By Amick B.
<img loading="lazy" decoding="async" class="aligncenter wp-image-18399 size-full" src="http://35.88.189.111/wp-content/uploads/2013/06/mug_drinking.png" alt="" width="507" height="407" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/06/mug_drinking.png 507w, https://blogcms.23andme.com/wp-content/uploads/2013/06/mug_drinking-300x241.png 300w" sizes="auto, (max-width: 507px) 100vw, 507px" />
There are many studies that look at the health impacts of drinking coffee, but you’d be forgiven if you weren’t clear about whether it’s good for you.
Research has found consuming coffee could potentially prevent heart disease, type-2 diabetes, Parkinson’s disease and liver cancer, but the results are often conflicting. Beyond that, other variables can potentially negate any benefits from drinking a cup of Joe.
<h6>Variables</h6>
Whether you like your coffee black or with a bit of cream and sugar, for example, makes a difference for your health.
How much you drink and even the kinds of filters you use to make coffee could also have an impact.
All the conflicting information is enough to keep non-coffee drinkers from lining up at Starbucks, while those who indulge are left scratching their heads about whether they need to cut back or keep on imbibing.
<h6>Love Coffee</h6>
But there’s one area where the science seems certain:   Some of us are just more genetically wired to like coffee. A number of studies have identified certain genetic variants associated with <a href="http://www.23andme.com/topics/wellness/caffeine-consumption/">caffeine consumption</a> and metabolism, which helps us know why some of us choose coffee, and others don’t.
Recently, a <a href="https://www.ncbi.nlm.nih.gov/pubmed/21876539" target="_blank" rel="noopener noreferrer">new study</a> found some additional genetic variants associated with a tendency toward java enjoyment, including one near NRCAM, a gene implicated in vulnerability to addiction.   The study looked at nearly 8,000 Caucasian coffee drinkers and found significant evidence of gene association at the single nucleotide polymorphism (SNP) near NRCAM.
Using coffee consumption as a model, this new research may help scientists better understand genetic problems with addiction and how to treat them.
<h6>Metabolizing Caffeine</h6>
The recent study also looked at two SNPs that lie in the region between CYP1A1 and CYP1A2 genes — CYP1A1 is known to metabolize polycyclic aromatic hydrocarbons, which are important constituents of coffee, whereas caffeine is primarily metabolized by CYP1A2. The study confirmed previous studies and added a new SNP, to the list of those associated with consumption of coffee and metabolism of caffeine.
23andMe looks at a variant that affects how quickly a person  metabolizes caffeine based on preliminary research of the SNP. People with and the slower version of the CYP1A2 enzyme who also drank at least two to three cups of coffee per day had a significantly increased risk of a non-fatal heart attack, according to the research, while, according to the study, fast metabolizers could actually reduce their heart attack risk by drinking coffee.
<h6>A Look Back</h6>
Additionally, in a 2011 blog post, 23andMe discussed <a href="https://blog.23andme.com/23andme-research/snpwatch/coffee-i-must-have-coffee/">two studies</a> that found an association between coffee and caffeine consumption and SNP variants near the CYP1A1 and AHR genes, helping us know which genes influence the amount of coffee people consume.   One study found the SNP near CYP1A1 had a fairly consistent effect – people with the T version were prone to drink about a quarter cup more of coffee a day — and the other showed that people with two copies of a T at near the AHR gene drank  about a third of a cup of coffee more each day than those without any copies.
To find out whether genetic variants influence their caffeine consumption, 23andMe customers can look up their data for and using the Browse Raw Data feature.
Amick Boone is a freelance writer who&#8217;s written about health and life sciences for nearly 10 years.  When she&#8217;s not at her computer, she&#8217;s usually in motion &#8211; doing yoga, riding her bike or traveling.

