from Bierut’s group published this month in the journal Addiction shows that the same version of previously associated with nicotine dependence is also linked to the pleasurable rush some first-time smokers get. Each A at increased a person’s odds of having found that first puff pleasurable by 1.6 times compared to people with no copies of an A. This “buzz” was in turn associated with an 8-fold increase in odds of being a current smoker.
&#8220;The finding of a genetic association with pleasurable early smoking experiences may help explain how people get addicted – and, of course, once addicted, many will keep smoking for the rest of their lives,&#8221; said the study’s senior author Ovide Pomerleau in a statement.
&#8220;It appears that for people who have a certain genetic makeup, the initial physical reaction to smoking can play a significant role in determining what happens next. If cigarette smoking is sustained, nicotine addiction can occur in a few days to a few months.&#8221;
Bierut’s research on SNP also extends to addictive substances other than nicotine. Back in June, her group released a study that examined cocaine addicts and non-drug abusing controls to <a href="https://www.ncbi.nlm.nih.gov/pubmed/18519132?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">show</a> that having the nicotine dependence-predisposing A version of this SNP actually decreases the risk for cocaine dependence. Having one A decreases the odds of cocaine dependence risk by about 33 percent; two copies decrease the odds by about 45 percent.
The involvement of this SNP in both nicotine and cocaine addiction, and its opposing effects, may seem perplexing. But Bierut and her colleagues suggest that the answer lies in how each addictive substance affects dopamine in the brain’s reward pathway — a key player in the pleasurable feelings produced by drugs that can lead to addiction.
Nicotine triggers the release of dopamine, a neurotransmitter that activates pleasure pathways in the brain. In contrast, cocaine produces pleasurable feelings by <a href="http://thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_cocaine.html#drogues" target="_blank" rel="noopener noreferrer">preventing</a> the dopamine that is naturally released in the brain from being reabsorbed when its job is done. Excess dopamine hangs around in the brain and produces the “high” associated with the drug.
The nicotine receptor that affects is involved in normal dopamine release, even in the absence of nicotine. So when the A version of this SNP dials down the receptor’s activity, natural dopamine release is reduced. This means there is less dopamine available for cocaine to keep around in the brain, and the amount of pleasure the drug can induce is diminished, possibly enough to keep a person from getting addicted.
Image from <a href="http://www.freedigitalphotos.net/details.php?gid=137&amp;sgid=&amp;pid=1389" target="_blank" rel="noopener noreferrer">FreeDigitalPhotos.net</a>

Gene Variant that May Counter Cigarette Cravings

In a recent post we used an analysis of Craig Venter’s genome to illustrate how much has yet to be learned about the relationship between genetic variation and health-related traits.
<img loading="lazy" decoding="async" class="alignright wp-image-916 size-medium" title="craigventer1" src="http://35.88.189.111/wp-content/uploads/2008/08/craigventer1-207x300.png" alt="" width="207" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/08/craigventer1-207x300.png 207w, https://blogcms.23andme.com/wp-content/uploads/2008/08/craigventer1.png 241w" sizes="auto, (max-width: 207px) 100vw, 207px" />
A new paper by Venter and colleagues at his Rockville, Maryland-based institute provides a prime example. Writing in the September issue of Clinical Phamacology &amp; Therapeutics, Venter et al. argue that knowing how genetic differences between ethnicities affect patients’ reactions to certain medications isn’t good enough. To make sure patients get the best healthcare, they say, doctors should be looking at how each person is likely to respond to a particular drug regimen based on his or her unique genetic makeup.
“Even the term ‘Caucasian’ can be deceptive,” the authors noted. “If a self-identified Caucasian originates from a founder population in which certain disease-specific alleles occur at higher frequencies (e.g. Quebec French Canadians or Ashkenazi Jews), his or her doctor may miss an important aspect of the patient’s medical history. One’s ethnicity/race is, at best, a probabilistic guess at one’s true genetic makeup.” 

