<img loading="lazy" decoding="async" class="aligncenter wp-image-10750 size-full" title="top10ten" src="http://35.88.189.111/wp-content/uploads/2011/12/top10ten.jpg" alt="" width="306" height="345" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/12/top10ten.jpg 306w, https://blogcms.23andme.com/wp-content/uploads/2011/12/top10ten-266x300.jpg 266w" sizes="auto, (max-width: 306px) 100vw, 306px" />
Take a moment to look back at the ten most interesting and significant genetic findings of 2012 or at least the ones that drew our attention.
In the last 12 months we’ve seen huge strides in genetic research giving us new insight into serious conditions such as Alzheimer’s as well as new treatments for cystic fibrosis. And in the last year scientists have made huge leaps in our understanding of the human genome itself with the culmination of a massive study of the so-called uncharted non-coding portions of our DNA – the ENCODE project.
Researchers at 23andMe continue to contribute to some of these important findings with groundbreaking work on the relative importance of family health history versus genetics when determining disease risk and a new method to screen for the genetic risk for certain types of blood disorders.
It’s been another great year of discovery and here’s our top ten.
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1) &nbsp;A Genetic Variant Protective Against Alzheimer’s Disease – The T version of rs63750847 &nbsp;– also known as the A673T variant in the APP gene – was associated with about five times lower odds of <a href="https://www.ncbi.nlm.nih.gov/pubmed?cmd=Search&amp;db=pubmed&amp;term=22801501">Alzheimer&#8217;s</a>. While this is a very rare variant – only about one in 10,000 people of European descent have it – the research, done by the Icelandic company deCODE Genetics in association with Genentech, adds more insight into the development of the disease. Many mutations in the APP gene actually cause Alzheimer’s through an overproduction of beta amyloid protein in the brain (a hallmark of Alzheimer’s), but the protective variant appears to do the opposite, according to the study. New drugs built on this finding could help protect against Alzheimer’s, or even the mental ravages of normal aging. 23andMe does offer customers reports on their own Alzheimer’s risk based on the more common APOE variant, as well as a report on this protective APP variant.
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2) &nbsp;ENCODE Project Creates a Map of the Uncharted Areas of the Genome – Much of the work in genetics has been focused on the areas in our DNA that code for proteins, but this is a very small part – just 1 percent – of our genome. The<a href="https://www.wired.com/wiredscience/2012/09/encode-human-genome/"> ENCODE project</a>, which has enlisted more than 400 scientists over several years, is attempting to map the rest of it, the so called<a href="https://blog.23andme.com/news/a-map-of-the-uncharted-genome/"> “dark matter” of the genome</a>. What they’ve created is the foundation of a sort of encyclopedia of the functions of many of these uncharted areas of the genome. It’s a resource that will be used by many scientists in the years to come.
3) &nbsp;Noninvasive Prenatal Sequencing – Two separate research groups reported within weeks of each other that they had<a href="https://blog.23andme.com/health-traits/noninvasive-sequencing-of-a-human-fetus/"> successfully sequenced a human fetus</a> and done so noninvasively. The breakthrough offers an opportunity for earlier prenatal screening than currently offered with amniocentesis or chorionic villous sampling (CVS) without the same risks for a developing fetus.
4) &nbsp;New insights into a group of rare blood disorders known as MPNs – In less than a year, 23andMe recruited a 1,000-person cohort with a group of rare blood disorders known as myeloproliferative neoplasms, or MPNs. Within months of reaching that goal we began reporting our<a href="https://blog.23andme.com/23andme-research/novel-genetic-findings-for-myeloproliferative-neoplasms/"> new findings</a>. Among them were replications of known genetic associations with the disease as well as new ones including an association between these conditions and variants in the TERT and ATM genes.