Amick Boone

Craving Coffee Might be Genetic

Robin Smith, Health Content Scientist
Some scientists believe that lobsters could live virtually forever, barring injury, disease, or capture. They are among a select group of animals, including tortoises, clams, and jellyfish, that are &#8220;negligibly senescent.&#8221;
<img loading="lazy" decoding="async" class="wp-image-17393 size-medium" src="http://35.88.189.111/wp-content/uploads/2013/01/Telomere_caps-300x236.gif" alt="" width="300" height="236" />
They don&#8217;t age much. So why aren&#8217;t we so lucky?
<h2>Consider the Lobster</h2>
Unlike lobsters, our cells cannot replicate and renew themselves throughout our lives. One cause of this limitation is our telomeres, which are DNA segments at the ends of our chromosomes that get shorter with each replication.
When a cell&#8217;s telomeres get too short, it can no longer replicate and eventually dies. A few cells—namely adult stem cells, sperm, and egg cells—are not limited by this process, though. These cells have a telomerase enzyme that can rebuild telomeres when they get too short. This process is hijacked by cancer cells, which become effectively immortal by turning on telomerase.
<h2>Telomeres and Aging</h2>
There are several indications that telomere length is a good predictor of longevity. In newborns, telomere length varies from about 8,000-13,000 &#8220;<a href="https://www.23andme.com/gen101/genes/#basics">base pairs</a>&#8221; (DNA letters) in length and declines by about 20-40 base pairs each year. Telomeres are also longer in <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1196417/">women than men</a>, mirroring the difference in lifespan between the sexes. In elderly twins, the twin with shorter telomeres is roughly <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=17925004">three times more likely</a> to die first.
The variability in telomere length between people of the same age is not random and has a genetic component that has interested scientists for decades. In a recent <a href="https://dx.doi.org/10.1038/ng.2528">study</a> in the Nature Genetics journal, scientists identified multiple markers associated with either shorter or longer telomeres.
The strongest of these resides near a gene named TERC. Each copy of a “T” at this position is associated with an average 117 base pair decrease in telomere length, equivalent to having the &#8220;biological age&#8221; of a person about four years older.
<h2>Other Factors in Aging</h2>
A person&#8217;s genetic makeup is not the only determinant of telomere length; environmental factors such as <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=16112303">smoking and obesity</a> bring about premature telomere shortening.
Telomere length is also highly influenced by the father&#8217;s age at conception. Because sperm cells are one of only a few types of cells that maintain or even increase their telomere length over time, the trend is for older fathers to have children with longer telomeres.
This effect can even carry over to a second generation, including grandchildren. It&#8217;s interesting to speculate that trends in some societies towards delaying parenthood may have the unexpected benefit of boosting life expectancy. Any such benefit, however, would have to be weighed against the known <a href="https://blog.23andme.com/health-traits/for-older-dads/">risks</a> of being an older dad.

23andMe Blog

23andMe Blog Team

Getting Long in the Telomeres

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-1138" title="fundus" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2008/08/fundus-300x222.jpg" width="300" height="222" /> 
Genetics plays a big role in the development of age-related macular degeneration (AMD), one of the leading causes of vision loss among older Americans.
Luckily, there are ways to lower the risk through diet.
Recently the National Institutes of Health slightly<a href="http://www.nei.nih.gov/news/pressreleases/050513.asp"> changed its recommendations</a> regarding a combination of vitamins and minerals recommended to protect against AMD.
About two million Americans have advanced AMD and another eight million are at risk, according to the NIH.
Millions of Americans are already taking high daily doses of vitamins C and E, beta-carotene and the minerals zinc and copper. Earlier studies showed that that formula – known as the Age-Related Eye Disease Study (AREDS) formulation – could significantly cut the risk for AMD.


Now the NIH is recommending replacing the beta-carotene with the carotenoids lutein and zeaxanthin, both found in leafy greens such as kale, spinach and broccoli. This is based on a new study that found that making the change improved the protective power of the formula.


Looking at participants in the study, researchers found that the revised formula reduced the risk of AMD by about 18 percent compared to the previous formula. For those individuals who prior to the study didn’t get a lot of lutein and zeaxanthin in the diet, the change had an even greater beneficial effect, cutting the risk of AMD by as much as 25 percent.

For Your Eyes Only

<img loading="lazy" decoding="async" class="alignright size-full wp-image-8490" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2011/02/mammogramblog.jpg" width="300" height="199">
<a href="https://www.nytimes.com/2013/05/14/opinion/my-medical-choice.html?ref=health">Angelina Jolie’s revelation</a> in the New York Times today that she had a double mastectomy after learning about her genetic risk for breast cancer focused attention on the difficult dilemma faced by many women in similar circumstances.
Jolie said she decided to write about her case to help other women.
&#8220;I chose not to keep my story private because there are many women who do not know that they might be living under the shadow of cancer. It is my hope that they, too, will be able to get gene tested, and that if they have a high risk they, too, will know they have strong options,&#8221; she wrote.
The revelation has also prompted some of our customers to ask about what 23andMe reports concerning breast cancer.
First 23andMe’s test is not diagnostic. Our report on BRCA1 and BRCA2 looks at only three mutations in those two genes associated with breast cancer.
Finally, we inform customers that the absence of the mutations does not rule out the possibility that they may carry another cancer-causing variation in one of those genes.