<img loading="lazy" decoding="async" class="alignnone size-medium wp-image-1005" title="james watson" src="https://blog-api.23andme.com/wp-content/uploads/2008/08/watson1-240x300.jpg" alt="" width="240" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/08/watson1-240x300.jpg 240w, https://blogcms.23andme.com/wp-content/uploads/2008/08/watson1-768x958.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2008/08/watson1-821x1024.jpg 821w, https://blogcms.23andme.com/wp-content/uploads/2008/08/watson1-705x880.jpg 705w, https://blogcms.23andme.com/wp-content/uploads/2008/08/watson1.jpg 885w" sizes="auto, (max-width: 240px) 100vw, 240px" />
To further emphasize the differences between people within the same ethnic group, the authors compare the publicly available genome sequences of Venter himself and Nobel Prize winner James Watson, focusing on six genes involved in drug metabolism.
One of those genes revealed a substantial difference between the two men. CYP2D6 is involved in the metabolism of various drugs for high blood pressure, heart arrhythmia and depression. Venter’s genotype indicates that like most Europeans he is an “extensive metabolizer” of such drugs; but Watson’s genotype puts him in the “intermediate metabolizer” category, which is more common among Asians.
Using race as a guide, the authors noted, a physician would have no reason to expect Venter and Watson to react differently to drugs that are metabolized by CYP2D6.
Venter and his colleagues conclude by emphasizing the need for personalized health care based on genomic information, adding that the cost to do so is dropping rapidly.
“Given the complex nature of drug responses, it would ultimately better serve all to dissect the relevant factors of a drug response instead of categorically stereotyping a culture with a presumed genetic background.”
Images: Venter photo by Michael Janich; Watson photo courtesy of the National Library of Medicine

The Rest of the Iceberg

Despite CNET&#8217;s assertion last week that Bigfoot couldn&#8217;t possibly be a hoax because people always bring their A game to Palo Alto, the carcass in the ice has turned out to be a rubber gorilla suit. And the freezer wasn&#8217;t that big either.
Sorry, Bigfoot believers, this means the DNA evidence presented at last week&#8217;s press conference almost certainly came from one or more non-Bigfoot sources, and probably not from a Giant Bipedal Possum of northern Georgia either.
With websites <a href="http://news.google.com/news?hl=en&#038;client=firefox-a&#038;rls=org.mozilla:en-US:official&#038;hs=otq&#038;q=bigfoot%20hoax&#038;um=1&#038;ie=UTF-8&#038;sa=N&#038;tab=wn" target="_blank" rel="noopener noreferrer">around the world</a> gleefully spreading the news, it&#8217;s perhaps best to let professional Bigfoot hunter Tom Biscardi – who arranged last week&#8217;s Palo Alto press extravaganza – speak for himself. But as it seems Biscardi wasn&#8217;t present at The Thawing, he&#8217;s deferred the task to someone else.
Here then is part of the eyewitness account from Tom Kulls of SquatchDetective.com, as <a href="http://www.searchingforbigfoot.com/" target="_blank" rel="noopener noreferrer">posted</a> on Biscardi&#8217;s site:
&#8220;On August 17th, 2008 Searching for Bigfoot Team Director of Field Operations, TJ Biscardi [Tom&#8217;s son] and myself, were up early to discover that some hair was now exposed. I extracted some from the alleged corpse and examined it and had some concerns. Bob Schmalzbach arrived and concurred. We burned said sample and said hair sample melted into a ball uncharacteristic of hair.
At that time we contacted Mr. Biscardi who gave us permission to begin an expedited melting process. We set up a salamander [portable] heater to heat the freezer. Within one hour we were able to see the partially exposed head, as I was now able to touch it, I was able to feel that it seemed mostly firm, but unusually hollow in one small section. This was yet another ominous sign. Within the next hour of thaw, a break appeared up near the feet area. As the team and I began examining this area near the feet, I observed the foot which looked unnatural, reached in and confirmed it was a rubber foot.&#8221;
Science in action.

