<img loading="lazy" decoding="async" class="alignright wp-image-17426 size-medium" title="heart health infographic" src="http://35.88.189.111/wp-content/uploads/2013/02/heart-health-infographic-300x263.jpg" alt="" width="300" height="263" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/02/heart-health-infographic-300x263.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/02/heart-health-infographic-768x673.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2013/02/heart-health-infographic-880x771.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2013/02/heart-health-infographic.jpg 897w" sizes="auto, (max-width: 300px) 100vw, 300px" />
February is American Heart Month and a time to focus on what remains the nation’s number one killer – heart disease – which is responsible for one in three deaths in the United States every year.
Why heart disease is so deadly has a lot to do with lifestyle and diet in America. Obesity, even among the very young, is increasingly commonplace, and the <a href="http://www.heart.org/HEARTORG/GettingHealthy/PhysicalActivity/StartWalking/The-Price-of-Inactivity_UCM_307974_Article.jsp">majority of Americans</a> do not get enough exercise, according to the American Heart Association.
Fortunately, we can all reduce our risk of heart disease. We can exercise more, eat right and reduce stress in our lives. But it’s also important to understand, that like many health conditions, genetic factors contribute to heart disease risk.
Understanding how your genetics plays a role can help you craft the most effective plan for a healthy heart.
23andMe reports on several genetic factors that impact heart health, such as those associated with coronary heart disease and atrial fibrillation, as well as a rare heart condition called hypertrophic cardiomyopathy. We also have reports on how your genes affect your response to anti-clotting drugs to reduce the risk of heart attack.
The role genetics plays in these different conditions varies greatly. In some cases, such as in coronary heart disease, many of the genetic factors involved are not yet fully known.
While you can’t change your genetics, you can do a lot to change your risks for heart disease by changing your lifestyle. Cutting out smoking, lowering cholesterol, exercising more and eating right can go a long way towards keeping your heart healthy.

23andMe Blog

23andMe Blog Team

Genetics and a Healthy Heart

<div id="attachment_17393" style="width: 310px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-17393" class="wp-image-17393 size-medium" title="Telomere_caps" src="http://35.88.189.111/wp-content/uploads/2013/01/Telomere_caps-300x236.gif" alt="" width="300" height="236" />Chromosomes tipped by telomeres.</div>
A study <a href="http://www.sciencemag.org/content/early/2013/01/23/science.1230062.long">published recently in Science</a> by Susanne Horn and colleagues is a noteworthy example of hypothesis-driven science done right. It exemplifies how seemingly obscure findings can lead to new hypotheses and provide insight into human health and disease.
Horn and her colleagues studied a family prone to melanoma and other cancers and found a mutation located near the TERT gene in a region that controls the gene. Researchers have long been interested in this gene because it encodes a protein called telomerase that is important for both aging and cancer.
The telomerase protein protects telomeres, the “caps” at the ends of chromosomes. Telomeres have been likened to the plastic tips on shoelaces because they stop the ends of chromosomes from coming apart and are critical for a healthy cell. Telomeres become shorter each time a cell makes a copy of itself and thus get shorter with age. Since the telomerase protein adds DNA back onto the telomere each time the cell divides, numerous researchers have studied it in the interest of prolonging human life. But others have cautioned that too much telomerase activity might contribute to cancer.
Horn looked to see if more people with melanoma also had the mutation discovered in the family but were unable to detect it in individual cases of melanoma, in other families with melanoma, or in large genetic databases. It seemed to be a genetic one-off, a mutation isolated to this one family.
Realizing that this unique mutation might provide insight into a mechanism of cancer, the researchers next looked at DNA from melanoma tumors and found very similar mutations. The mutations in the tumors were not present in the person’s DNA at birth but rather arose during his or her lifetime. By analyzing the mutations very closely the researchers concluded that both the mutation found in the family and those found in the tumors contribute to cancer through a similar mechanism.
Both types of mutations influence the regulation of the TERT gene and result in increased levels of the telomerase protein. Normally telomerase is not active in adult cells that aren’t dividing &#8212; for instance cells in the skin, heart and other places. In people with these mutations, more telomerase likely leads to longer telomeres, more dividing cells and ultimately cancer. Though scientists <a href="https://www.nytimes.com/2013/01/25/science/new-mutations-discovered-in-melanomas.html?_r=0">have also cautioned</a> that it might not be this simple and that too much telomerase protein could also promote cancer through other mechanisms.

