June 19th is <a href="http://worldsicklecellday.webs.com/">World Sickle Cell Awareness Day</a> and commemorates the date in 2008 when the United Nations began recognizing this group of genetic blood disorders as a public health concern.
Sickle cell disease affects millions around the globe and nearly 100,000 people in the United States. It’s relatively common in Latin America, the Caribbean, Saudi Arabia, India, Mediterranean countries, and especially prevalent in those with ancestry tracing to sub-Saharan Africa. In the US roughly <a href="https://www.cdc.gov/ncbddd/sicklecell/data.html">one in 500</a> black or African-American babies is born with the disease. 

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<h6>Geno Atkins and Sickle Cell Trait</h6>
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In his two seasons in the NFL playing with the Cincinnati Bengals, defensive tackle Gene Renard “Geno” Atkins Jr. has shown few weaknesses, notching up 48 tackles and eight sacks.
But throughout his time on the field – not just professionally, but when he was a standout player in college and high school– Geno has played with what is called the “<a href="https://www.cdc.gov/ncbddd/sicklecell/traits.html">sickle cell trait</a>.”
While it isn’t full-blown <a href="https://www.23andme.com/topics/carrier/sickle-cell-anemia">sickle cell anemia</a>, the sickle cell trait can pose health risks for those who don&#8217;t know they have it. For instance, people with the trait may be more vulnerable to heatstroke and muscle breakdown as a result of strenuous exercise.  Geno hopes to bring attention to the issue and recently wrote about his own experience in a piece on the CDC website. Because testing isn&#8217;t currently in place for high school athletes, many play without knowing they are at risk.
“I was blessed to not suffer any side effects or have any health-related issues due to the <a href="https://www.cdc.gov/ncbddd/sicklecell/traits.html">sickle cell trait</a>,” Geno <a href="http://www.genostacks.blogspot.com/2010/09/sickle-cell-trait-and-athlete.html" target="_blank" rel="noopener noreferrer">wrote in his blog two years ago</a>. “I would urge parents, friends, and extended families of all Athletes participating in any sports or working out at a high level to have their Athlete tested.&#8221;
After he learned of his risk in college, both Geno and his coaches paid particular attention to whether he was healthy during practice and games.
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<h6>Sickle Cell Trait</h6>
Prevalence of sickle cell disease in African populations is high due to the fact that many people with African ancestry carry a genetic mutation in the HBB gene that causes the condition. You need two copies of this mutation (one from each parent) to have the disease, but if you have just one, you have what’s known as “<a href="https://blog.23andme.com/2012/02/14/did-you-know-one-in-twelve-african-americans-has-sickle-cell-trait/">sickle cell trait</a>”.
This trait protects you from malaria which is why the mutation has become relatively common in sub-Saharan Africa, where malaria is endemic. Unfortunately, it also increases the risk that your child may be born with sickle cell disease if your partner also has one copy of the mutation.
<h6>One in 13</h6>
Roughly one in 13 African Americans carries a copy of the HBB mutation and the World Health Organization estimates that sickle cell disease contributes to 5 percent of deaths in children under 5 years of age in some African countries. World Sickle Cell Awareness Day aims to highlight and combat this public health burden.
Although improved access to care is needed to counteract some of the public health burdens, appropriate genetic screening could lower the rates of disease and/or equip families with knowledge about their chances of passing the disease to future generations.
<h6>Raising Awareness</h6>
To raise awareness about sickle cell disease, the Centers for Disease Control (CDC) is piloting a data collection system called the <a href="https://www.cdc.gov/ncbddd/hemoglobinopathies/index.html">Registry and Surveillance System for Hemoglobinopathies</a> (or RuSH) to find out exactly how many US individuals suffer from sickle cell disease and related red blood cell disorders like <a href="https://www.23andme.com/topics/carrier/beta-thalassemia">beta-thalassemia</a>. They are also addressing unmet needs in research, surveillance, and education.
So we ask you today – do you suffer from sickle cell disease or know anyone living with it? What about sickle cell trait – have you been screened for a mutation that you could pass on to your child? We welcome your comments on this important health topic and encourage you to also raise awareness about this disease.
Find out more about 23andMe&#8217;s Sickle Cell report <a href="https://www.23andme.com/topics/carrier/sickle-cell-anemia">here</a>.