Defrosted Disappointment

Throughout the history of our species there has been one constant:   movement.   Since the origin of Homo sapiens nearly 200,000 years ago in East Africa, humans have journeyed around the globe, ultimately inhabiting every continent save Antarctica. Scientists have traditionally used archaeology, and more recently genetics, to understand the timing and scope of these ancient migrations.   The field of historical linguistics has also been used in the same way,   reasoning that if people migrated to new regions, they would have brought their languages with them.   In this way, linguistics can be used as an additional resource in understanding our species’ past movements. However, this concept is rarely — if ever — that straightforward.   For example, a language might spread from local population to local population, while the original speakers of the language stayed put.   This concept, called ‘cultural diffusion’ is at the core of many debates about our species’ prehistory:   did people (and therefore their genes) migrate to a new region, or was it just a transfer of cultural traits (such as language) from one region to the next?

There are two famous examples in human prehistory that delved deep into this very question.
<h6> Bantu Expansions in sub-Saharan Africa</h6>
 About 5,000 years ago, the majority of sub-Saharan African peoples still relied on hunting, gathering, and foraging as their main source of food.   But some people in west-central Africa were developing new techniques of survival.   They began to experiment with herding and agriculture, cultivating the yams, legumes, peppers, and gourds that would became staples of a sub-Saharan African diet.   Then, about 4,000 years ago, they began to move.   As they traveled over a period of centuries, they both displaced and absorbed groups that were already living throughout Africa.   The languages that they brought with them from their ancestral homeland, belonging to the Bantu family, also spread throughout sub-Saharan Africa.   Today the majority of sub-Saharan African languages are Bantu. What both genetics and linguistics have told us about the Bantu expansions is that it was an expansion of both peoples and cultures.   Though these early Bantu speakers may have intermarried as they expanded,   their genetic signature still shows West African ancestry.   The distribution of Bantu languages throughout sub-Saharan Africa confirms this prehistoric migration.   In fact, this example marks one of the most straightforward instances of a combined genetic and cultural expansion.  
<h6> The Spread of Agriculture and Indo-European Languages</h6>
 Unfortunately, the spread of agriculture from the Near East into Europe and its connection to the spread of Indo-European languages is far more complicated.   Agriculture is believed to have originated in the Near East about 13,000 years ago.   Starting about 10,000 years ago, the archaeological record indicates that the practice expanded westward into Europe. By 9,000 years ago, agriculture existed in Greece.   By 5,000 years ago it had reached Scandinavia. But was this spread of technology accompanied by farmers themselves, as in the Bantu migrations?   Linguists felt they had the answer: the vast majority of languages spoken in Europe today are members of the Indo-European language family.   Languages such as Greek, Latin, Celtic, and English all belong to this group.   In fact, only a few isolated European languages (such as Basque and Finnish) are unrelated.   Linguists argued that the geographical origin for this language family was probably somewhere in the Near East or Caucasus Mountains, and that these languages spread — along with the farmers themselves — into Europe, replacing the older languages that were already in existence.   The archaeology appeared to support this idea, and soon many scholars had argued for an expansion of agriculturalists from the Near East. However, the genetics told a somewhat different story.   Though there are genetic footprints in Europe of these early Near Eastern agriculturalists, there are pre-agricultural genetic footprints as well.   In fact, more Europeans trace their ancestry back to ancient European hunter-gatherers, who survived the harsh Ice Age in the southern fringes of Europe 20,000 years ago, expanding into northern Europe as glaciers receded several thousand years later.   They were not replaced or marginalized by the arrival of agriculturalists. This discordance has made the question of the arrival of agriculture and Indo-European languages in Europe one of the most contentious in the fields of archaeology, genetic anthropology, and linguistics.   It remains unresolved, though many scientists now argue for lower levels of genetic diffusion into Europe than originally thought. There are countless other examples in human prehistory of cultural vs. genetic diffusion, with different disciplines often yielding different hypotheses.   The connection between genetic diffusion and cultural diffusion is anything but straightforward, and the best research will take into account not only genetic and linguistic evidence, but evidence from the archaeology, human skeletal remains, and paleobotany.   As noted scientist and author Jared Diamond has put it, &#8220;It is quite a challenge, but a uniquely fascinating one.&#8221;

Genes and Languages: Not So Strange Bedfellows?