Rare Mutation Leads to New Insights into Melanoma

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-17362" title="Woman weighing herself on scales in health club" src="https://blog-api.23andme.com/wp-content/uploads/2013/01/womenScale-300x214.jpg" alt="" width="300" height="214" />
There are lots of things we can&#8217;t change, but our lifestyle isn&#8217;t one of them. Good thing, too  – our weight, nutrition habits, and exercise behaviors impact us beyond whether we look good in a swim suit. They also influence our risk for many different diseases.
In the same way, our DNA also contributes to our risk for various diseases. It&#8217;s where our lifestyle and DNA intersect that we have the greatest potential for positive change. For instance, the knowledge that my genes put me at higher-than-average risk for heart disease may make me think twice about the extra slice of bacon (so long as it&#8217;s not within smelling distance!). And going light on the bacon for the long haul may ultimately lower my risk for many conditions besides heart disease.
So where might your genetic incentives be?
<div>Obesity</div>
Extra pounds equate to extra risk for numerous <a href="https://www.23andme.com/dna-health-ancestry/">health conditions</a>. The obese are seven times more likely to develop type 2 diabetes, three times more likely to develop gallstones, and twice as likely to develop coronary heart disease or venous thromboembolism (blood clots) compared to those at a healthy weight.
Each of these obesity-associated conditions has at least one 23andMe genetic report (see the links above).  If you find that your genetics puts you at higher-than-average risk for one of these conditions, perhaps this knowledge will motivate you to keep your weight in check.  To the fortunate few with lower-than-average genetic risk for all the conditions above, don’t grab that donut yet.  Obesity still increases your risk compared to those at a healthy weight, and there are likely many additional genetic factors that are as-of-yet unknown but may contribute to your risk.
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<img loading="lazy" decoding="async" class="alignleft size-full wp-image-12163" title="small_23andMe_logo" src="https://blog-api.23andme.com/wp-content/uploads/2012/04/JRBgdIBXKIeVIdETJrxYIw_ttam_logo.jpg" alt="" width="24" height="40" />
Not yet a 23andMe customer? Learn what your DNA says about your ancestry. <a href="https://www.23andme.com/store" target="_blank" rel="noopener noreferrer">Visit our store</a>!
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Nutrition 
Poor nutrition, even discounting its effect on your waistline, certainly doesn’t keep the doctor away.  People who consume red meat ten times per week or more have about a 50 percent higher risk for age-related macular degeneration, an eye condition that can lead to blindness. Furthermore, studies suggest that a diet high in fiber, vegetables, nuts, and foods typically found in Mediterranean cuisine is associated with 20-40 percent lower risk for coronary heart disease. Colorectal cancer is also linked with poor diet habits, and experts suggest that  diets high in fiber and low in fat can lower your risk.
If you find that you are at increased genetic risk, this knowledge may help you prioritize which dietary changes to make. For example, a person who has a strong genetic risk for age-related macular degeneration might consider eating more fish, nuts, and leafy greens  – foods linked to lower risk for that disease.
Exercise 
A gym membership (if actually used) may positively impact your health. For starters, exercise helps keep one’s weight in check; people who exercise regularly are up to 60 percent less likely to be overweight than people who don&#8217;t exercise.
Even beyond that, exercise can strengthen one of your most important muscles: your heart. People who don&#8217;t exercise are about twice as likely to develop coronary heart disease as people who exercise regularly. In women, walking just an hour a week is associated with 50 percent lower risk for coronary heart disease and in men, vigorous activity and playing sports may lower the risk for heart disease.   If your genetics suggest you&#8217;re at higher than average risk for heart disease, take that as extra incentive to hit the gym regularly!
Poor exercise also influences your risk for type 2 diabetes.   People who engage in moderate physical activity on a regular basis or simply walk for at least two and a half hours a week at a brisk pace are about 30 percent less likely to develop type 2 diabetes compared to people who don&#8217;t exercise.   If your genetic report shows you are already at higher than average risk for type 2 diabetes, perhaps you may want to go the extra mile to make a change.
The Competitive Advantage 
Unfortunately, health isn&#8217;t an even playing field. Just as some people have genetic variants associated with lower than average risk for disease, some are born with skinny genes (and can wear skinny jeans).
<div>Still, there are other genetic factors that may help in the battle of the bulge. One that&#8217;s received a lot of attention is in a gene called PPARG. Normally, high fat intake is associated with weight gain, but in people with a certain variation of the PPARG gene, a diet high in monounsaturated fat is actually linked to weight loss. Monounsaturated fat is found in olive oil, so this type of diet has been nicknamed the &#8220;Mediterranean&#8221;-style diet.</div>
Very few genetic factors have been reliably linked to diet and exercise but some of the preliminary findings..
Whatever your health goals may be, we wish you success that outlasts the month.  May this knowledge about your DNA  – whether that be the genetics of disease risk or the genetics of losing weight  – help you towards a fitter you.