23andMe Blog

23andMe Blog Team

Raising Awareness For Sickle Cell Disease

A new paper in <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002746">PLoS Genetics</a> describes discoveries related to the genetics of male pattern baldness, with substantial contributions from the 23andMe community.
<h2>Early Onset Baldness</h2>
Led by Dr. Brent Richards of McGill University, the study combined genome-wide association data from seven cohorts, comparing men with &#8220;early onset&#8221; male pattern baldness with older men who had experienced little or no hair loss. The combined analysis allowed us to identify six new genetic factors associated with <a href="http://www.23andme.com/topics/traits/early-hair-loss/">early onset baldness</a>, in addition to replicating two previously known loci.
<img loading="lazy" decoding="async" class="alignright wp-image-7918 size-medium" title="baldness" src="http://35.88.189.111/wp-content/uploads/2010/11/baldness-300x214.jpg" alt="" width="300" height="214" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/11/baldness-300x214.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2010/11/baldness.jpg 435w" sizes="auto, (max-width: 300px) 100vw, 300px" />
23andMe participants represented more than half of all the cases in the study &#8212; not that we have an unusual number of bald customers, it&#8217;s just that we&#8217;ve got lots of data! We also used additional data provided by 23andMe participants to show that a risk score based on genotypes at the eight associated loci strongly predicted whether someone would report early-onset male pattern baldness.
<h2> New Genetic Associations</h2>
Two new loci are in or near histone deacetylase genes HDAC4 and HDAC9. Histone deacetylases regulate the expression of other genes by modifying histones, which are proteins responsible for packaging our long strands of DNA into the tiny spaces within the middle of cells.
One mechanism cells use to regulate gene expression is to tightly bundle up and pack away the DNA of genes that should not be active and to unpack and expose the DNA of genes that should be turned on. Both of these HDAC genes are thought to have roles in the regulation of androgen hormone pathways, which are thought to play an essential role in prostate cancer and male pattern baldness. Several previous studies have linked baldness and prostate cancer risk, and our new findings may help explain these observations.
<h2>Surprising Associations with Certain Diseases</h2>
Unexpectedly, we found that one of the newly associated loci is also associated with Parkinson&#8217;s disease. 23andMe was uniquely positioned to investigate this relationship further. This is in part because of our existing <a href="https://www.23andme.com/pd">Parkinson&#8217;s disease community. </a> Many of those in our Parkinson&#8217;s research community have also taken our hair loss survey. This particular genomic region is unique because it is spanned by a large, common inversion polymorphism. That is a long stretch of DNA flipped end-to-end in many people.
A consequence of this rearrangement is that genes in this region tend to be inherited together. It is difficult to say whether the shared association is due to variation in a single gene that affects both conditions or to variation in two unrelated genes inherited together due to the inversion. We found that even after accounting for this shared association, men were still more likely to report both male pattern baldness and Parkinson&#8217;s disease than would be expected by chance. This suggests that additional shared genetic or environmental risk factors may predispose towards both conditions.
This study gives an excellent example of a relatively easy question to ask using the 23andMe customer community. However, it would be complicated in a traditional genetic research setting. These are all complex conditions with many genetic and environmental factors at play. Just because you have one condition doesn&#8217;t necessarily mean you will develop the other conditions. However, shared genetic factors between Parkinson’s disease and male pattern baldness may offer exciting avenues for research. Similarly, the link between prostate cancer and male pattern baldness provide hints at possible mechanisms.