<img loading="lazy" decoding="async" class="alignright size-full wp-image-969" title="potassium_channel" src="https://blog-api.23andme.com/wp-content/uploads/2008/08/potassium_channel.jpg" alt="" width="350" height="299" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/08/potassium_channel.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/08/potassium_channel-300x256.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />A potassium channel/David S. Goodsell,The Scripps Research Institute
Ion channels are pore-forming proteins that poke through cell membranes to control the movement of ions like calcium, potassium, and chloride in and out of cells. Movement of these ions is critical for a wide-array of physiological processes &#8212; everything from controlling the heartbeat to flexing muscles to firing neurons.
Because ion channels are so essential, mutations in these proteins can lead to serious disease. For example, cystic fibrosis is caused by mutations in a chloride channel protein and certain forms of epilepsy are caused by mutations in sodium channel genes.
Three studies published online yesterday in the journal Nature Genetics show that common variants in ion channel genes may also contribute to disease risk. Two groups found evidence that a potassium channel protein is associated with type 2 diabetes, while another group discovered that a calcium channel and a protein that regulates sodium channels might be associated with bipolar disorder.

<h6>Type 2 Diabetes</h6>
Of all the conditions that have so far been studied with genome wide association study methods, type 2 diabetes has been one of the blockbusters.  Research continues and variants associated with the condition are constantly being found and/or validated.
This week <a href="https://dx.doi.org/10.1038/ng.207" target="_blank" rel="noopener noreferrer">Yasuda et al</a> contribute their finding that a variant associated with an increased risk for developing type 2 diabetes.
This variant is in the gene KCNQ1, which encodes part of a potassium channel that has known roles in cardiac muscle. It is not yet known how this gene could affect the risk for type 2 diabetes, but there is evidence that it is turned on in the pancreas. Yasuda et al found that people with who were homozygous for the variant had evidence of impaired insulin secretion. Another potassium channel gene, KCN11 has previously been associated with type 2 diabetes in several studies.
Genomewide association studies have struggled to find SNPs that are associated with diseases in more than one ethnic group. That’s why it is surprising that the variant was associated with type 2 diabetes not only in the original Japanese set of cases and controls used in this study, but also in Chinese, Korean, and European samples.
<h6>Bipolar Disorder</h6>
Bipolar disorder is a serious mental illness that affects about one to three percent of the world’s population. As with many other common diseases, researchers have been using genomewide association studies in an effort to find SNPs associated with bipolar disorder in order to begin to understand how and why this disease strikes and how best to treat it. So far, however, progress has been slow and there has been little agreement from study to study.
In their quest to tease out the genetics of bipolar disorder, <a href="https://dx.doi.org/10.1038/ng.209" target="_blank" rel="noopener noreferrer">Ferreira et al</a> took an approach that is becoming more popular&#8211;they combined data from several smaller studies to get the larger sample size that is often needed to find variants with modest effect. In total, they looked at 10,596 people of European ancestry — 4,387 people with bipolar disorder and 6,209 controls.
Two variants stood out as candidates for bipolar disorder. Both were in genes related to ion channels.
The first variant in in the gene CACNA1C, which encodes a calcium channel. Previous studies had hinted that this gene might be associated with bipolar disorder. The second variant is in the gene ANK3. This gene encodes a protein that has been shown to regulate sodium channels.
Further evidence for the involvement of these SNPs in bipolar disorder comes from previous studies by these same researchers. In <a href="https://www.ncbi.nlm.nih.gov/pubmed/17622937?ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">mice</a> they found that lithium, the most effective drug for treating bipolar disorder, appears to decrease the amount of protein made by the ANK3 and CACNA1C genes.
“Finding statistically robust associations linked to two proteins that may be involved in regulating such ion channels — and that are also thought to be targets of drugs used clinically to treat bipolar disorder — is astonishing,” said Pamela Sklar, a lead author of the study, in a statement.