Your Lifestyle, Your Health, Your Genes

<img loading="lazy" decoding="async" class="alignright size-full wp-image-7425" title="ancestry-photo-sheridan" src="https://blog-api.23andme.com/wp-content/uploads/2010/09/ancestry-photo-sheridan.png" alt="" width="280" height="152" />
We first met <a href="https://blog.23andme.com/23andme-and-you/23andme-how-to/ancestry-at-23andme-introducing-sheridan/">Sheridan</a>* in the fall of 2010. As an adoptee, she was curious about her DNA and what 23andMe might be able to tell her.
With the help of old friends and some new ones on 23andMe, Sheridan learned about her <a href="https://blog.23andme.com/23andme-and-you/23andme-how-to/ancestry-at-23andme-sheridans-global-origins/">global origins</a>,  which include an African-American father and a mother of European descent, and <a href="https://blog.23andme.com/23andme-and-you/23andme-how-to/ancestry-at-23andme-sheridans-got-relatives/">connected with DNA relatives</a>.
She even discovered that she and her good friend Brian are <a href="https://blog.23andme.com/23andme-and-you/23andme-how-to/ancestry-at-23andme-finding-connections/">4th cousins</a>, which means she has some Irish ancestry. Together, they <a href="https://blog.23andme.com/23andme-and-you/23andme-how-to/ancestry-at-23andme-old-roots-and-new-horizons/">figured out a branch of her family tree</a>.