Talking About Breast Cancer Risk

<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-17920" title="Football" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2013/04/Football-300x200.jpg" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/04/Football-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2013/04/Football.jpg 424w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Mounting <a href="http://www.nejm.org/doi/full/10.1056/NEJMp1007051">evidence</a> points to brain trauma as a risk factor for mental decline. Football players who’ve had multiple concussions <a href="https://www.ncbi.nlm.nih.gov/pubmed/10485682">perform worse</a> on tests of brain function and are more likely to have memory <a href="https://www.ncbi.nlm.nih.gov/pubmed/16239884">problems</a> later on. Repeated blows to the head can also cause certain types of dementia &#8212; medically referred to as “chronic traumatic encephalopathy” and historically called “<a href="https://en.wikipedia.org/wiki/Dementia_pugilistica">punch-drunk syndrome</a>” in boxers. These <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3400421/">athletes</a> usually suffer repeated onslaughts, but <a href="http://www.nejm.org/doi/full/10.1056/NEJMp1007051">research suggests</a> that even an isolated severe brain injury might be enough to increase risk for conditions like Alzheimer’s disease.
(A severe traumatic brain injury is one that leads to a concussion and unconsciousness for 30 minutes or more.)
Research also suggests that DNA may play a role in how susceptible we are to mental decline after head trauma. Numerous genes have been <a href="https://www.sciencedirect.com/science/article/pii/S1474442212702260">implicated</a> but the most plausible connection is with a gene named APOE. A version of this gene called e4 is firmly linked to higher risk for Alzheimer’s and researchers are studying people with the e4 variant to see if they are more likely to show signs of mental decline after brain injury compared to people without this genetic variant.
But how might the APOE e4 variant affect our ability to recover from a traumatic brain injury? Research on Alzheimer’s offers some clues.
<div style="float: right; text-align: justify; width: 250px; background-color: #e6e6e6; padding: 10px; margin-left: 15px; margin-bottom: 15px; font-size: 12px;">Sizing up head trauma 
More than <a href="https://www.ncbi.nlm.nih.gov/pubmed/18162698">10 million</a> people around the world suffer a traumatic brain injury every year and a staggering <a href="https://www.cdc.gov/traumaticbraininjury/statistics.html">1.7 million</a> of these injuries occur in the USA. This makes traumatic brain injury the leading cause of death and disability in Americans under the age of 35. Most <a href="http://www.mayoclinic.com/health/traumatic-brain-injury/DS00552/DSECTION=causes">cases of brain injury</a> result from falls and car accidents, but contact sports and modern warfare are also contributors. </div>
It’s not clear exactly why people with the e4 variant are more likely to develop Alzheimer’s, but it is known that the brains of people with this variant <a href="http://ghr.nlm.nih.gov/gene/APOE">have more protein clumps</a>, called amyloid plaques, than the brains of people without the variant. It’s possible that these plaques cause neurons in the brain to die.
Up to <a href="https://www.ncbi.nlm.nih.gov/pubmed/8163989">30% of people</a> who suffer a severe traumatic brain injury also have plaques. These plaques seem to develop very quickly &#8212; sometimes <a href="https://www.sciencedirect.com/science/article/pii/S0014488604002420">within two hours</a> &#8212; after injury. It’s possible that people with the e4 variant are simply more likely to develop plaques in their brains &#8212; perhaps even more so with trauma &#8212; and this predisposes them for developing cognitive problems.
Scientists have long thought that our genes interact with our environment to impact our health. In the case of mental decline and dementia, preliminary research suggests a connection between the APOE e4 variant and severe brain injury, but findings are inconsistent and more research is needed to know for sure.
Not everyone who suffers a brain injury or has the e4 variant will develop dementia or other cognitive problems. But being aware of the risk can help you be proactive in avoiding head injuries in the first place. You can keep your brain active, through social engage ­ment or “<a href="https://abcnews.go.com/blogs/health/2012/01/23/brain-games-may-help-thwart-alzheimers-study/">brain games</a>” like Sudoku, in order to lower your risk of mental decline.
Recommended reading:

<a href="http://www.mayoclinic.com/health/alzheimers-disease/AN01710">What types of brain injury carry a risk for mental decline?</a> 
<a href="http://www.alz.org/dementia/traumatic-brain-injury-head-trauma-symptoms.asp">Traumatic brain injury and Alzheimer’s disease</a> 
Prevention strategies for Alzheimer’s disease 
<a href="https://dopasolution.com/dementia/">Online Resources That Meet W3C Guidelines for Accessibility</a>