Variants in Ion Channel Genes are Associated with Type 2 Diabetes and Bipolar Disorder

by Esther Dyson
Last weekend I attended Science Foo Camp, a sort of grown-up summer camp for scientists sponsored by Google (an investor in 23andMe), Nature Magazine and O’Reilly Media.
Aside from the science itself (which is worth many blog posts on its own), one question really grabbed my attention: What motivates people to do science in the first place?<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2008/08/estherzerog-300x198.jpg" alt="" title="estherzerog" class="size-medium wp-image-929 alignright" width="300" height="198" />
 
In two different sessions, I felt that scientists were ignoring one critical element of the equation – themselves.
<h6>Compelled by Curiosity</h6>
Many scientists say they do what they do out of a thirst for knowledge. Yet in the 23andMe session, I found that many researchers don’t recognize curiosity as a motivating factor when it extends to oneself.
There was a sense that of course scientists are interested in scientific data. But why would “normal people” want to use 23andMe for anything other than health care information? Many scientists at the session seemed to think that if you’re motivated by personal curiosity rather than “serious health concerns,” your curiosity is somehow less legitimate. Ironically, this is at a time when we are all struggling with how to get kids interested in science. Why not appeal to people’s innate curiosity and fascination with themselves?
I’m lucky enough to have about 30 family members plus another 80-odd people in my personal circle of friends. I love combing through the data to see how everyone compares to me and one another. (You’re welcome to add yourself! My user name is edyson, and I will accept an invitation at whatever level you set. NOTE: I will freely disclose your overall similarity to others, and your ancestry painting, but not the health information unless you give permission.)
At SciFoo, I encountered a 23andMe customer who was adopted. “The first time I saw a blood relative was when my first baby was born,” she said. “I wanted to know more about my own kids.” Did she find out anything “serious” or actionable? No, but she satisfied a lot of curiosity … and indeed, she now knows something about health issues her child may face down the road.
<h6>Data = notches on your belt</h6>
In addition to curiosity there’s money, which scientists mostly hate to discuss in public, but which is fairly well understood as a motivator for some scientists — not to mention for all the engineers, applied scientists and others who turn scientific insights into useful technology and products. â€¨â€¨But there’s another motivator that seems to be less understood or acknowledged. I’m not sure of the best word to describe it, but it’s an interest in being part of the effort and being acknowledged for it, sometimes leavened by fascination with one’s own data (either alone or compared with others’).
This came up in a session I attended about data-sharing. The focus was mostly data about insect species, viruses and human medical records, but it could just as easily have been genetic data.
The discussion reflected how science has changed over time. In the past, much of it was about individual discovery and experiments. But increasingly we need lots of data, collected by lots of people, to make progress. Yet scientists, and even more so scientific institutions, often operate in a climate of secrecy — at least until their results are published in a peer-reviewed journal. But what if you need the data before you can produce the results?
In science as in sports, teamwork can mean the difference between victory and defeat. At the Beijing Olympics, one of the big stories is how Michael Phelps swam to victory by following a teammate who let him swim in his wake until the final sprint, when Phelps was able to use the energy he had not expended earlier in the race to win it. That’s a benefit of collaboration.
There’s also the odd but totally understandable fact that Olympians tend to set records in competition, when they’re trying to beat another person. (I know I personally always swim faster when there’s someone about my speed in the next lane.)
Scientists aren’t immune to such effects. Biologist Dan Janzen and medical researcher/doctor Scott Layne both talked about how scientists like to add data to the pot in a way that gets them recognition for their contributions — karma points so to speak. On Flickr, you post photos. In science, you post data … and you can measure your contribution to the general welfare not just in citations, but in page views, reuse, whatever. The tools for doing that are still being developed. Meanwhile, through 23andMe and PatientsLikeMe, a social network for patients with ALS or Parkinson’s, even individuals can play by contributing their own data (medical or genetic) rather than isolating enzymes in a lab or bugs in a hospital. 
Scientists may scoff, but I’m sure the evidence will show that social recognition can do a lot for science.
Esther is a director at 23andMe and investor in numerous private aviation, space and health care ventures, including PatientsLikeMe.

