<img loading="lazy" decoding="async" class="alignright size-full wp-image-1702" title="milkshake" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/milkshake.jpg" alt="" width="284" height="423" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/10/milkshake.jpg 284w, https://blogcms.23andme.com/wp-content/uploads/2008/10/milkshake-201x300.jpg 201w" sizes="auto, (max-width: 284px) 100vw, 284px" />
Although obesity was seen as a sign of social status during the Renaissance, it’s been known since <a href="http://classics.mit.edu/Hippocrates/aphorisms.2.ii.html" target="_blank" rel="noopener noreferrer">long before then</a> that being overweight is actually unhealthy.
We all know that carrying around extra pounds increases the risk for high blood pressure, diabetes and cardiovascular disease, yet one out of three Americans is obese.
New research, published online today in <a href="https://dx.doi.org/10.1126/science.1161550" target="_blank" rel="noopener noreferrer">Science</a>, suggests that for some obese people, genetic variations may desensitize the brain&#8217;s reward centers, making food less satisfying and leading to the consumption of more calories followed by the predictable result – weight gain.
<h6>Dopamine</h6>
When we eat, feelings of pleasure are produced by the release of a chemical called dopamine into the brain. Recent research has shown that the brains of obese people have fewer dopamine-responsive receptors; this deficit may decrease the pleasure obese people get from food and prompt them to overeat in order to compensate.
“Individual differences in how the brain processes food reward have been postulated to play a role in explaining why some, but not all, people are gaining weight in an environment where calories are plentiful. Our finding is exciting because it supports this possibility by demonstrating an association between an abnormal response to food and future weight gain — and it shows that this relationship depends on your genetic make-up,” said study author Dana Small in a statement.
<h6>The Study</h6>
Small and her colleagues examined 43 college women and 33 adolescent girls using functional magnetic resonance imaging scans, which analyze brain activation by measuring blood flow in the brain, while the study subjects tasted either a chocolate milkshake or a flavorless solution.
In both study groups, women with higher body mass indices (BMI) had lower levels of activation in dopamine-responsive areas of their brains as they tasted the milkshake. This relationship was significantly stronger in women with one or two copies of a variation in the dopamine receptor gene DRD2 that scientists call the “Taq1A A1 allele”.
The A1 allele has been associated with fewer dopamine receptors in the brain. Previous research has shown that people with one or two copies of the A1 allele are more likely to be obese. Other traits – such as alcoholism, obsessive-compulsive disorder, and error avoidance — have also been linked to the A1 allele and thus the brain’s reward pathways.
After one year, the researchers found, women with one or two copies of the A1 allele who had also shown lower brain activation in response to food gained more weight, possibly because of their diminished pleasure response.
“Identifying changes in behavior or pharmacological options could correct this reward deficit to prevent and treat obesity,” said the study’s lead author Eric Stice.

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Genetics May Dull Pleasure Response to Food

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Obesity affects about one out of three adults in the United States. Because obese people are at increased risk of high blood pressure, diabetes, cardiovascular disease, and other health problems, many authorities consider it one of the most significant public health problems in the developed world.
Of course, diet and exercise are important parts of maintaining a healthy weight, but some people need a little more help. Sibutramine (marketed by Abbott Laboratories as Meridia ® in the U.S.) is a drug that creates a feeling of fullness, prevents the decline in metabolic rate usually associated with low-calorie diets and causes weight loss, especially when combined with behavioral therapy.
<h6>Genetics and Responsiveness to Treatment</h6>
But success with sibutramine is variable — for some people it just doesn’t work. New research, published in the October issue of <a href="http://www.gastrojournal.org/article/S0016-5085(08)01317-6/abstract" target="_blank" rel="noopener noreferrer">Gastroenterology</a>, shows that genetic differences might be to blame.
“Our results suggest the genetic make-up of patients could predispose their responsiveness to a drug. This could have important implications for the future of personalized molecular-based or individualized medicine,” said the study’s lead author Dr. Michael Camilleri in a statement.
Using a sample of 158 overweight and obese people, researchers at the Mayo Clinic tested the effectiveness of sibutramine therapy compared to placebo over 12 weeks. All participants also received behavioral therapy.
<h6>Study Results</h6>
The researchers found that weight and body mass index were significantly reduced in patients taking sibutramine compared to placebo, as was expected from previous research. But upon further inspection of the data, the researchers found that only people with certain versions of three different genes experienced significant weight loss.
People with a variant in the GNÎ²3 gene, had success with sibutramine, losing about 13 pounds. People with another variant in the Î±2A gene, lost even more weight — more than 17 pounds on average.
The third genetic marker scientists investigated, known in the scientific literature as 5-HTTLPR, is a stretch of DNA that comes in a long and short form. Only people with one or two copies of the short version of this marker had significant weight loss with sibutramine.
“Genetic variations may help select obese patients who are more likely to experience improved outcome with this treatment. Since the different markers were present in almost 50 percent of patients, the inclusion of screening for the genetic markers before prescribing the medication may even be cost-effective from a public health perspective,” Camilleri said.
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Genetic Variants Affect Weight Loss Drug Effectiveness