Brain Injury, Mental Decline, and the APOE Gene

<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-17819" title="mediterranean diet" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2013/03/mediterranean-diet-200x300.jpg" width="200" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2013/03/mediterranean-diet-200x300.jpg 200w, https://blogcms.23andme.com/wp-content/uploads/2013/03/mediterranean-diet.jpg 283w" sizes="auto, (max-width: 200px) 100vw, 200px" />
Your diet has a huge impact on your health, particularly influencing your risk for things like heart disease, the leading cause of death worldwide.
Your genetics equally contributes to your risk for heart disease the same as your diet, your environment and overall lifestyle does.
Understanding your risks can help you take the right actions to stay as healthy as you can. With heart disease, the simplest ways to reduce your risk is with diet and exercise. A recent<a href="http://www.nejm.org/doi/full/10.1056/NEJMoa1200303?query=featured_home?=article"> Spanish study</a> published in the New England Journal of Medicine showed that changing what you eat may go a long way at protecting you from heart disease. The study suggests a Mediterranean diet – which is rich in vegetables, fruit, legumes, fish, olive oil and nuts – can significantly reduce the risk of death from heart attack or stroke in people at highest risk.
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How Your Body Responds 

A Mediterranean diet could ward off heart disease, but how does it effect whether you gain or lose weight?
Your genetics can influence how your body metabolizes and uses food. This   explains a bit about why some people have a much easier time losing weight than others.
</div>
The study gives hope. The researchers looked at more than 7,000 Spaniards who were overweight, smoked or had other conditions that put them at them at higher risk for heart disease. The participants ranged in age from 55 to about 80. Researchers at the University of Barcelona separated the participants into three groups, one on a Mediterranean diet, another group that were on a Mediterranean diet that included additional extra virgin olive oil, nuts, fish, vegetables, fruit and wine. And a third group that was simply advised to stay on a low-fat diet.
About five years into the work, the benefits of the Mediterranean diet were so strong – groups on the Mediterranean diets were 30 percent less likely to have a heart attack or stroke – that the researchers stopped the study early.
While there are some caveats to the study, it strongly suggests a simple change in what you eat – independent of whether you lose weight or exercise – could significantly reduce your risk for heart disease. This is particularly good news for people who want to lower their risk but are having a hard time losing weight.
While the benefits for this high-risk, elderly population of Spaniards seems pretty clear, what is less clear is whether changing to a Mediterranean diet would offer the same benefits for everyone. Because the study specifically looked at people who were at high risk for heart disease, it’s unclear if diet alone can reduce heart disease risk in the general population, too. Unfortunately the study also didn’t look at how people with different genetics might respond to the diet changes. We know genetics has a strong influence on your risk for heart disease, but we don’t know if people with different genetics would respond differently to this diet.
Whether the benefits could apply to people who are at low risk is not yet known, but it probably couldn’t hurt to reduce the amount of sweets, saturated fats and processed foods in favor of a diet rich in olive oil, nuts, beans, fish, fruits and vegetables. The fact that the diet also includes a drink of wine with each meal is a nice bonus as well.

Heart Disease, Genetics and the Mediterranean Diet

<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-8468" title="Flour wheat celiac" src="https://blog-api.23andme.com/wp-content/uploads/2011/02/iStock_000014686955XSmall-300x199.jpg" alt="" height="199" width="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/02/iStock_000014686955XSmall-300x199.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2011/02/iStock_000014686955XSmall.jpg 425w" sizes="auto, (max-width: 300px) 100vw, 300px" />

Editor&#8217;s note: This post has been altered to reflect 23andMe&#8217;s new product offering.


By Amick B.

Like other autoimmune diseases, <a href="http://www.23andme.com/topics/health-predispositions/celiac-disease/">celiac disease</a> has a strong genetic component, but new research shows that environmental factors, including an exposure to a variety of microbes in our water and in dust, may also play an important role.
A recent<a href="https://www.nytimes.com/2013/02/24/opinion/sunday/what-really-causes-celiac-disease.html?pagewanted=all&#038;_r=0"> New York Times article</a> reported that the amount of bacteria in the gut affects whether the immune system treats glut
en as food or as a deadly invader.  Research also showed that breast-feeding, which increases this important group of intestinal bacteria — called bifidobacteria — may protect against the disease.
This finding is related to other<a href="https://blog.23andme.com/news/is-autoimmunity-a-result-of-genetic-adaptation-to-pathogens/"> recent research that suggests</a> versions of SNPs associated with increased risk for autoimmune diseases may come from immune defenses originally evolved to protect people from infectious organisms.  This means that the very same genetic adaptations that protected our ancestors from harmful pathogens may now have undesirable consequences in our “cleaner” modern societies where those pathogens are no longer common. 
For people with celiac disease, the simple act of eating food with gluten – a protein found in wheat and other grains – triggers an immune response that mistakenly attacks their digestive system. The disease strikes people who inherit certain versions of a protein called HLA-DQ, one of the proteins the immune system cells use to mark foreign proteins for attack.
The versions of HLA-DQ that are associated with celiac disease bind to gluten as if it were a threat; this mistaken immune response damages the villi lining the small intestine, undermining the absorption of nutrients and ultimately causing symptoms ranging from stomach aches and diarrhea to iron deficiency.
While 30-to-40 percent of all people have the versions of HLA-DQ that increase the risk for celiac disease, only about one percent of the U.S. population, or about two million people, actually gets the disease. While genetic proclivity makes us susceptible, some kind of other immunological trigger is required to kick the disease into gear.
Along with certain genetic markers, the risk factors for celiac include having European ancestry, a family history of celiac disease and a personal history of other autoimmune disorders.