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For a quick Ancestry primer, check out:
<a href="https://blog.23andme.com/23andme-and-you/genetics-101/ancestry-at-23andme-what-can-you-learn/">Ancestry at 23andMe: What Can You Learn?</a>
Follow Sheridan’s journey from the beginning:*
<a href="https://blog.23andme.com/23andme-and-you/23andme-how-to/ancestry-at-23andme-introducing-sheridan/">Introducing Sheridan</a> 
<a href="https://blog.23andme.com/23andme-and-you/23andme-how-to/ancestry-at-23andme-sheridans-global-origins/">Sheridan’s Global Origins</a> 
<a href="https://blog.23andme.com/23andme-and-you/23andme-how-to/ancestry-at-23andme-sheridans-got-relatives/">Sheridan’s Got Relatives</a> 
<a href="https://blog.23andme.com/23andme-and-you/23andme-how-to/ancestry-at-23andme-finding-connections/">Finding Connections</a> 
<a href="https://blog.23andme.com/23andme-and-you/23andme-how-to/ancestry-at-23andme-old-roots-and-new-horizons/">Old Roots and New Horizons</a>
*Sheridan and her story are works of fiction and any resemblance to actual people or events is purely coincidental.
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<h6>Using DNA Relatives</h6>
For Sheridan, learning about herself on 23andMe did more than just kindle a love for the Irish. By combining the information she learned about her ancestral origins with information from some of the <a href="https://www.23andme.com/dna-ancestry/">DNA Relatives</a> she found, she and Brian were able to fill in the first pieces of her genealogical history.
Since then, Sheridan’s filled in even more of the family tree on her mother’s side.
Her second cousin Mike, identified through 23andMe as a DNA Relative, was able to track down the name of his grandmother’s sister &#8212; a woman very likely to be Sheridan’s own grandmother. To Brian’s delight, Mike also found the name of his grandmother’s sister’s husband, a Fitzpatrick descended from the same Irish ancestors as Brian.
<h6>Neanderthal</h6>
<img loading="lazy" decoding="async" class="alignleft wp-image-17249 size-medium" title="Neanderthal-friends-sheridan" src="http://35.88.189.111/wp-content/uploads/2013/01/Neanderthal-friends-sheridan-272x300.png" alt="" width="272" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/01/Neanderthal-friends-sheridan-272x300.png 272w, https://blogcms.23andme.com/wp-content/uploads/2013/01/Neanderthal-friends-sheridan-768x849.png 768w, https://blogcms.23andme.com/wp-content/uploads/2013/01/Neanderthal-friends-sheridan-927x1024.png 927w, https://blogcms.23andme.com/wp-content/uploads/2013/01/Neanderthal-friends-sheridan-796x880.png 796w, https://blogcms.23andme.com/wp-content/uploads/2013/01/Neanderthal-friends-sheridan-1068x1180.png 1068w, https://blogcms.23andme.com/wp-content/uploads/2013/01/Neanderthal-friends-sheridan.png 1192w" sizes="auto, (max-width: 272px) 100vw, 272px" />
Brian always kept her in the loop on 23andMe, though. Some more mutual friends joined and they quickly started sharing on 23andMe. Sheridan remembers when the <a href="https://www.23andme.com/you/labs/neanderthal/">Neanderthal Ancestry feature</a> came out. There was an unofficial contest over who had the most <a href="https://blog.23andme.com/ancestry/find-your-inner-neanderthal/">Neanderthal DNA</a>; Brian was disappointed that he was solidly average for a Northern European person. Sheridan tried to cheer him up by pointing out that he still had the most caveman of their friends with mostly European ancestry.
“Besides,” she said, “I only have 2.2 percent Neanderthal!”
“That’s because Neanderthals were never even in Africa to begin with,” he snorted, but he seemed mollified.
Sheridan, far from feeling shortchanged, found it fascinating that even a small percentage of her DNA could be traced back to these prehistoric “cousins.”
<h6>Ancestry Composition</h6>
But Brian’s Stone Age enthusiasm paled in comparison to his excitement over Ancestry Composition. A new and improved replacement for the popular Ancestry Painting feature, <a href="https://blog.23andme.com/ancestry/23andmes-newest-feature-explores-your-ancestry/">Ancestry Composition</a> gives a much more detailed breakdown of a person’s genetic ancestry. Brian called Sheridan at two in the morning when it came out.
“It’s here!” he exclaimed when she groggily answered the phone.
“Unghh wha&#8211;?” she mumbled.
“Ancestry Composition! Like Ancestry Painting, but way better. Remember? Your Ancestry Painting was cool, but your Composition is even cooler. Mine’s still kind of boring, though. But you should look at yours! And I can see it split it up by which side I got from my mom and which side from my dad and you can zoom in and out and change the thresholds&#8230; hey, you still there? Sheridan? Hello?”
So maybe two in the morning wasn’t the best time for Brian to tell Sheridan about Ancestry Composition. But the next day they met up at the coffee shop to explore the new feature together.
Brian quickly explained that 23andMe had updated its main ancestry feature with lots of examples of people with full ancestry from different parts of the world &#8212; like South Asia, France, or Finland. Some of these people were part of research studies and their genetic data is publicly available. But many of the people 23andMe used to develop its ancestry analysis are 23andMe customers themselves.