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“I feel like a fish with no water.”
That’s how the child in the public service announcement featuring flopping, gasping goldfish describes what it feels like to have an asthma attack. The spot encourages parents of the close to nine million kids who suffer from asthma to take steps to decrease the number of attacks their kids have because, as the announcer says, “even one attack is one too many.”
Both environmental factors — things like mold, pollen, cold air and cigarette smoke &#8212; and genetic factors are thought to contribute to childhood asthma, a disease that causes more than 10 million missed days of school and leads to about two million trips to the emergency room each year.
Researchers are beginning to realize that asthma that strikes early in life may be a distinct disease from cases that set in later. In 2007, <a href="https://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Search&amp;db=pubmed&amp;term=17611496" target="_blank" rel="noopener noreferrer">a genomewide association study</a> linked several related SNPs in a region of chromosome 17 specifically to childhood asthma. 
<h6>Childhood Asthma and Secondhand Smoke</h6>
New research published online today in the <a href="http://content.nejm.org/cgi/content/full/NEJMoa0806604" target="_blank" rel="noopener noreferrer">New England Journal of Medicine</a> confirms these genetic findings and adds a new twist: the SNPs have an effect only in kids exposed to tobacco smoke.
Bouzigon and colleagues studied several hundred French families and found a number of SNPs linked with asthma on chromosome 17, just as in earlier studies. The SNPs were associated only with asthma that began at age four or younger.
Like previous researchers, Bouzigon et al could not determine exactly how the SNPs are related to childhood asthma risk; but they could clearly show that the variants’ effects are triggered by exposure to tobacco smoke.
<h6>Variants Associated with Risk</h6>
The researchers found that the overall risk of early-onset asthma was increased at least 1.7-fold for people with two risky copies of any of the SNPs compared to those with none or only one. But when they took smoking into account, they saw that children with two risky copies of any of the SNPs who were also exposed to tobacco in utero, during infancy or both actually had risk at least 2.3-fold higher than those with the more favorable genotypes. The SNPs had no statistically significant effect among children who were not exposed to tobacco smoke early in life.
In an accompanying <a href="http://content.nejm.org/cgi/content/short/NEJMe0807576v1" target="_blank" rel="noopener noreferrer">editorial</a> in NEJM, two researchers not involved in the study &#8212; John Holloway and Gerard Koppelman &#8212; say that the influence of early life events in the development of asthma is well supported and that the interaction of genes and tobacco smoke seen by Bouzigon and colleagues “further highlights the detrimental effect of such early life exposure on respiratory health.”
But, say Holloway and Koppelman, the importance of the exact timing of exposure to tobacco smoke is not clear, as Bouzigon et al could not differentiate between prenatal and postnatal exposure.
Although more research will be needed to confirm the results in this new report, Holloway and Koppelman think that as more is learned about how chromosome 17 variants affect asthma risk, this knowledge may help physicians better treat the disease.

Genes and Environment Work Together to Increase Risk of Childhood Asthma

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People naturally yearn to know where they came from. Genealogists scratch that itch by poring over historical documents such as vital records, tax rolls, census lists and diaries to reconstruct their family history.
In recent years, genealogists have also begun using genetic information as another way of understanding their identity and establishing kinship. With the growth of several genetics companies specializing in genetic ancestry — including 23andMe’s <a href="https://23andme.com" target="_blank" rel="noopener noreferrer">Personal Genome Service</a>â„¢ — genealogists now have an entirely new approach to use in tracing their roots. DNA is especially useful for recent immigrants, Native Americans or African-Americans whose ancestors left few historical records, but passed down a trail of genetic breadcrumbs that can lead back to a specific geographic region — and in some cases even a particular tribe.