Male Pattern Baldness and Unexpected Associations with Disease

By Lauren Anderson
For many, the decision to participate in genetic research is not a trivial one. But for Gary Schmitz, he didn’t think twice. “For me,” he says, “the question was why wouldn’t you want to contribute?”
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Not long after The Michael J. Fox Foundation and 23andMe, <a href="https://www.23andme.com/pd/" target="_blank" rel="noopener noreferrer">announced</a> a new research community for Parkinson’s patients, Gary signed on. In January 2010, he became part of what would become the world’s largest Parkinson&#8217;s community. He shared his spit, using 23andMe’s DNA kit.
“It was easy to do and didn’t require much from me,” Gary says. He found the results from his test interesting–and comprehensive. Diagnosed with Young-onset Parkinson’s at 38, Gary, now 50, learned he was only at a slightly higher than normal risk for developing PD. He was most surprised by the amount of information he received–about his maternal and paternal bloodlines, food preferences, muscle performance. Happily, he learned he was not likely to go bald, which he hopes is right. “I even found out if my <a href="https://www.23andme.com/topics/traits/earwax-type/">earwax</a> was moist or not,” he says.
Learning more about his genetic profile was actually something of a relief to Gary. Since he had little genetic predisposition to Parkinson’s, such as carrying the LRRK2 mutation, he now worries less about his two children developing Parkinson’s. But even if his results had been different, having that knowledge makes a difference, he says. “If you’re at risk for something, then you can do something about it. You may know you need to see a certain type of doctor twice a year versus once.”
<div style="float: right; text-align: justified; width: 180px; background-color: #eee; padding: 15px; margin-left: 10px;">For Father&#8217;s Day 
If your Dad has Parkinson&#8217;s, show him you care by making a long-term investment in his health and the future of Parkinson&#8217;s disease research. At no cost, give him access to his genetic data and the growing Parkinson&#8217;s Research Community (~7,500 strong!) at 23andMe. Visit <a href="https://www.23andme.com/pd/" target="_blank" rel="noopener noreferrer">www.23andme.com/pd</a> to sign him up.</div>
Participating in genetic research was only the beginning for Gary. Since then, he completed a profile on <a href="https://foxtrialfinder.michaeljfox.org/" target="_blank" rel="noopener noreferrer">Fox Trial Finder</a>, The Michael J. Fox Foundation’s clinical trial matching site. Through this tool, he found–and completed–a study on cognition and Parkinson’s at the University of Texas Southwestern Medical Center, which is near his home in the Dallas area. He also connected with Ceregene’s CERE-120 trial, for a potentially neuro-protective gene therapy. However, as he was being screened for this trial, Gary learned he had suffered a small stroke at some point. While this made his participation in the trial no longer possible, it was information he didn’t have before. And it hasn’t dampened his determination to participate in future clinical trials–he’s still looking to contribute wherever he can.
Like his attitude toward genetic research, Gary wonders why you wouldn’t participate in clinical research. “I want everyone to get involved through Fox Trial Finder,” he says. And he’s encouraging friends and family members to sign up.
Gary has also taken action through Team Fox–“to do something positive,” he says. In Texas, he has hosted several Team Fox events, including a pancakes breakfast and a shopping event on his town’s Main Street. His sister in Milwaukee, Wisconsin, has gotten involved, too. She hosted a comedy night and an event at a Milwaukee Brewers’ game.
Through Team Fox and clinical trial participation, Gary is happy to do his part to help speed a cure and support MJFF’s efforts. “The Michael J. Fox Foundation is a sign of hope for me,” he says. “I know they’re working in one direction–toward improved treatments and a cure. That’s just what I need.”