<img loading="lazy" decoding="async" class="aligncenter wp-image-6487 size-full" title="neanderthal_bones" src="http://35.88.189.111/wp-content/uploads/2010/05/neanderthal_bones.jpg" alt="" width="350" height="421" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/05/neanderthal_bones.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2010/05/neanderthal_bones-249x300.jpg 249w" sizes="auto, (max-width: 350px) 100vw, 350px" />
5) &nbsp;New Insights into Human Origins and Evolution – Several different studies highlight ongoing research on our early ancestors and the evolution of modern humans. Beyond the compelling tale of our early ancestors, the journey out of African and the intermixing with Neanderthals and Denisovans, the new research also gives us insight into the<a href="https://www.wired.com/wiredscience/2012/11/recent-human-evolution-2/"> significance of rare genetic variants</a>.
6) &nbsp;Family Medical and Genetics Used Together to Predict Disease – 23andMe <a href="https://blog.23andme.com/23andme-research/using-genetics-and-family-history-for-health/">developed a model</a> to show that both family history and genetic tests have strengths in predicting disease risks, but when used together they provide the best predictor for disease.
&nbsp;7) &nbsp;Older Dads’ Biological Clocks – For a long time prospective fathers could wile away the years without much worry about when to have kids, while prospective moms were constantly checking their ticking biological clocks.<a href="https://www.nature.com/nature/journal/v488/n7412/full/nature11396.html"> A study</a> may turn the tables a bit, pushing men to think a little more about how long they wait to start a family. The study says that as men grow older the number of de novo mutations they<a href="https://blog.23andme.com/health-traits/for-older-dads/"> pass onto their children increases</a>, and preliminary studies suggest that the more de novo mutations passed onto a child the higher the risk that child could develop certain types of conditions, such as autism and schizophrenia. That said becoming a dad can actually be good for you. There’s evidence linking <a href="https://blog.23andme.com/health-traits/ah-fatherhood-dirty-diapers-skinned-knees-and-healthier-hearts/">fatherhood to healthier hearts.</a>
8) &nbsp;Breast Size Matters, But Not How You Think – Researchers at 23andMe found that genetic factors influence breast size and that in turn these factors are connected to the genetics of breast cancer.
&nbsp;9) &nbsp;New Treatment for Cystic Fibrosis – &nbsp;Early in 2012 the FDA approved ivacaftor (Kalydeco ®) as a new treatment for cystic fibrosis, one of the most common recessively inherited diseases. The drug<a href="https://online.wsj.com/article/SB10000872396390444024204578046911440223842.html?mod=WSJ_TechInnovationAwards1012_MiddleSecondSummaries%20."> developed by Vertex Pharmaceuticals Inc</a>. is the first treatment that targets one of the underlying causes of cystic fibrosis – a specific genetic mutation – rather than its symptoms.
10) &nbsp;Autism Study Reveals No Genetic Associations – It may be strange to <a href="https://blog.23andme.com/health-traits/autism-study-reveals-no-genetic-associations/" target="_blank" rel="noopener noreferrer">point to a study that finds no genetic associations</a>, but sometimes an absence of evidence can hint toward new routes of study. Cases of Autism spectrum disorders – which run the gamut from mild to severe impairment and include autism, Asperger syndrome and other disorders – have become increasingly common in the U.S. Why that is, is not so easy to discern. The lack of an association doesn’t mean that genetics isn’t important. In fact twin studies suggest that autism is at least moderately heritable, but it may be that genetic variations play a smaller role than rare mutations or copy number variation in the risk of a person developing autism.