The growth of genetic ancestry services, combined with the availability of resources on the internet, has also led many genealogists to share their stories and connect with others. Now Roots Television is adding viral video to the modern genealogist&#8217;s tool box. Roots Television markets itself as a video-based genealogy website, created for and by avid genealogists and family history lovers. They create online web shows on a variety of topics, while also licensing other programs. A recent glance at their programming line-up revealed a brief video on the art of document restoration, interviews with well-known genealogists, and reviews of new genealogy computer software. There is even an area of the site dedicated to user-submitted video, called RootsTube. Here, anyone can tell their story &#8211; whether it is an interesting discovery about their family history, a family reunion video, or even a tip on how to best utilize a particular genealogy resource.
So far there isn&#8217;t much content related to genetic genealogy, but the website is still in its infancy; we hope to see more genetics-related content over time.

Roots Television: The Internet TV Channel for Genealogists

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As talks began Saturday at Cold Spring Harbor&#8217;s first &#8220;Personal Genomes&#8221; conference, the first half of which I blogged on <a href="https://blog.23andme.com/2008/10/11/fuhgetabouddit-notes-from-long-island-the-frontier-of-personal-genomics-this-weekend/">here</a>, several leading explorers of the strange new world of &#8220;structural variation&#8221; in the human genome, such as Evan Eichler and Mike Snyder, shared some of their latest findings.
You can observe the most common kind of structural variation by lining up two corresponding chromosomes; if you notice that one of them is missing a stretch of DNA letters that is present in the other, that&#8217;s a deletion (or an insertion from the other chromosome&#8217;s viewpoint). Geneticists call these types of variations insertion/deletions, or indels for short.
The main way these variations seem to happen is during the production of sperm and eggs, when an individual&#8217;s homologous chromosomes recombine with one another. Usually, chromosome pairs line up perfectly for recombination, but when they don&#8217;t, you end up with chromosomes that have a little more or a little less DNA than the originals.

Problems can arise when the stretch of DNA lost in the shuffle was part of an essential gene. Recent work has shown that one form of autism is caused by a deletion, and the same is true for forms of schizophrenia and cystic fibrosis.
Both basic research and clinically-motivated research were presented Saturday. Eichler, of the University of Washington, and Snyder, of Yale, are among those making detailed maps of structural variation in the human genome. The consensus is emerging that there is a *lot* of it. Snyder showed that, at least in the handful of individual genomes he&#8217;s looked at so far, any two individuals differ by more than one thousand indels of at least 3,000 DNA letters. Eichler made a similar observation with respect to his comparison between a sample individual&#8217;s sequence and the reference human genome and commented that this means there are at least 3 million DNA letters (3,000 times 1,000) in the sample individual&#8217;s sequence not present in the reference genome. That&#8217;s on top of the 3 million one-letter SNP variants between any two humans. So it looks like genetic variation is the rule and not the exception, and the very notion of a &#8220;reference&#8221; sequence may need to stretch a bit in order to stay consistent with the data.
Derek Chiang of the Broad gave a fascinating talk about progress in trying to understand how structural variation can cause medical problems. Chiang, of the Broad Institute of MIT/Harvard, has developed sophisticated software to find structural variants associated with cancerous tissue based on microarray data. His efforts have already yielded a new oncogene for lung cancer. Chiang also described a clever algorithm for finding structural variants from next-generation sequence data that appears to work quite well by comparison to methods based on microarray data. Like the work Elaine Mardis presented Friday, Chiang&#8217;s talk suggests a future in which cancerous tumors could easily be distinguished from normal tissue using genetic scans.
The task of understanding what these differences *do* is another, very difficult, question entirely. And being able in turn to develop a therapy tailored to that specific change is yet another challenge.
Sunday&#8217;s talks took us into the world of *next next* generation sequencing, as though the prospect of plain old next-generation sequencing weren&#8217;t already shaking up the field enough. Steve Turner gave a talk on <a href="http://www.pacificbiosciences.com">Pacific Biosciences</a>&#8216; sequencing technology that kept the audience rapt. The technology is ingenious and solves a number of problems that have bedeviled sequencing since its inception. I will punt on explaining the basics of the technology since it&#8217;s so well-explained on their <a href="http://www.pacificbiosciences.com/index.php?q=technology-introduction">website</a>.
Turner offered an update that doesn&#8217;t appear on the website yet; the technology depends critically on the use of an enzyme, called DNA polymerase, which is responsible for copying DNA. Their team has modified the DNA polymerase used in the machine from the version that exists naturally in humans using a technique called experimental evolution. They generated a collection of mutant polymerases that each differ from the original at random. Then they tried each variant in their machine, retained the ones that do best, and repeated the process. It&#8217;s fair to say that horticulture and animal husbandry are slower, less direct forms of experimental evolution. After several generations, they ended up with a polymerase that was better suited to the environment of their machine than natural human polymerase is.
The meeting ended Sunday as Maynard Olson of the University of Washington, an eminent geneticist and one of the architects of the Human Genome Project, closed the conference with a witty and thoughtful summary of the proceedings. Olson suggested that true personalized medicine could be a long time coming, and expressed skepticism that it would arrive at all. One generalization from the talks, he said, was that it appears increasingly that the genetic mutations that impact health are rare, and it may be the case that many diseases can be caused in a large number of ways. The difficulty of working out what each version means could make it hard to work out therapies for so many different possibilities. He predicted a near-term future of unpredictability, especially in guessing which sequencing technologies will come to be adopted the genetics community. He closed by reciting the lyrics to Bob Dylan&#8217;s &#8220;<a href="http://www.bobdylan.com/#/songs/times-they-are-changin">The Times They Are A-Changin&#8217;</a>,&#8221; which seemed fitting to me.
&lt;span=&#8221;caption&#8221;&gt;Photo: Henryk Kotowski