“Of course, you can only learn what, say, ‘Welsh DNA’ looks like if you have some examples of it,” he said. “The more examples you can learn from, the better your analysis will be. And 23andMe has a lot of different types of examples.”
<img decoding="async" class="aligncenter size-large wp-image-17254" title="Brian-composition" src="https://blog-api.23andme.com/wp-content/uploads/2013/01/Brian-composition-700x421.png" alt="" width="350" />
Brian clicked on the ‘+’ symbol in the “Resolution” bar to zoom in. “It’s still all European for me &#8212; no surprise &#8212; but now it can break it down into sub-regions.” The list of ancestries on the right of the screen expanded as he clicked and when he hovered the mouse pointer over the darker blue ring the map zoomed in to the British Isles.
“See? 99% British and Irish!” he said, puffing out his chest, which today was sporting, perhaps not accidentally, a green “Kiss me, I’m Irish!” t-shirt.
Sheridan rolled her eyes.
“Ok, ok, you were saying mine was cooler, though, right?”
“Oh, right. Yeah.”
Sheridan scooted him aside and pulled her Ancestry Composition up on the screen. The rings quickly morphed into concentric stacks of bright colors with a rainbow-colored map in the middle.
“Ooh,” she breathed. “Yeah, that’s pretty cool.”
<img decoding="async" class="aligncenter size-large wp-image-17299" title="sheridan-composition" src="https://blog-api.23andme.com/wp-content/uploads/2013/01/sheridan-composition-700x500.png" alt="" width="700" />
According to the new analysis, Sheridan’s DNA was about 62% European, 37% Sub-Saharan African, and 1.2% East Asian or Native American. The rest of her DNA was unassigned, meaning it couldn’t be mapped confidently to any specific population.
&#8220;Africa isn&#8217;t broken down into sub-regions yet the way Europe is,&#8221; Brian said, pointing to the pink stripe, &#8220;but 23andMe is going to update this soon.&#8221;
&#8220;Hm, I guess I can wait a little longer,&#8221; said Sheridan. &#8220;It&#8217;s nice to see all the European populations, though. Look, there’s the Irish ancestry for me, too!”
She already knew that she probably had some Irish ancestry based on the fact that she and 99% Irish Brian were 4th cousins and they’d traced their Irish family connection through her second cousin Mike, but it was somehow gratifying to see it spelled out so clearly on her screen. She could also see that she had some Eastern European and even a bit of Native American ancestry.
<img decoding="async" class="aligncenter size-medium wp-image-17257" title="Miguel-composition" src="https://blog-api.23andme.com/wp-content/uploads/2013/01/Miguel-composition-300x161.png" alt="" width="350" /> 
<img decoding="async" class="alignright size-medium wp-image-17258" title="Mesut-composition" src="https://blog-api.23andme.com/wp-content/uploads/2013/01/Mesut-composition-300x154.png" alt="" width="350" /> 
<img decoding="async" class="aligncenter size-large wp-image-17262" title="Ancestry Composition Native American" src="https://blog-api.23andme.com/wp-content/uploads/2013/01/Ancestry-Composition-Native-American-700x331.png" alt="" width="350" />
There was also a small dark blue band in her Composition labeled as “Ashkenazi”.
“That might actually be interesting,” Brian mused, “Let’s look into that later.”
For now, Ancestry Composition kept them busy as they explored their friends’ results. Miguel had a colorful Composition like Sheridan, except it had much more Native American and much less African. Mesut, Sheridan’s Turkish friend, was mainly Middle Eastern and European.
“Did Camille know she has Native American ancestry?” she asked, pointing to the 3.3% Native American in her Ancestry Composition.
“Not before she did 23andMe,” said Brian. “When she saw that result she did some digging and it turns out that her paternal grandfather was one-eighth <a href="https://en.wikipedia.org/wiki/Ojibwe_people">Chippewa</a>!”
He went to the drop down menu and selected another friend of theirs, Jamie. “This is pretty cool, too. Jamie’s half Askhenazi Jewish, and since her parents are also on 23andMe you can use the ‘Split View’ setting to see which side of the family it’s from.”
The map in the middle disappeared and the labels “Father” and “Mother appeared on either side of a vertical line splitting the colored rings in half. Sheridan could see that the Ashkenazi ancestry was clearly from Jamie’s mother’s side.
“Wow, that’s cool,” said Sheridan.
She thought for a second.
“So if I do end up learning who my mother is, and if I’m able to find her, and if she wants to do 23andMe&#8230; would this be able to tell me more about my father’s side, too?”
Brian nodded.
“That’ a lot of ‘ifs’, but yeah, I think so. You just need one parent for it to tell which half of your DNA came from that parent. Then by default, the other half came from the other parent.”
“Whew.” Sheridan sat back. “This whole genetic ancestry thing just got even more interesting.”
To be continued&#8230;