23andMe Blog

23andMe Blog Team

Top Genetic Findings of 2012

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For decades, a patient’s family health history has been a keystone to any wellness plan.
A simple record of medical conditions your siblings, your parents, aunts, uncles and grandparents struggled with can help you and your doctor know what to watch for to keep you healthy. Like family health histories, genetic testing also offers people insights they otherwise might not have about their own health.
Unfortunately there has often been a false division between family health histories and genetic testing where the approaches are portrayed as opposing alternatives. It’s an odd argument. No one would juxtapose the utility of a stethoscope against a thermometer. They are both useful in their own way.
A <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002973?__utma=261502610.914248644.1349999882.1349999882.1349999882.1&amp;__utmb=261502610.12.10.1349999882&amp;__utmc=261502610&amp;__utmx=-&amp;__utmz=261502610.1349999882.1.1.utmcsr=google|utmccn=%28organic%29|utmcmd=organic|utmctr=%28not%20provided%29&amp;__utmv=-&amp;__utmk=28925503" target="_blank" rel="noopener noreferrer">new paper in</a> PLoS Genetics by 23andMe shows that neither family health histories nor genetic testing is perfect in predicting health risks, but they each have their strengths.
More importantly using them together improves upon the risk prediction by capitalizing on the situations where each method is at its strongest. Along with making comparisons between family health history and genetic testing to make risk prediction, the paper describes a model to combine the two methods together to assess risk.
Lead author and 23andMe scientist Chuong “Tom” Do, Ph.D, worked with our senior medical director Uta Francke, MD, and scientists David Hinds, Ph.D., and Nicholas Eriksson Ph.D. to make a comprehensive comparison of family health histories and genetic testing to assess risk for 23 different conditions.
“We show that family history is most useful for highly common, heritable conditions,” Tom said.
So for relatively common diseases that may have many genetic and environmental factors – coronary artery disease, for instance – knowing that your father had the disease is helpful at predicting whether or not you might be at risk for the same condition.
But for less common diseases with many genetic factors influencing them, knowing your family history seldom helps in making a risk prediction, said Tom.
In part, that’s because these diseases are uncommon enough that they would rarely show up in the health history of your immediate family. When family histories are uninformative, genetic testing may still reveal the genetic variants that would put you at a higher or lower risk for the condition. So for example Crohn’s disease might not show up in a family history, but the risk prediction from a genetic test is relatively strong. As an aside there is also the issue of people who simply don’t know their family health history. And we’ve written about how genetic testing <a href="../news/inside-23andme/tales-of-23andme/my-heart-my-family-and-mybpc3/">can alert them to risks they wouldn’t have otherwise suspected.</a>
To be fair, even though new genetic discoveries are being made every day, only a fraction of the genetic contributions to whether or not a person develops a disease is currently known in many cases. But even after accounting for this, existing genetic testing – that use single nucleotide polymorphism (SNP)-based methods to determine risk for some rare complex diseases – are already as good at predicting risk as family histories for common heritable conditions.
“These results indicate that for a broad range of diseases, already identified SNP associations may be better predictors of risk than their family history-based counterparts, despite the large fraction of missing heritability that remains to be explained,” Tom writes in the paper.
Finally, it’s important to remember that having a family history for a disease is generally not the same as a diagnosis. Just because your mom had diabetes doesn’t mean that you will get it too.  But knowing that you’re at increased risk based on family history can be a motivating factor in helping you to make appropriate lifestyle changes.  In much the same way, knowing your genetic risks can also be useful in helping you live healthier.

Using Genetics and Family History for Health

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A study published yesterday in <a href="http://stm.sciencemag.org/content/early/2012/04/02/scitranslmed.3003380">Science Translational Medicine</a> from a group at Johns Hopkins University set out to determine the best-case power of genetics to provide clinically meaningful information about risk of common diseases. The authors did this using data from identical twin pairs: by seeing how often twins with identical genomes develop the same diseases, we can judge the extent to which those diseases are determined by genetics, and the extent to which they might be predictable if we completely understood their genetics.
The study&#8217;s key findings were that most people could obtain a result that they are at significantly elevated risk of at least one disease. But for most diseases, they would learn that their genetic risk places them not far from the average risk across the population. In a few cases, the authors found that a genetic test could potentially identify most individuals who eventually will develop a disease: this was true for thyroid autoimmune disease, type 1 diabetes, Alzheimer&#8217;s disease, and coronary heart disease in men. The authors conclude that genetic testing will not replace conventional preventive medicine.
We agree with the authors that it is important to set reasonable expectations for what genetic testing can and cannot do. We think the positive finding that genetic testing can have some clinical utility for risk assessment for common disease is encouraging. We also think it is very encouraging that there are a few diseases where genetic testing could be particularly powerful &#8212; Alzheimer&#8217;s disease and coronary heart disease are not small potatoes and early alerts of increased risk of these conditions could have substantial public health benefits.
Many of our more than 125,000 23andMe customers receive a risk report for a common disease that indicates that they are at substantially increased or decreased risk, using criteria similar to the ones used in this study. In addition to disease risks, 23andMe customers also receive information about their carrier status for inherited diseases and possible drug responses based on genetics, both of which already make an impact in personalized medicine today.
On a more technical note, the study&#8217;s finding that negative genetic test results are mostly uninformative is largely an artifact of the authors&#8217; mathematical modeling procedure and the fact that risk predictions for each disease were binned into just two buckets for &#8220;negative&#8221; and &#8220;positive&#8221; results. The authors pre-specify a baseline risk that for most diseases is not much smaller than the population average risk, and disease risk associated with different genotype classes is constrained to fall between the baseline value and 100%. Thus, it is impossible for anyone to have disease risk much less than the population average, and most individuals with &#8220;negative&#8221; results are pegged at the baseline risk level. Models that place some individuals at substantially lower risk would also be consistent with the observed twin data, but this study is not effectively exploring the potential utility of these negative findings.
Do we believe that genetic testing could ever substitute for conventional preventive medicine? No, and we don&#8217;t think it should. Instead, it is more useful to think about genetic testing as one of many sources of information &#8212; along with family history, lifestyle, and conventional clinical testing &#8212; that can inform disease risk assessment and preventive medicine. Genetics will not be equally informative for everyone, and will not replace these other approaches, but this is actually quite compatible with personalized medicine &#8212; that we should find and leverage the information that has the biggest impact on care at an individual level.