Science in the Suburbs, Part II: More from the Personal Genomes Meeting at Cold Spring Harbor

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1651" title="skincancer" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/skincancer.jpg" alt="" width="320" height="211" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/10/skincancer.jpg 320w, https://blogcms.23andme.com/wp-content/uploads/2008/10/skincancer-300x198.jpg 300w" sizes="auto, (max-width: 320px) 100vw, 320px" />
Basal cell carcinoma is not only the most common form of skin cancer in the United States — it’s the most <a href="http://www.nlm.nih.gov/medlineplus/ency/article/000824.htm" target="_blank" rel="noopener noreferrer">common cancer overall</a>. Close to a million new cases are diagnosed each year. Luckily, this type of cancer is easily treated and unlikely to spread. It can, however, cause extensive damage to surrounding tissue and bone if it’s not removed.
The biggest risk factor for basal cell carcinoma (BCC), as well as several other types of skin cancer, is sun exposure. People with light skin, hair, and eyes — who have low levels of the protective skin pigment melanin — are at especially increased risk. It’s therefore not surprising that many of the genetic variants associated with skin cancer are also linked to fair pigmentation.
A new study, published online Sunday in <a href="https://dx.doi.org/10.1038/ng.234" target="_blank" rel="noopener noreferrer">Nature Genetics</a>, has identified two SNPs on chromosome 1 that increase the risk of BCC, but are not linked to a person’s coloring.

After studying more than 2,000 people with BCC and close to 36,000 controls from Iceland and Eastern Europe, Stacey et al found that each A at rs7538876 and each G at rs801114 increased the odds of developing BCC 1.28 times over those with two Gs or two Ts, respectively. 
 (23andMe customers can check their data by clicking on the links above that lead to our Browse Raw Data feature)
The authors of the study estimate that about 1.6% of people with European ancestry have two copies of the riskier versions at both of these SNPs, and that these people have 2.98 times the odds of BCC compared to people who have no risky copies.
The researchers then looked at the DNA of people with two other types of skin cancer that, like BCC, are related to sun. But in about 400 people with squamous cell carcinoma and about 2,000 with cutaneous melanoma, they saw no association with the SNPs.
“One unifying theme may be that genes associated with fair pigmentation confer cross-risk of all three skin cancer types because of their roles in protection from the shared risk factor of UV light, whereas the more specifically associated variants may act through different pathways,” the authors write in their report.
To investigate this idea further, the researchers looked to see if the two new BCC-associated SNPs were related to pigmentation at all. In a sample of about 5,000 Icelandic people they found that neither SNP was linked to eye or hair color, nor were either of them linked to a propensity to freckle or sun sensitivity.
“Taken together, these data suggest that the [SNPs] act through pathways other than those related to UV-susceptible pigmentation traits,” the authors write.