Ancestry at 23andMe: New Insights for Sheridan

<img loading="lazy" decoding="async" class="aligncenter wp-image-2804 size-full" title="smoking" src="http://35.88.189.111/wp-content/uploads/2009/02/smoking.jpg" alt="" width="350" height="260" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/02/smoking.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/02/smoking-300x223.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
You probably know that smoking and excessive drinking are bad for you. But did you know that your genetics also factor into how much those vices can impact your health?
Healthy lifestyle choice – like avoiding cigarettes – make you less susceptible to a host to diseases. For instance, non-smokers live, on average, a decade longer than smokers. Genetics aside it just makes a lot of sense to avoid lighting up.
But genetics also plays a role. Your genes – regardless of your health habits – may put you at higher risk for certain diseases associated with smoking and drinking.  That can make the healthy choices you make that much more important.
Your genetic information, when taken together with information about your lifestyle and environment, will give you the most complete picture of your health risks.
But, in a few cases, your genetics can increase the risks of smoking and drinking by much more than either risk factor alone. Heightening the importance of making healthy choices. Here are a few examples.
A variant in a single gene, <a href="http://www.23andme.com/topics/health-predispositions/alpha-1-antitrypsin-deficiency/">alpha-1 antitrypsin</a>, leads to deficiency in a protein that protects fragile lung tissue. This can put one at more risk for emphysema and liver disease. Because smoking can further reduce the levels of the protective protein, it can further increase the risks for lung disease.
Another variant in the ALDH2 gene causes a deficiency in its enzyme product – aldehyde dehydrogenase. Those lacking this enzyme are at increased risk for esophageal cancer, especially for those who smoke or drink.
The magnitude of the combined effect varies from study to study, but the basic finding that these three risk factors synergistically increase the risk of esophageal cancer is definitive.
In the case of smoking, a variant in the CHRNA gene is strongly associated with how many times you light up in an average day. In people with European ancestry, each copy of an A at the single-nucleotide polymorphism (SNP) rs1051730 is associated with smoking one more cigarette per day on average. It’s unclear if the association also holds true for people of African or Asian ancestry.
As for drinking, a number of previous studies found an association between the SNP rs1800497 and alcoholism, with each copy of A at that location increasing a person’s odds of being alcoholic by 1.2 times.
Keep in mind that there are many of other conditions associated with smoking and drinking that are also impacted by your genetics. For instance, if you light up regularly, you’re putting yourself at a higher risk for such things as lung cancer, esophageal cancer, age-related macular degeneration, multiple sclerosis, psoriasis, rheumatoid arthritis, venous thrombosis and coronary heart disease.
Heavy drinking increases your risk for esophageal cancer, colorectal cancer, and atrial fibrillation 
esophageal cancer, colorectal cancer and atrial fibrillation.

Barfly Genetics

<img loading="lazy" decoding="async" class="aligncenter wp-image-17185 size-full" title="underarm odor" src="http://35.88.189.111/wp-content/uploads/2013/01/underarm-odor.jpg" alt="" width="425" height="282" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/01/underarm-odor.jpg 425w, https://blogcms.23andme.com/wp-content/uploads/2013/01/underarm-odor-300x199.jpg 300w" sizes="auto, (max-width: 425px) 100vw, 425px" />
Here’s something to file under “Thank Goodness!” Researchers at the University of Bristol found that people with the genetic variant making them more prone to smelly armpits are also more likely to wear deodorant.
The paper, published in the <a href="https://www.nature.com/jid/journal/vaop/ncurrent/full/jid2012480a.html">Journal of Investigative Dermatology</a>, looked at variants in the ABCC11 gene that had previously been identified with what scientists describe as “axillary osmidrosis,” known to most people as underarm odor.
Individuals with a certain version of the single-nucleotide polymorphism (SNP) rs17822931 don’t produce as much sweat as other genotypes making conditions less ripe for underarm body odor. Ancestry also plays a role – a higher percentage of people with East Asian ancestry have this version of the SNP. Fewer people with European or African ancestry have this variant.
Since we’re talking about bodily functions we might as well mention that this same SNP is also associated with whether you have <a href="https://www.23andme.com/topics/traits/earwax-type/">wet or dry earwax</a>.
While these associations have to do with physical traits, what the researchers in Bristol were looking at was behavior. Specifically, they investigated if use deodorant depended on whether or not an individual had a genetic predisposition toward sweating.
What they found was not too surprising: if you have the genetic variant that is associated with more body odor you’re more likely to use deodorant.
But the study – which looked at more than 17,000 people – also found that behavior may be explained by cultural influences. For instance, while the percent of women who probably should use deodorant but choose not to was pretty small, a whopping 13 percent of the men in the same genetic boat don’t use deodorant when they probably should. Yikes.

