You are on page 1of 23

8/2/12

23andMe Printable Report

23andMe Genetic Health Overview
Prepared for: Printed on: JOAKIM
JARDENBERG Aug
2,
2012

What this overview includes
This overview includes brief summaries of your 23andMe results for: diseases for which you are at greater than average genetic risk, heritable diseases for which you carry one or more genetic variants (carrier status), and drugs to which you are likely to have an atypical response based on genetics. These results are based on your genetic data and any sex and ancestry information you have provided along with population-level risk data for specified age ranges. They do not take into account non-genetic factors, family history, or additional genetic factors that may influence these conditions. Only results for genetic associations that are scientifically well established are included. This overview does not provide details regarding diseases for which you are at typical or lower than average genetic risk, heritable diseases for which you aren't known to carry a variant, or drugs to which you are likely to have a typical response. If you would like more information on any of your 23andMe results, please go to that topic's individual report page on our website at https://www.23andme.com/you/health/.

https://www.23andme.com/user/report/health/

1/23

8/2/12

23andMe Printable Report

Overview
of
Genetic
Health
Joakim Jardenberg Year of Birth: 1966 Northern European Disease risk results are included in this overview only if your risk based on genetics is greater than 1%. Note that certain conditions may have genetic information applicable only to specific populations.
Components
of
this
test
were performed
in
a
clinical
laboratory regulated
under
the
Clinical Laboratory
Improvement Amendments
of
1988
(CLIA)
to perform
high-complexity
testing.
The data
provided
are
intended
for informational
and
educational
use and
are
not
for
diagnostic
use. *All
conditions
tested
are
listed
at
the end
of
the
report.
You
may
not
have data
for
every
report.

Disease
risk Coronary Heart Disease Venous Thromboembolism Atrial Fibrillation Age-related Macular Degeneration Restless Legs Syndrome Ulcerative Colitis 23 conditions* Carrier
status

Your
risk 67.4% 41.8% 33.9% 11.9% 2.5% 1.1%

Average
risk 46.8% 12.3% 27.2% 6.5% 2.0% 0.8%

Typical or decreased risk

Status Variant Present Variant Absent Response Increased Increased Typical Response

Congenital Disorder of Glycosylation Type 1a (PMM2CDG) 45 heritable conditions* Drug
response Pseudocholinesterase Deficiency Warfarin (Coumadin®) Sensitivity 6 other drugs*

https://www.23andme.com/user/report/health/

2/23

8/2/12

23andMe Printable Report

How
to
read
your
reports

https://www.23andme.com/user/report/health/

3/23

8/2/12

23andMe Printable Report

Coronary
Heart
Disease
Coronary heart disease (CHD), also called coronary artery disease, is a condition characterized by blockage of the arteries that supply the heart with blood. CHD can result in shortness of breath, chest pain (angina) and heart attack. It is a leading cause of death in both men and women worldwide. In the United States, about 1.2 million people will have a heart attack each year, and many of those heart attacks will be fatal. Healthy lifestyle choices play a major role in preventing CHD. If a heart attack does strike, prompt medical attention is vital.

Joakim's
Genetic
Risk

What
is
my
risk
based
on?

67.4%
Joakim's risk of developing Coronary Heart Disease between the ages specified

46.8%
Chance that the average person will develop Coronary Heart Disease

45 - 79

Men

European ancestry 15 genetic markers
rs10757278 (9p21 region), rs12526453 (PHACTR1), rs1746048 (CXCL12), rs1122608 (SMARCA4), rs9982601 (MRPS6), rs17465637 (MIA3), rs6725887 (WDR12), rs2306374 (MRAS), rs3798220 (LPA), rs11556924 (ZC3HC1), rs579459 (ABO), rs12413409 (CNNM2), rs964184 (APOA5), rs4773144 (COL4A2), rs2895811 (HHIPL1)

compared to average

1.44x

Genes
vs.
Environment
Heritability for coronary heart disease ranges from 39% to 56%, depending on the exact subtype of heart disease. This means that genetic factors and environmental factors contribute about equally to risk for coronary heart disease. There is also evidence that genetic factors may contribute slightly more to risk of death from coronary heart disease in men than they do in women. Genetic factors that play a role in coronary heart disease include both unknown factors and known factors such as the SNPs we describe here. Other factors that increase your risk include being older, being male, being African-American, smoking, having high blood cholesterol or high blood pressure, physical inactivity, being overweight, having diabetes, alcohol use, and stress.