Two DNA Variants Linked to Basal Cell Carcinoma, the Most Common Form of Skin Cancer

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Almost half of all men will eventually be affected by male pattern baldness. This form of hair loss, which begins above the temples, continues to form a characteristic “M” shape and sometimes progresses to complete baldness, has been shown to be related to certain hormones, such as testosterone, called androgens.
Genetics has long been known to play the dominant role in determining whether a man would go bald, but it wasn’t until <a href="https://www.ncbi.nlm.nih.gov/pubmed/15902657?ordinalpos=2&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">2005</a> that a specific gene was connected to male pattern baldness.
The gene, which encodes an androgen receptor (AR), is on the X chromosome. This means that men inherit only one copy of the gene, and that this copy always comes from their mothers. It’s possible that this is part of the reason behind the adage that male pattern baldness skips a generation.
But the AR gene doesn’t completely explain the inheritance of male pattern baldness, suggesting that there are still genes to be found. New research, published online Sunday in Nature Genetics, provides evidence that one of these genes might be on chromosome 20.

<a href="https://dx.doi.org/10.1038/ng.228" target="_blank" rel="noopener noreferrer">Axel Hillmer</a> and colleagues at the University of Bonn in Germany, who were involved in the research that first connected the AR gene and baldness, have now shown that the approximately 80% of Europeans with one or two Ts at rs2180439 have increased odds of male pattern baldness compared to the men with two Cs.
Just how much these odds are increased depended on how the researchers conducted their experiments. In one sample, 296 Germans who went bald before age 40 were compared to 347 male and female German controls, some of whom may have had some degree of balding. The researchers found that each T at rs2180439 increased the odds of male pattern baldness 1.82 times. But in another sample, 319 bald German men were compared with 234 German men who had made it past age 60 without going bald, and the authors found a 2.17 times increase in odds for each T.
<a href="https://dx.doi.org/10.1038/ng.255" target="_blank" rel="noopener noreferrer">Richards et al</a> conducted an independent study of baldness in more than 2,700 men from Switzerland, England, Iceland and The Netherlands. They found a different SNP on chromosome 20 linked to male pattern baldness. Each A at rs1160312 increased the odds of baldness by 1.6 times over men with two Gs. 23andMe does not currently provide data for this SNP.
There is no obvious direct connection between the SNPs the two research groups found, but the fact that they independently linked chromosome 20 to male pattern baldness suggests that scientists may be zeroing in on another “baldness gene.” Finding this gene and the causative variation for baldness could have implications for research on several other common medical disorders which tend to be associated with baldness: coronary heart disease, hypertension and insulin resistance.
Discoveries about the genetics of male pattern baldness could also lead to new treatments, which according Richards et al is really big business. They cite financial disclosures from Merck that said global annual sales of an exisiting medical therapy for male-pattern baldness at upwards of $405 million.
“Clearly most men know if they are bald or not — but early prediction before hair loss starts may lead to some interesting therapies that are more effective than treating late stage hair loss,” said study author Tim Spector, of King’s College London, in a statement.

Two Groups Discover DNA Variations Linked to Male Pattern Baldness

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The structure of DNA was first publicly described 55 years ago by James Watson at Cold Spring Harbor Laboratory (CSHL) on Long Island in New York.
<h2>Personal Genomes Meeting</h2>
Thursday night, the now 80-year-old Watson opened up the <a href="http://meetings.cshl.edu/meetings/person08.shtml">2008 Personal Genomes meeting</a> at <a href="http://www.cshl.edu">CSHL</a> by telling the story of the origins of the Human Genome Project, which he headed from 1990 to 1992. In 2003, the Human Genome Project produced a (nearly) complete reference DNA sequence of a human genome that is now essential to basic and applied human genetic research.
These days, Watson pointed out, scientists can read the DNA letters of the double helix so quickly and inexpensively that it is becoming practical to sequence the genomes of large numbers of people. With this progress comes a flood of research questions and technological challenges, and I hope these insights from the lab will translate into advances in personalized medicine.