Celiac disease should not be confused with other problems related to gluten, namely wheat allergies and gluten intolerance. Wheat allergies trigger responses that range from hives to sneezing and wheezing. Unlike celiac disease, gluten intolerance triggers a response that comes from innate immunity — the body using its normal immune response to repel gluten as if it were an invader — causing a direct response in the form of inflammation inside and outside of the digestive tract.


Celiac disease comes from adaptive immunity, a more sophisticated system in which genes activate specific cells to fight foreign bodies. With celiac disease, one’s own tissue lining of the small intestine is attacked as a result of this adaptive immunity. The only treatment for celiac disease is adherence to a completely gluten-free diet. Luckily this completely alleviates symptoms for most people with the disease and allows the damage to their intestines to heal.
Unfortunately, we don’t have much control over the microbes in our environment, but we can at least educate ourselves to recognize the symptoms of Celiac Disease if and when they appear.
Amick Boone is a freelance writer who&#8217;s written about health and life sciences for nearly 10 years.  When she&#8217;s not at her computer, she&#8217;s usually in motion &#8211; doing yoga, riding her bike or traveling.

Genetics, Microbes and Celiac Disease

<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-13288" title="CancerInfographic" alt="" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/CancerInfographic-300x254.jpg" width="300" height="254" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/CancerInfographic-300x254.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/05/CancerInfographic-768x650.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/05/CancerInfographic.jpg 849w" sizes="auto, (max-width: 300px) 100vw, 300px" />
A new study by researchers at Boston’s<a href="http://www.brighamandwomens.org/"> Brigham and Women’s Hospital</a> draws attention to the value of online resources to document family medical history.
23andMe customers can record their family medication information in several ways, including through our Cancer Family History survey – men’s version and women’s version.
Having a simple record of the conditions your siblings, parents, aunts, uncles and grandparents have faced can help both you and your doctor know what to watch out for to keep you healthy. But often people don’t know or have failed to keep track of that valuable information, making it harder for doctors to assess risks for things like cancer or other chronic diseases.
Scientists at 23andMe<a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002973"> have shown</a> how using family history information together with genetic testing can offer even better risk prediction for disease.
The new study published in the<a href="http://rd.springer.com/article/10.1007%2Fs11606-013-2338-z"> Journal of General Internal Medicine</a> found that offering a simple online tool to track that history can help. About 10,000 patients were given an opportunity to fill out their family health histories and lifestyle information online while they waited for their physician visit.  When they completed the questionnaire, patients were given a report that summarized their risks for cancer, heart disease, diabetes and stroke. The physician could also choose to transfer the submitted information into the patients’ electronic medical records. About 6,000 other patients in the study simply saw their physician as usual.
The study found that the online tool offered patients a chance to document important family medical history and helped doctors document histories of disease that otherwise would have been missed.
About 1,000 patients ended up filling out the tool, or 10 percent of those who were given the opportunity. Overall, two percent of those who had a chance to fill out the online tool had their family history information incorporated into their medical record within 30 days compared to 0.6 percent of patients that were not given the tool. Of those who filled out the tool, 10 percent had family history information incorporated into their medical record compared to 0.8 percent of patients that would have been likely to fill out the tool had they been given the chance. This may indicate that among patients motivated to provide their family history information, the tool increases the probability that the information is captured in their medical record.
While the study’s findings are very preliminary, it does suggest the value of online tools for better documenting family medical history information. Still, only 10 percent of those given the chance actually filled out the online tool, citing lack of time as the main reason. This suggests that providing access to the online tool well before the appointment (rather than in the waiting room) would increase uptake.
In a press release concerning the study, Baer said “This type of risk assessment tool may be useful for collecting information on family history and lifestyle factors and may also help increase communication between physicians and patients about their risk.”

23andMe Medical History

<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.

Health + Traits — Page 26