Additional
Information
Symptoms Treatment for heart attack is most effective when started within one hour of the beginning of symptoms, which can include: chest discomfort or pain (uncomfortable pressure, squeezing, fullness that can recur and subside), upper body discomfort in one or both arms, the back, neck, jaw, or stomach, shortness of breath with or before chest discomfort, nausea or vomiting, lightheadedness/fainting, cold sweats. If you or someone else experiences any of these symptoms and a heart attack is suspected, call 911 or seek medical help immediately. Other
Medical
Conditions High cholesterol, diabetes, and hypertension can all increase your risk for coronary heart disease and its complications. Your health care provider can work with you to treat these related conditions to keep your heart healthy. Lifestyle
Factors Keep
a
healthy
diet: Eating right will help you keep your heart healthy, even if you have no underlying
https://www.23andme.com/user/report/health/ 4/23

8/2/12

23andMe Printable Report

cardiovascular disease. The American Heart Association has numerous resources and tools to help you make smart choices. Exercise
regularly: Having a sedentary lifestyle is a major risk factor for cardiovascular disease. For healthy people, the American Heart Association recommends performing any moderate-to-vigorous intensity aerobic activity for at least 30 minutes on most days of the week at 50-80% of your maximum heart rate. You can accumulate 30 minutes in 10 or 15 minute sessions. It’s a good idea to consult your health care provider before changing or beginning a new exercise regimen. Don't
smoke: Smoking greatly increases the risk of many cardiovascular diseases, including heart attack.
View
the
full
report
online
for
links
to
resources,
references,
and
more
detailed
genetic
results
and
information.

https://www.23andme.com/user/report/health/

5/23

8/2/12

23andMe Printable Report

Venous
Thromboembolism
Venous thromboembolism (VTE) encompasses two related conditions. The first, deep vein thrombosis or DVT, is the formation of a blood clot in a vein deep within the body, usually in the legs. The second, pulmonary embolism (PE), occurs if the clot breaks free and travels through the circulatory system to the lungs. DVT always precedes PE. It is estimated that about 250,000 people are hospitalized with venous thromboembolism in the United States each year, but the incidence is probably much higher as many cases go undiagnosed. Pulmonary embolism is potentially life threatening if prompt medical attention is not received. Therefore, recognizing the symptoms of venous thromboembolism and avoiding risk factors is of paramount importance.

Joakim's
Genetic
Risk

What
is
my
risk
based
on?

41.8%
Joakim's risk of developing Venous Thromboembolism between the ages specified

12.3%
Chance that the average person will develop Venous Thromboembolism

0 - 79

Men

European ancestry 3 genetic markers
rs6025 (F5), i3002432 (F2), rs505922 (ABO)

compared to average

3.39x

Genes
vs.
Environment
The heritability of venous thromboembolism is estimated to be 55%. This means that genetics (including unknown factors and known ones such as the SNPs we describe here) and environment play nearly equal roles in this condition. There are a number of environmental factors of various strengths that contribute to venous thromboembolism. Strong risk factors include hip or leg fractures, hip or knee replacement, major surgery or trauma, and spinal cord injury or surgery. Moderate risk factors include arthroscopic knee surgery, having central venous lines, congestive heart or respiratory failure, hormone replacement or oral contraceptive use, cancer, pregnancy, paralytic stroke, previous venous thromboembolism, and thrombophilia. Weak risk factors include bed rest for more than three days, immobility due to sitting (such as a long car or plane trip), specific types of chemotherapy, increasing age, laparoscopic surgery, obesity, and varicose veins.