<h2>Bending the Curve in Healthcare Costs</h2>
Watson was followed on Thursday night by Francis Collins, who also followed him as director of the Human Genome Project, and later by Mary-Claire King, the renowned breast cancer geneticist from the University of Washington. Collins pointed out that healthcare costs have risen steadily to roughly 20 percent of the US GDP.
How much of this is spent on treatments that might have been identified as unnecessary with the availability of genetic information?
He suggested that widespread genomic sequencing and analysis could lead to the discovery of the genetic causes of common diseases, such as lung cancer and Type II diabetes, for which some genetic links are now known, but much more remains to be learned.
<h2>Personalized Medicine</h2>
Mary-Claire King considered breast cancer as a case study for personalized medicine. In the case of breast cancer, she noted, there are more than a thousand known mutations in each of the genes BRCA1 and BRCA2 that can predispose a woman to the disease. Many of these are unique to specific families or specific localities &#8212; she gave the example of one BRCA mutation endemic to a Norwegian valley.
King illustrated through recent breast cancer studies that linking newly-discovered mutations to disease is a formidable technical challenge, but emphasized that the rewards for succeeding in doing so would be immense.
Roughly 5 percent of new breast cancer cases in the US each year – around 10,000 – are linked to known BRCA1/2 mutations and thus might have been prevented through such measures as prophylactic mastectomy.
<h2>Next Gene Sequencing</h2>
Friday moved into reports from the trenches. The morning session consisted of talks by researchers from major genome sequencing centers and from the companies behind the so-called &#8220;next generation&#8221; sequencing methods that underlie this conference.
The new technologies, namely <a href="http://www.illumina.com">Illumina&#8217;s</a> Solexa, 454&#8217;s FLX, and <a href="http://www.appliedbiosystems.com">ABI&#8217;s</a> SOLiD, follow the same general plan as the venerable Sanger sequencing method: scan short fragments, or &#8216;reads&#8217;, of DNA letters, and then reconstruct the original sequence from the reads. They just do it much faster than before, mainly by scanning many reads in parallel.
Much of the concern these days is on the reliability of these new techniques – considering that a single changed DNA letter can mean the difference, for example, between getting Alzheimer&#8217;s or not – and so the presentations focused on technical topics like error rates and comparisons across platforms.
<h2>New Findings</h2>
Even so, there were suggestions that some exciting new scientific findings might be around the corner; Richard Gibbs of Baylor showed early data from their sequencing of a HapMap trio (a father, mother, and child) suggesting that the human mutation rate might be much higher than previously thought. Elaine Mardis from Washington University showed that her lab had found mutations unique to tumor tissue in a lung cancer patient. Known as somatic mutations, they had arisen in the patient during their lifetime and were not found in non-tumorous skin tissue from the same patient. Her study did not show that one of these mutations had actually caused the cancer, but demonstrating that such changes may even be found is intriguing.
The afternoon session moved into the imposing task of storing, processing, and interpreting the flood of data these new technologies generate.
<h2>Storing All that Data</h2>
Paul Flicek from the European Bioinformatics Institute produced that rarest of things, the funny bioinformatics talk, in describing the travails of dealing with the 100 terabytes (that&#8217;s 100,000 gigabytes or 100 million megabytes) generated so far by the pilot phase of the <a href="http://www.1000genomes.org">1000 Genomes Project</a>, and the specter of dealing with a petabyte (1,000 terabytes) of sequence data.
Carlos Bustamante of Cornell described some of the insights into human evolutionary history that have made possible by the DNA deluge, including using sequence data to infer possibly the most detailed models yet of historical human population size and migrations. He also described his lab&#8217;s and John Novembre&#8217;s recent findings on the relationships between geography and human genetics, a topic we&#8217;ve blogged on recently at the Blog <a href="https://blog.23andme.com/2008/09/03/a-different-kind-of-gene-mapping-comparing-genetic-and-geographic-structure-in-europe-the-return/">here</a> and <a href="https://blog.23andme.com/2008/08/13/a-different-kind-of-gene-mapping-comparing-genetic-and-geographic-structure-in-europe/">here</a>.
There&#8217;s another big day of talks to come here at CSHL. I&#8217;m glad to be here keeping up to date on the latest research so we can incorporate it into 23andMe and show off the site to many people on the cutting edge of genetics.

Notes from Long Island, the Frontier of Personal Genomics

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!

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