Smells Like Gene Spirit

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You may lack the enzyme thiopurine methyltransferase (TPMT) and not even know it.



<h6 class="wp-block-heading" id="h-serious-side-effects">Serious Side Effects</h6>



<figure class="wp-block-image alignright size-medium"><img loading="lazy" decoding="async" width="300" height="285" src="http://35.88.189.111/wp-content/uploads/2010/11/cartoon-pills-300x285.png" alt="An image of prescription bottles. " class="wp-image-7843" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/11/cartoon-pills-300x285.png 300w, https://blogcms.23andme.com/wp-content/uploads/2010/11/cartoon-pills.png 478w" sizes="auto, (max-width: 300px) 100vw, 300px" /><figcaption class="wp-element-caption">Some of the more common thiopurine drugs:
6-Thioguanine (Lanvis ®)
6-Mercaptopurine (Purinethol ®)
Azathioprine (Azasan ®, Imuran ®)</figcaption></figure>



For most of those who lack the enzyme, it will never be a problem, but, for those who are prescribed thiopurine medication, the lack of functional TPMT enzyme could lead to <a href="https://blog.23andme.com/articles/23andme-customers-reported-side-effects-to-drugs">serious side effects</a>.



Thiopurines are a family of drugs that are used to “turn down” or suppress the immune system, which can be useful when you want to reduce inflammation, for instance.



They&#8217;re used in a variety of treatments for such conditions as <a href="https://blog.23andme.com/articles/more-than-100-genetic-variations-associated-with-leukemia-treatment-response">leukemia</a>, organ transplant rejection, rheumatoid arthritis, Crohn&#8217;s disease, and inflammatory bowel disease.



<h6 class="wp-block-heading" id="h-pharmacogenetic-testings">Pharmacogenetic Testings</h6>



While these are important drugs for many individuals, for those who lack functional TPMT enzyme, thiopurines cause serious side effects, such as bleeding and low blood count. &nbsp;Because of these potential side effects, a doctor can test for TPMT enzyme activity before prescribing thiopurine drugs, but a test isn’t always done.



There are a couple of different types of tests available. &nbsp;One type of test looks at the levels of TPMT enzyme directly. &nbsp;Another type of test looks for mutations in the gene that encodes the TPMT enzyme. &nbsp;Approximately 10 percent of people with European ancestry have reduced TPMT activity due to having inherited one mutant TPMT gene. About 0.3 percent have none at all due to having inherited two mutant copies.