Lauren Anderson

Why Not Participate? One Patient’s Perspective

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-13513" title="Teenage boy and girl stick out tongues to each other" src="https://blog-api.23andme.com/wp-content/uploads/2012/06/siblings-300x199.jpg" alt="" width="300" height="199" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/siblings-300x199.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/06/siblings.jpg 425w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Theories abound about the effects of birth order on personality, success, and other life outcomes. Last week we <a title="Oldest vs. Youngest – Let the Sibling Rivalries Begin!" href="https://blog.23andme.com/traits-2/oldest-vs-youngest-let-the-sibling-rivalries-begin/">quizzed our readers</a> on traits that differed between 23andMe customers who were oldest children (firstborns) versus youngest children (lastborns). Congratulations to Kay, the winner of the quiz! Kay got all three answers correct and will receive a $25 Amazon gift card. So what were the correct answers? Read on&#8230; 

Some researchers have theorized that firstborns are more successful than younger children (lastborns). Though they don’t have a leg up on all potential measures of success, 23andMe’s firstborns are more educated than lastborns. Even controlling for age, sex, and correcting for multiple tests (as we did for all the findings reported here), firstborns reported greater educational attainment than lastborns. We can’t say that this fully confirms the idea that firstborns are more successful, as they did not report higher incomes or higher subjective socioeconomic status.
Personality theorists have also postulated that firstborns are more conscientious, more socially dominant, less agreeable, and less open to new ideas than lastborns. In actuality, we found that firstborns are more full of ideas, but less altruistic than lastborns. These results are consistent with some but not all of the existing, but controversial, research on firstborn children’s personalities. While altruism is a component of agreeableness, and therefore might seem to support the theory, firstborns did not differ significantly in overall agreeableness, just altruism. Why might this be? We’re just not sure. Perhaps lastborns have to learn to share from an earlier age than do firstborns. Have a theory? Leave it in the comments below.
Finally, firstborns are more likely to have had chicken pox or mumps. This was really interesting and completely unexpected. It’s possible that having an older sibling might reduce your chance of contracting certain childhood diseases.
As an aside, one of the red herrings for this last question was that firstborns are more likely to smoke. In fact, the opposite was true. Lastborns were significantly more likely to have smoked than firstborns. About a third of lastborns had smoked regularly at some point in their life, compared to roughly a quarter of firstborns.
Have your own theories about birth order effects? Leave a comment below!

Quiz Answers: Oldest vs. Youngest — Success, Personality, and Health

<img loading="lazy" decoding="async" class="alignright wp-image-13764 size-medium" src="http://35.88.189.111/wp-content/uploads/2012/06/doctorMan1-300x202.jpg" alt="" width="300" height="202" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/doctorMan1-300x202.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/06/doctorMan1.jpg 422w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Prostate cancer affects more men than any other type of cancer &#8212; approximately one in six men will be diagnosed with it.
Although two-thirds of prostate cancers grow slowly and are largely asymptomatic, the remaining third of prostate cancers are aggressive and deadly, killing more men than any other cancer besides lung cancer. Prostate cancer is caused by the unchecked proliferation of cells in the prostate &#8212; the male gland that makes some of the fluids found in semen. The underlying cause of this cellular proliferation, however, is still not well understood.
Age and ethnicity are two of the most significant <a href="http://www.webmd.com/prostate-cancer/guide/prostate-cancer-risk-factors">factors</a> influencing a man’s risk of prostate cancer. Risk increases with age, and two-thirds of cases occur in men over the age of 65. &nbsp;In fact, 80% of men aged 80 or older have cancerous prostate cells. Ethnicity is another risk factor; the cancer is most common in men of African ancestry and least common in men of Asian ancestry, with individuals of European ancestry at intermediate risk. The high rate of prostate cancer in African Americans may not be totally attributable to ethnicity, however; African Americans have higher prostate cancer rates than Africans living in Africa, suggesting that diet or other non-genetic factors may also contribute.