Esther Dyson

A Matter of Motivation

If anybody could turn the history of genetic anthropology into a page-turner, it would be Bryan Sykes. Sykes, Professor of Human Genetics at the University of Oxford, has spent the better of part the last 25 years decoding the mystery of our species’ genetic ancestry through mitochondrial DNA analysis. He recounts his work in his 2001 book, The Seven Daughters of Eve: The Science that Reveals our Genetic Ancestry.
But Sykes doesn&#8217;t simply relate the major discoveries in the field. He goes one step further by breathing life into each of the seven major mitochondrial DNA clusters that are common today in European populations.

The Seven Daughters of Eve can be divided into two major parts. In the first, Sykes discusses some of his most fascinating work. He relives how he and his colleagues extracted ancient DNA from the 5,000-year-old Ã–tzi the Iceman, examines his work on understanding the origins of the Polynesians, and tells how he and his team discovered the true fate of Tsar Nicholas II and the Romanovs. With each story, Sykes easily manages to explain the scientific details behind his conclusions in a way that nearly any reader can comprehend.
23andMe customers will be most interested in Sykes&#8217; explanation of how mitochondrial DNA can be used to trace individuals’ maternal ancestry. Mitochondrial DNA (mtDNA) is a small segment of circular DNA that is found in tiny organelles called mitochondria. It is believed that hundreds of millions of years ago, mitochondria were free-living bacteria who invaded more advanced cells and never left. Now, they are an integral part to every cell. For people like Bryan Sykes, however – not to mention 23andMe customers who are interested in their ancestry – mitochondria are mostly important for what their DNA can tell us.
Because of the way fertilization takes place, mitochondria (and thus mtDNA) are only passed from mother to child, like a kind of &#8220;matrilineal surname.&#8221; In the same way that surnames can change gradually over generations, so too does mtDNA. So while two siblings are almost certain to have identical mtDNA, people whose most recent common maternal ancestor lived thousands of years in the past are likely to bear substantially different mtDNA signatures.
As it turns out, the different mtDNA patterns found in populations around the world can be organized together into a global family tree. At the tips of the tree are present-day human populations from around the world. At the root of the tree is the common mtDNA ancestor of every human alive today, a real woman who lived in Africa about 175,000 years ago.
As with any family tree, some people are more closely related than others. Scientists have given these more closely related clusters, or ‘haplogroups,’ specifically designated letters. There are seven such haplogroups (and thus, seven letters) among people of European descent – U, K, H, V, X, T, and J.
These seven haplogroups form the basis for the second part of Sykes’ book. As a way of making them seem more personal to the reader, he gives them each a name. For example, haplogroup U becomes Ursula, X become Xenia, H becomes Helena, and so on. These are the so-called &#8220;Seven Daughters of Eve.&#8221;
Sykes uses these names to create stories based on where in Europe the descendants of each &#8220;daughter&#8221; are concentrated. In a chapter on haplogroup K (Katrine), he relates the domestication of wolves. The chapter on haplogroup J (Jasmine) is dedicated to the beginnings of agriculture in the Near East more than 10,000 years ago.
Sykes concludes his journey into our species’ genetic past by explaining why he feels it important to understand genetics from a personal standpoint. He writes, &#8220;I like this kind of genetics because it puts the emphasis back where it belongs: on individuals and their actions.&#8221; There are so many stories hidden in our genes, he reasons, and it is best to tell them to the public in this fashion.
This book is not without flaws. The anecdotes about Sykes&#8217; research in the field are, by definition, centered on how he was the major player in each discovery. As a result, many important players in the field are marginalized or left out completely. In addition, the dramatic benefit of assigning each haplogroup its own story comes at the expense of accuracy and completeness. For example, haplogroup J (Jasmine) is not the only one associated with the origin and spread of agriculture form the Near East to Europe; but in The Seven Daughters of Eve, it is the only one mentioned.
However, simplifying and romanticizing genetic anthropology does make for a good story — which was Sykes’ goal in the first place. Indeed, Sykes has discovered many amazing stories in his years of research at Oxford, and The Seven Daughters of Eve proves to be an engaging journey that can be enjoyed by general audiences and genetic ancestry enthusiasts.
The Seven Daughters of Eve: The Science that Reveals our Genetic Ancestry 
Bryan Sykes 
2001 
New York: W.W. Norton &amp; Co.
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