Genetics and Response to Thiopurine Medications

<img loading="lazy" decoding="async" class="aligncenter wp-image-17124 size-full" title="Flu" src="http://35.88.189.111/wp-content/uploads/2013/01/Flu.jpg" alt="" width="283" height="424" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/01/Flu.jpg 283w, https://blogcms.23andme.com/wp-content/uploads/2013/01/Flu-200x300.jpg 200w" sizes="auto, (max-width: 283px) 100vw, 283px" />
A sure way to make you more diligent about washing your hands is to read some<a href="https://www.nytimes.com/2013/01/10/health/flu-widespread-leading-a-range-of-winters-ills.html?ref=health"> coverage</a> of what’s turning out to be the worst flu season in recent memory.
<h2>Norovirus</h2>
A lucky few of us, however, have defenses that go beyond trusty soap and water – our genes. Approximately 30 percent of people with European ancestry and 20 percent of those with African ancestry carry a mutation that gives them extra protection against the most common strains of norovirus.
Norovirus is one of the three flu or flu-like viruses now spreading across the globe during this sick season.
<h2>Flu Season</h2>
What makes this so bad is what the New York Times <a href="https://www.nytimes.com/2013/01/10/health/flu-widespread-leading-a-range-of-winters-ills.html?ref=health">describes</a> as “the convergence of three flu or flu-like epidemics” hitting all at once. These three illnesses include an unusually virulent flu virus,  a nasty norovirus, and a whooping cough outbreak that&#8217;s as bad as it&#8217;s been in 60 years. As the article indicates, this all happens “amid the normal winter highs for the many viruses that cause symptoms on the colds and flu spectrum.” It&#8217;s not a pretty picture for those who fret about getting ill.
The Centers for Disease Control (CDC) is a little less breathless in its description of flu season, but officials there are still heralding a warning.
According to the CDC&#8217;s Dr. Joe Bresee, “Reports of influenza-like illness (ILI) are nearing what have been peak levels during moderately severe seasons.” The CDC continues to recommend flu shots and antiviral medication when appropriate.
<h2>Norovirus Symptoms</h2>
So, let’s focus on the norovirus, which is sometimes described as the “stomach flu.” In reality, it isn’t the flu but “viral gastroenteritis.”
This nasty bug is hugely contagious and pretty unpleasant, with symptoms that include abdominal pain, vomiting, and diarrhea. It spreads quickly, especially in close quarters, and can rapidly rip through schools, retirement communities, and hospitals. This latest outbreak is hitting the US right as the flu is spreading. This particular strain hit England a few weeks ago, making more than a million people ill, according to<a href="http://www.guardian.co.uk/society/2013/jan/08/norovirus-vomiting-bug-festive-period"> the Guardian</a>.
<h2>Genetic Protection</h2>
&#8216;Some people may be safer than most during this illness. About 30 percent of people with European ancestry and about 20 percent with African ancestry carry the AA version of SNP rs601338 in the FUT2 gene. These lucky folks need not fear the most common strain of norovirus like the rest of us. They lack the molecules noroviruses use to enter the digestive tract cells.  It doesn’t mean they are bulletproof from getting sick, but they are protected against most norovirus strains. Unfortunately, very few people of Asian ancestry carry the resistant genetic variant.
Whether you belong to the fortunate ones who carry this extra genetic protection or not, it is still a good idea to keep washing your hands. If you haven&#8217;t already, you might also consider getting a flu shot if it is available.

Genetic Armor in Flu Season

<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-17116" title="Virginia Hughes" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2013/01/Virginia-Hughes-300x173.jpg" width="300" height="173" />
Thank you, Virginia.
In<a href="https://www.slate.com/articles/health_and_science/medical_examiner/2013/01/ethics_of_genetic_information_whole_genome_sequencing_is_here_and_we_need.single.html"> a recent article</a> in Slate, <a href="http://virginiahughes.com/" target="_blank" rel="noopener noreferrer">Virginia Hughes</a>, who also blogs for National Geographic, nails it, hammering home the point that people are much smarter and tougher than they’re depicted in many news articles about genetic testing.
We’ve written before about what feels like fear mongering in some stories about DNA testing. Hughes writes that a lot of the media coverage is stuck on the same refrain that people won’t be able to handle the information they get from genetic testing.
“&#8230;this is the wrong question, or at least one that’s becoming increasingly irrelevant,” Hughes writes. “The personal genomics horse has bolted, and yet many paternalistic members of the medical community are still trying to shut the barn door. In doing so, they’re fostering a culture of DNA fear when what we really need is a realistic and nuanced genetics education.”

That last point, the need for more genetic literacy is key. Instead of covering the gap in genetic knowledge, some writers play up this diffuse fear that a test is going to tell you your destiny or that the information is just too difficult to handle.
Hughes argues that the commonly-expressed opinion, “…that a nonexpert couldn’t possibly understand the concept of uncertain risk and would therefore be harmed by the knowledge” is “patronizing” and “probably false.”
She goes on to say that it’s better to deal with the reality that people want access to their genetic information, and that more and more people are getting tested every day. It’s time to bring a more nuanced approach to how we talk about it.
A Hughes writes, “There’s no way around the fact that genomes are complicated and, at least for now, difficult to interpret. And sometimes, yes, they will lead to unpleasant information. But [genetic information] isn’t going to suddenly fade away. More and more people are getting their DNA sequenced and eager to find out what secrets, if any, it holds. So let’s figure out how to tell them.”
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