In addition, genetics significantly contribute to prostate cancer risk. &nbsp;Twin studies suggest that <a href="https://blog.23andme.com/articles/quiz-answers-heritability-demystified">heritability</a> of prostate cancer is around 40%, making it one of the most heritable of cancers. &nbsp;The genetic aspect of prostate cancer is further underscored by the increased incidence observed in those with a family history; having a brother or father with prostate cancer doubles a man’s risk. &nbsp;Many studies have attempted to uncover the genes responsible for this genetic and familial risk, and when all the known associations are taken together, they explain approximately a <a href="https://www.ncbi.nlm.nih.gov/pubmed/21743467">quarter</a> of the familial risk.
<img loading="lazy" decoding="async" class="aligncenter wp-image-13488 size-full" src="http://35.88.189.111/wp-content/uploads/2012/06/NationalMensHealthWeek.jpg" alt="" width="626" height="691" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/NationalMensHealthWeek.jpg 626w, https://blogcms.23andme.com/wp-content/uploads/2012/06/NationalMensHealthWeek-272x300.jpg 272w" sizes="auto, (max-width: 626px) 100vw, 626px" />
Screening for and managing prostate cancer is yet another big question mark. The widely-used PSA test, which measures levels of prostate-specific antigen, has recently come under fire as a screening and diagnostic tool for prostate cancer. Generally speaking, cancerous prostate cells produce more prostate-specific antigen than healthy prostate cells, but there is considerable variation between healthy individuals and many non-cancerous conditions can lead to increased prostate-specific antigens levels. A report by the U.S. Preventive Services Task Force argues that overdiagnosis resulting from PSA screening is actually doing more harm than good due to unnecessary surgeries and treatments that can have complications ranging from erectile dysfunction and incontinence to life-threatening blood clots and heart attacks. Because of this, the task force no longer recommends regular PSA screening, although not all physicians agree.
Given our current, limited understanding, prostate cancer is a paradox: it is arguably both one of the most deadly and one of the most benign cancers. Prostate cancer kills more men over the age of 75 than any other cancer, but the vast majority of cases are non-aggressive, slow-growing, and asymptomatic, to the point where doctors debate whether to screen for it. More research may help uncover more genetic and non-genetic factors that predict or distinguish different forms of prostate cancer or lead to better ways to screen effectively for this common disease.

Understanding Prostate Cancer

<img loading="lazy" decoding="async" class="aligncenter wp-image-13489 size-full" src="http://35.88.189.111/wp-content/uploads/2012/06/FatherBikeKid.jpg" alt="" width="416" height="288" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/FatherBikeKid.jpg 416w, https://blogcms.23andme.com/wp-content/uploads/2012/06/FatherBikeKid-300x208.jpg 300w" sizes="auto, (max-width: 416px) 100vw, 416px" />
You claim that Junior is giving you gray hairs, but is he really? In actuality your kids may be adding years to your life &#8212; one recent <a href="https://www.ncbi.nlm.nih.gov/pubmed/21946940">study</a> suggests that fatherhood may actually reduce a man’s risk of dying from a heart attack.
The study, which was conducted last year and led by Michael Eisenberg at Stanford and Mark Pletcher at the University of California, San Francisco, addresses the relationship between heart health and fatherhood. Nearly 138,000 men between the ages of 50 and 71 participated in the study, which used data from the NIH-AARP Diet and Health Study, a national survey in retired persons. Only men free of heart disease and stroke at the beginning of the study were included, and the heart health of these individuals was followed for over ten years, on average. After adjusting for income, education, health habits, and age, men without children died from heart disease 17% more frequently than men who were fathers.

One possible explanation for this heart health discrepancy is a difference in testosterone production. Studies have shown that low levels of androgen hormones, such as testosterone, result in both a higher risk for cardiovascular disease and for infertility. The correlation between lower testosterone and infertility may partially explain the higher rate of cardiovascular death observed in childless men.
Eisenberg and Pletcher did not take into account the fertility of the women in these families (male infertility accounts for about half of infertility cases in couples) nor did they take into account the many fertile couples who did not wish to have children. Fatherhood is, therefore, far from a perfect proxy for male fertility.  Furthermore, the theory that testosterone deficiency underlies both infertility and heart disease just a theory, and some older research suggested that very high testosterone levels also increase a man’s risk for heart disease.  Another biological or social factor may, in actuality, be the underlying source of the correlation.  More research is needed to better understand the link between heart health and fatherhood.
So, Dads, next time you’re on diaper duty, don’t think of the sacrifices you are making for your children; think instead of the great health benefits you may be reaping for yourself. Let your children bring joy to your heart.