Additional
Information
Symptoms Seek out medical attention immediately if you experience any of the following: DVT
(leg
clot)
symptoms: Swelling, usually in one leg Leg pain or tenderness Reddish or bluish skin discoloration Leg warm to touch PE
(lung
clot)
symptoms: Sudden shortness of breath Chest pain-sharp, stabbing; may get worse with deep breath Rapid heart rate Unexplained cough, sometimes with bloody mucus Medications
and
Treatment
https://www.23andme.com/user/report/health/ 6/23

8/2/12

23andMe Printable Report

Estrogen containing oral contraceptives and oral hormone replacement therapy are two commonly used medications that have been linked to increased clotting. Women taking these medications who also have genetic changes in their clotting factors and/or inhibitors are at especially high risk. Read more in the Oral Contraceptives, Hormone Replacement Therapy and Risk of Venous Thromboembolism Drug Response Report. Lifestyle
Factors Don't
smoke: A large Danish study found that women who smoked had a 52% increased risk for venous thromboembolism compared with women who had never smoked. For men, smoking conferred a 32% increase in risk. Heavy smokers had even higher risks. Maintain
a
healthy
weight: Obesity increases the risk of venous thromboembolism. Stay
active: Venous thromboembolism is sometimes called "economy class syndrome" because sitting still for long periods of time, as on a cramped airplane, can cause sluggish blood flow, which in turn increases the risk for the formation of blood clots.
View
the
full
report
online
for
links
to
resources,
references,
and
more
detailed
genetic
results
and
information.

https://www.23andme.com/user/report/health/

7/23

8/2/12

23andMe Printable Report

Atrial
Fibrillation
Atrial fibrillation is characterized by chaotic electrical signals in the heart that cause the upper chambers (atria) to quiver. It is the most common type of sustained irregular heart rhythm, and while it is not usually life threatening on its own, it can have deadly complications. Atrial fibrillation can disturb smooth blood flow, increasing the risk of clots that can cause organ damage or stroke. The heart's ability to pump blood can also deteriorate, leading to heart failure. The most common causes of atrial fibrillation are heart abnormalities and heart muscle damage, but in at least 10 percent of cases there is no underlying heart disease that explains the condition.

Joakim's
Genetic
Risk

What
is
my
risk
based
on?

33.9%
Joakim's risk of developing Atrial Fibrillation between the ages specified

27.2%
Chance that the average person will develop Atrial Fibrillation

0 - 79

Men

European ancestry 2 genetic markers
rs2200733 (4q25 (1)), rs10033464 (4q25 (2))

compared to average

1.25x

Genes
vs.
Environment
The heritability of atrial fibrillation is estimated to be 62%. This means genetic factors contribute more to differences in risk for this condition than environmental factors. Genetic contributions to atrial fibrillation include both unknown factors and known factors such as the SNPs described in this report. There are familial forms of atrial fibrillation caused by rare mutations, but most affected people do not have a family history of the condition. Non-genetic factors that can increase the risk of atrial fibrillation are age, obesity, stress, heavy alcohol or caffeine consumption, electrolyte imbalances, severe infections, diabetes and high blood pressure.

Additional
Information
Other
Medical
Conditions If you have a history of heart disease (including heart valve problems or a history of heart attack or surgery) your health care provider may work with you to manage these diseases to lower your risk for atrial fibrillation. Other medical problems, such as hyperthyroidism and sleep apnea, can also increase your risk for atrial fibrillation. Medications
and
Treatment If you have atrial fibrillation, your health care provider may prescribe medications that help control your heart rate and/or rhythm, or to prevent blood clots. If your atrial fibrillation cannot be controlled by medications, your health care provider may suggest a surgical procedure as treatment. Lifestyle
Factors Eat
healthy: A healthy diet will help keep your heart healthy, even if you have no underlying cardiovascular disease. The American Heart Association has numerous resources and tools to help you make smart choices. Consume
in
moderation: Heavy drinking has been associated with increased risk for atrial fibrillation.
View
the
full
report
online
for
links
to
resources,
references,
and
more
detailed
genetic
results
and
information.

https://www.23andme.com/user/report/health/

8/23

8/2/12

23andMe Printable Report

Age-related
Macular
Degeneration
Age-related macular degeneration (AMD) is the most common cause of irreversible vision loss in the western world among people over 60. The disease affects the central part of the retina, which is critical for activities like reading, driving, or even recognizing faces. AMD can develop so slowly that some people may not even realize they have it, while others suffer a rapid loss of sight in both eyes. More than 1.7 million people in the U.S. have AMD (about 7% of people over 75). It is estimated that by 2020, almost 3 million people will have the disease. Regular, comprehensive eye exams can detect the early signs of AMD. Though any vision that is lost to the disease cannot be restored, there are treatments that can slow AMD's progress.

Joakim's
Genetic
Risk

What
is
my
risk
based
on?