Great Expectations for Personal Genomes

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by David Hinds
A small study conducted by researchers at the Cleveland Clinic and reported at last week&#8217;s American Society of Human Genetics annual meeting found that family health history (FH) often gave different assessments of cancer risk than SNP-based personal genomic (PG) risk assessments obtained from <a href="http://www.navigenics.com/" target="_blank" rel="noopener noreferrer">Navigenics</a>. The results have been characterized in the popular press as demonstrating that FH is superior to PG in predicting who is at increased risk of disease. We believe that research in this area is important, but felt that the conclusions of the study were not necessarily supported by the study&#8217;s design. 
What is family history risk assessment?
An identifying feature of many genetic diseases is that they tend to &#8220;run in families&#8221;.  Families also tend to share similar environmental risk factors. Collecting health information about family members can thus provide important clues about an individual&#8217;s risk of disease. Family history risk assessment is typically performed by genetic counselors using structured methods so that the results can be easily compared with guidelines for relating history to disease risk. There are also <a href="http://www.hhs.gov/familyhistory/portrait/index.html" target="_blank" rel="noopener noreferrer">online tools</a> for recording family histories, and <a href="https://familyhealthlink.osumc.edu/Notice.aspx" target="_blank" rel="noopener noreferrer">some disease risk calculators</a> can take advantage of this information.
Family history is known to be especially helpful for identifying individuals at substantially elevated risk of disease because their families carry rare, high-risk variants (such as mutations in BRCA1 and BRCA2, for breast and ovarian cancer).
<h6>What is SNP-based risk assessment?</h6>
SNP-based personal genomic risk assessment is currently based on results of studies demonstrating that specific common genetic variants are correlated with disease risk. These common variants generally have small effects, but in aggregate, may contribute to more cases of disease in the population than rare variants like BRCA1/2.  Navigenics and 23andMe use similar methods for combining information from multiple markers to arrive at an estimate of an individual&#8217;s risk.  As with family history, SNP-based tests only account for a subset of risk factors, and are most informative for the subset of individuals whose estimated risk is substantially different from the population average.
Some personal genomics services, such as 23andMe, include variants other than common SNPs in their risk assessments. In the future, personal genomic risk assessments may routinely apply technologies beyond SNP-based genotyping to form a more comprehensive picture of an individual&#8217;s genetic landscape.
<h5>What did the study show?</h5>
The researchers identified 22 patients in a genomic medicine clinic who either had cancer themselves or a family history of cancer, and their spouses. All 44 received FH assessments, as well as the Navigenics SNP-based PG risk assessment. There was generally poor agreement between the FH results and PG results. In addition, five of the 22 patients were later found to carry high risk mutations for an inherited form of colon cancer, but were not identified as high risk by the PG test.
<h6>What does this really mean?</h6>
The inconsistency between FH and PG observed in this study is largely due to a fundamental difference between the two types of tests. Family history is most effective at identifying individuals with familial cancer syndromes related to rare mutations with large effects, while SNP-based tests use common variations with smaller effects. The two types of tests are thus measuring very different things.
The two methods also may not be assessing the same underlying conditions. There is no doubt that individuals with <a href="https://en.wikipedia.org/wiki/Hereditary_nonpolyposis_colorectal_cancer" target="_blank" rel="noopener noreferrer">hereditary nonpolyposis colorectal cancer</a> or <a href="https://en.wikipedia.org/wiki/Familial_adenomatous_polyposis" target="_blank" rel="noopener noreferrer">familial adenomatous polyposis</a> have a different spectrum of disease than typical colon cancer patients. Familial syndromes also represent only a small proportion of all cancers (5% of all colon cancers).
Furthermore, the Cleveland Clinic study started from the presumption that FH was the &#8220;gold standard&#8221;, so any deviations in the PG results were considered errors. In our opinion, this is not an appropriate starting point for performing a head-to-head assessment of test performance. Such an assessment would, ideally, evaluate the accuracy of the two tests in a set of individuals not previously screened for a positive family history, as some of the participants in this study were.
Perhaps the most troubling suggestion from the study was that individuals at high risk based on family history might choose a PG  test, and be misled by a result indicating they were at low risk. 23andMe disease risk reports all discuss the limitations of the tests and the importance of family history as well as other environmental and undiscovered genetic risk factors.  The suggestion also neglects any benefits of PG testing for the large majority of individuals who do not have a positive family history of disease.
<h6>Where do we go from here?</h6>
At 23andMe, we are committed to increasing scientific knowledge of the genetic basis of human diseases and traits, and we are conducting research to evaluate and improve the predictive accuracy of our genetic risk models. As we learn more about the genetic factors underlying disease, genetic information should become increasingly valuable in developing risk assessments, and will be complementary to methods such as family history. Ultimately, we believe that the path forward will involve integrated, individualized risk assessment based on family history, personal genetics, and environmental risk factors.