Ah, Fatherhood — Dirty Diapers, Skinned Knees … and Healthier Hearts?

The American Society of Clinical Oncology recently wrapped up its annual meeting, bringing together health care professionals focused on the fight against cancer.
The five days were packed with mind-expanding science and encouraging updates on new efforts for research collaboration between doctors, scientists, advocates, and, most importantly, patients themselves.
<img loading="lazy" decoding="async" class="aligncenter wp-image-13533 size-full" title="ASCO-2012-23andme-FINAL-poster-2012" src="http://35.88.189.111/wp-content/uploads/2012/06/ASCO-2012-23andme-FINAL-poster-2012.jpg" alt="" width="1651" height="1275" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/ASCO-2012-23andme-FINAL-poster-2012.jpg 1651w, https://blogcms.23andme.com/wp-content/uploads/2012/06/ASCO-2012-23andme-FINAL-poster-2012-300x232.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/06/ASCO-2012-23andme-FINAL-poster-2012-768x593.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/06/ASCO-2012-23andme-FINAL-poster-2012-1024x791.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2012/06/ASCO-2012-23andme-FINAL-poster-2012-880x680.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2012/06/ASCO-2012-23andme-FINAL-poster-2012-1180x911.jpg 1180w" sizes="auto, (max-width: 1651px) 100vw, 1651px" />
<h6>Sarcoma Research</h6>
23andMe’s Dr. Kim Barnholt, the project manager for both our<a href="https://www.23andme.com/sarcoma/"> Sarcoma</a> and<a href="https://www.23andme.com/mpn/"> Myeloproliferative Neoplasms</a> (MPN) research communities, got to present some of the highlights of<a href="https://blog-api.23andme.com/wp-content/uploads/2012/06/ASCO-2012-23andme-FINAL-poster-2012.pdf"> 23andMe’s work on sarcoma</a>, which is all about collaboration.
But the conference also allowed members of our MPN and Sarcoma Advisory Panels to talk about some of their latest work, bringing home how lucky we are to have them working with us. They all have impeccable standing in the community of oncologists and cancer researchers.
<h6>Online Communities</h6>
One of the highlights of the whole conference was Dr. Demetri’s talk on the “Dynamics of Partnerships between Professionals and Patient Online Communities to Accelerate Clinical Research and Improve Care.” For 23andMe, the theme is at the heart of what we call our “research revolution.”
Dr. Demetri, who is a charismatic forward thinker, talked about how “interactive social networking models offer great potential to increase meaningful partnerships between patients, caregivers, family and friends, and health care professionals.”
Dr. Demetri used 23andMe’s Sarcoma Research Initiative as an important example of crowdsourcing that integrates the patient’s experience and voice into research and clinical care.
<h6>Patient Centered</h6>
This also got to another theme of the conference that marks a change from the old approach to medicine involving a one-way line of communication from doctor down to patient. Clearly this approach is no longer acceptable, and the conference highlighted how online tools and social media have helped to change that dynamic as well as offer new opportunities for collaboration.
“This type of research could not be done in traditional ways,” Dr. Demetri said.
<img loading="lazy" decoding="async" class="aligncenter wp-image-9055 size-full" title="sarcoma image" src="http://35.88.189.111/wp-content/uploads/2011/05/sarcoma-image1.jpg" alt="" width="315" height="257" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/05/sarcoma-image1.jpg 315w, https://blogcms.23andme.com/wp-content/uploads/2011/05/sarcoma-image1-300x245.jpg 300w" sizes="auto, (max-width: 315px) 100vw, 315px" />
Demetri, whose work on our advisory board is unpaid, said the research model pioneered by 23andMe, “can be extrapolated to (the study of) other common diseases as molecular profiling divides all cancers into subsets of rare diseases.”
We think so too and are encouraged by the progress and promise our research communities can offer.
We look forward to sharing even more of our findings as our research initiatives progress.

Fighting Cancer Together

<img loading="lazy" decoding="async" class="alignnone size-medium wp-image-13464" src="https://blog-api.23andme.com/wp-content/uploads/2012/06/thumbnail-300x200.jpg" alt="" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/thumbnail-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/06/thumbnail-768x513.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/06/thumbnail-1024x684.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2012/06/thumbnail-880x588.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2012/06/thumbnail-1180x789.jpg 1180w" sizes="auto, (max-width: 300px) 100vw, 300px" />
(Editor&#8217;s note: This post originally ran in June, but we thought it was worth a second look on the eve of the election.) 
As Americans approach the elections this November, discussions of what influences economic and political preferences will surely flood our television sets and news feeds. Pundits use factors like income, gender, and education level to make predictions on how people will vote.
<h6>Genetics and Politics</h6>
But do they ever consider genetics in making their predictions?  Probably not. A new study, however, suggests that such preferences may indeed be influenced by our genetic makeup.
Led by Daniel Benjamin of Cornell University and Peter Visscher of the University of Queensland a team of researchers studied 3,200 individuals for four traits believed to influence economic preferences (risk-aversion, patience, trust, and fair-mindedness), as well as five categories of political preferences (immigration/crime, economic policy, environmentalism, feminism/equality, and foreign policy). Each individual’s preferences in these areas were determined using an extensive survey. The results of the study were published in the <a href="https://www.pnas.org/content/109/21/8026.long">Proceedings of the National Academy of Sciences</a> in May.
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Technical note:
<a href="https://blog.23andme.com/articles/quiz-answers-heritability-demystified/">Heritability</a> is a common measure of the average influence genetics has on a trait relative to other, non-genetic influences in a population.The heritability of a trait can range from zero (variance in the trait is independent of genetics) to one (variance in the trait completely explained by genetics). Heritability is often estimated using using twin studies; if identical twins are, on average, more similar than fraternal twins in a given trait, this increase in similarity is attributed to shared genetics.
The Visscher team, however, used a newer method for estimating heritability that relies on the genetically-determined relatedness of study subjects, which is potentially more accurate. The heritability estimates generated by this method were noisy, but three of the nine traits had statistically-significant heritability estimates: trust (heritability = 24%, p-value = 0.05), foreign policy (heritability = 35%, p-value = 0.01), and economic policy (heritability = 34%, p-value = 0.01). Despite the noisiness, the heritability estimates are not inconsistent with earlier findings from twin-designed studies (after for accounting for the biases in the two estimation methods).
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<h6>Trust and Economic Policy</h6>
Before asking which genes are involved, we have to ask: are genes involved in economic and political preference, or are these preferences solely determined by environmental factors, such as family and friends? Three of the nine traits Benjamin and Visscher’s team analyzed appeared to be heritable to some extent &#8212; trust, foreign policy, and economic policy &#8212; which is consistent with previous studies.
Although Visscher and his fellow researchers were able to establish that genetics likely influences some aspects of our economic and political preferences, they were not able to determine which genes or genetic variants may be involved.
<h6>Many Genes</h6>
Visscher and his co-workers conclude that economic and political preferences are, most likely, influenced by many different genes, each affecting these traits in very small ways. In order to capture such small effects, much larger sample sizes are needed. Thus, economic and political preferences, along with the canonical examples of height and schizophrenia, fall into a group of very complex traits that are heritable but for which we may never find one single gene as the “smoking gun.”
If you’re voting in today’s primaries in California, Montana, New Jersey, New Mexico, or South Dakota, it’s likely that genetic influences are with you in the voting booth. Which genes are involved in economic and political preferences, however, remains to be discovered. Perhaps by the 2016 election we’ll better understand the genetics of politics.