Family History and Personal Genetic Risk Assessments: A Perspective on the Cleveland Clinic Study

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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. &nbsp; Not only can DVT be painful, but it can also lead to a potentially fatal condition called pulmonary embolism if the clot breaks free and travels through the circulatory system to the lungs.
In addition to environmental factors, there are genetic variations that can raise a person’s chances of having DVT. &nbsp; But providing genetic testing to everyone is not feasible, leading researchers from the Leiden University Medical Center in the Netherlands to question whether a family history of DVT could also be of value as a risk indicator.
The researchers looked at records and family histories of 3,764 people — 1,605 who had had DVT and 2,159 who had not. &nbsp; Their results, published online this week in the <a href="http://archinte.ama-assn.org/cgi/content/abstract/169/6/610" target="_blank" rel="noopener noreferrer">Archives of Internal Medicine</a>, show that in people with no environmental or genetic risk factors, having a first-degree relative (parentor sibling) with DVT increased the odds of having a first episode of DVT by 2.5 times. &nbsp; This was about the same as the increase in odds (2.3 times) caused by genetic risk factors in people with no family history or environmental risk factors.
Only 29.7% of people with family history of DVT carried a known genetic risk factor, but a family history was more common in DVT patients than controls with similar known genetic and environmental risk factors. &nbsp; This suggests that there are unknown, probably genetic, factors at work. &nbsp; The researchers say that unknown genetic factors probably have small effects that contribute to DVT only when other, larger risk factors are present, such as the factor V Leiden genetic variation or an environmental risk factor such as surgery, immobilization or oral contraceptive use.
Based on the fact that a positive family history increases the risk of DVT to about the same degree as known genetic risk factors, and the fact that most people with a family history of DVT don’t actually carry a known genetic risk factor, the researchers conclude that genetic testing for variations associated with DVT is of little additional value compared to collecting family history alone.
However, while a cost-effectiveness argument might be made, the authors’ own data shows that known genetic risk factors substantially increase the odds of DVT whether or not a person has a family history of the condition. &nbsp; A family history of DVT or a known genetic risk factor alone increases the odds of DVT by about two and a half times, but the presence of both increases the odds by 6.3 times. &nbsp; The presence of an environmental risk factor raises the odds of DVT about nine and half times. &nbsp; Add in a positive family history and the odds go up to more than 16 times those of someone who lacks known risk factors (both genetic and environmental) as well as a family history of DVT. &nbsp; But in those unlucky enough to have a family history of DVT, an environmental risk factor and a known genetic risk factor, the odds of DVT are increased a whopping 64 times.

Family Health History — Page 2

Top Genetic Findings of 2012

Using Genetics and Family History for Health

Great Expectations for Personal Genomes

Family History and Personal Genetic Risk Assessments: A Perspective on the Cleveland Clinic Study

Family History, In Addition To Genetic and Environmental Risk Factors, Predicts Risk of Deep Vein Thrombosis

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