Elephants Are Red, Donkeys Are Blue, Genetics Can Influence Politics, Too

<img loading="lazy" decoding="async" class="aligncenter size-full wp-image-13429" title="ASCO image" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/ASCO-image.jpg" alt="" width="557" height="102" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/ASCO-image.jpg 557w, https://blogcms.23andme.com/wp-content/uploads/2012/05/ASCO-image-300x55.jpg 300w" sizes="auto, (max-width: 557px) 100vw, 557px" />
Starting today cancer researchers will be gathering in Chicago at the meeting of the<a href="http://www.asco.org/"> American Society of Clinical Oncology</a>.
Researchers and doctors at the annual meeting – the world’s largest oncology conference – will hear about the most promising drugs being developed to fight cancer. They’ll spend five days learning about the new science around a vast array of cancers, and discuss the newest therapies as well as the latest and most innovative clinical trials. They’ll wrestle with broader issues on ethics and hunt out presentations about the most successful cancer prevention.
But this year we hope that a few will also take notice of a new approach to cancer research being pioneered by 23andMe.
Along with our scientific advisors – who include <a href="http://doctors.dana-farber.org/directory/profile.asp?dbase=main&amp;setsize=16&amp;pgt=George+D%2E+Demetri%2C+MD&amp;picture_id=0000273&amp;grouptype_typeid_data=1&amp;gs=c&amp;nxtfmt=r&amp;display=Y&amp;lookup=Y&amp;oldurl=Y&amp;pict_id=0000273">Drs. George Demetri</a>, Robert Maki, Judy Garber, and Mark Robson, – our very own Dr. Kim Barnholt, the Research Project Manager for both our<a href="https://www.23andme.com/sarcoma/"> Sarcoma</a> and<a href="https://www.23andme.com/mpn/"> Myeloproliferative Neoplasms</a> (MPN) research communities, is attending. Kim will be presenting some of the highlights of our 23andMe’s work on sarcoma.
We’ve been able to recruit almost 1,000 people with these cancers that develop in bone and soft tissue, making our sarcoma research cohort one of the world’s largest. Sarcoma, which strikes about 14,000 people each year, is not one kind of cancer, but many different ones.
The complexity of what turns out to be dozens of subtypes of sarcomas makes treating and studying them difficult. But using web-based tools allows for both quick recruitment and efficient large-scale genome-wide studies of the disease. It also gives people with sarcoma, who might be geographically isolated or far away from cancer research centers, or too sick to travel, an easier way to participate in research.
Kim is most encouraged by the engagement of the community with more than 80 percent of participants having completed important surveys. &nbsp;Last summer, she put together an<a href="https://www.23andme.com/sarcoma/videos/"> evening gathering</a> for the community giving patients a chance to directly interact with her and other scientists at 23andMe, as well as with sarcoma researchers and advocates.
<img loading="lazy" decoding="async" class="aligncenter wp-image-6395 size-full" title="sarcoma-large" src="http://35.88.189.111/wp-content/uploads/2010/04/sarcoma-large.jpg" alt="" width="350" height="289" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/04/sarcoma-large.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2010/04/sarcoma-large-300x248.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
“It’s important for researchers to meet patients,” Kim said recently. “It gives more meaning to what we do. There’s more than just numbers in research. Understanding the personal stories and each person’s journey gives what we do more relevance and meaning, but it also gives us a better picture of the disease. It all goes back to the quality of measurement in research. If you can talk and interact with patients and they have a voice and that is part of the data collection, it improves the what we do. I know it does for my work.”
Kim plans to present some preliminary data in Chicago and report back over the next few days on some of the most interesting presentations.

Health + Traits — Page 30