11.9%
Joakim's risk of developing Agerelated Macular Degeneration between the ages specified

6.5%
Chance that the average person will develop Agerelated Macular Degeneration

43 - 79

Men

European ancestry 5 genetic markers
rs1061147 (CFH), rs547154 (C2), rs3750847 (LOC387715/ARMS2), rs2230199 (C3), rs9621532 (TIMP3)

compared to average

1.81x

Genes
vs.
Environment
Estimates of the heritability of AMD vary from 45% to 71%. This means that genetic factors contribute at least as much as environmental factors do to risk of AMD. Genetic factors that play a role in AMD include known factors, such as the SNPs we describe here, and unknown factors. Established environmental risk factors include age, family history of AMD, cigarette smoking, low dietary intake or blood levels of antioxidant vitamins and zinc, and European ancestry. Other possible risk factors may include being female, having light-colored irises, a history of cardiovascular disease, or increased exposure to sunlight.

Additional
Information
Screening
and
Risk
Assessment Regular eye exams can help detect AMD early. Some websites have tools that can be used to check for macular degeneration. These tools do not replace an eye exam with a physician. Lifestyle
Factors Eat
fruits
and
vegetables: Having a diet rich in fresh fruits and dark green, leafy vegetables may delay or reduce the severity of AMD. Eat
fish
and
nuts: Eating fatty fish such as salmon, tuna or mackerel two to three times per week has been shown to slow the progression of AMD. Nuts, which contain healthy omega-3 fatty acids, also contain copper, which may play a role in preventing age-related eye diseases. Avoid
red
meat: People who consume red meat 10 times per week or more have a 47% higher risk for AMD. Don't
smoke: Smokers have two to three times increased risk for AMD compared to those who've never lit up.
View
the
full
report
online
for
links
to
resources,
references,
and
more
detailed
genetic
results
and
information.

https://www.23andme.com/user/report/health/

9/23

8/2/12

23andMe Printable Report

Restless
Legs
Syndrome
Imagine what it would be like to crawl into bed every night, ready to catch some much-needed Zs, only to be struck by an irrepressible urge to move your legs as soon as you began to relax. No matter how tired you were, instead of drifting off peacefully, you would be compelled to get up and move around. It may sound crazy, but this is exactly the situation people with restless legs syndrome (RLS) experience. Though the symptoms in many people are milder, it is estimated that about 4% of the U.S. population suffers from this puzzling disorder.

Joakim's
Genetic
Risk

What
is
my
risk
based
on?

2.5%
Joakim's risk of developing Restless Legs Syndrome between the ages specified

2.0%
Chance that the average person will develop Restless Legs Syndrome

0 - 79

Men

European ancestry 1 genetic markers
rs3923809 (BTBD9)

compared to average

1.25x

Genes
vs.
Environment
The heritability of restless legs syndrome is estimated to be 54%. This means that genetic and environmental factors contribute nearly equally to differences in risk for this condition. Genetic factors that play a role in restless legs syndrome include both unknown factors and known factors such as the SNPs we describe here. Environmental factors include pregnancy. Low iron levels, dialysis for end-stage renal disease, and damage to the nerves of the hands and feet tend to worsen the condition.

Additional
Information
Other
Medical
Conditions Chronic diseases such as kidney failure, diabetes, Parkinson's, and peripheral neuropathy can exacerbate symptoms of RLS. If you have RLS, your health care provider may work with you to manage these conditions to reduce your symptoms. Pregnancy can sometimes trigger symptoms of RLS. If this happens, the symptoms will usually disappear once the pregnancy is completed. Lifestyle
Factors Limit
caffeine,
alcohol,
and
tobacco
use: Caffeine, alcohol, and tobacco intake can trigger or aggravate symptoms in predisposed individuals. Get
enough
iron: Insufficient iron levels can also trigger or aggravate symptoms. Medications
and
Treatment Taking certain drugs can sometimes cause symptoms of RLS. These symptoms usually disappear once the drug regimen is stopped. Your health care provider can work with you to manage drug regimens that may be triggering RLS.
View
the
full
report
online
for
links
to
resources,
references,
and
more
detailed
genetic
results
and
information.

https://www.23andme.com/user/report/health/

10/23

8/2/12

23andMe Printable Report

Ulcerative
Colitis
Ulcerative colitis is an inflammatory bowel disorder that causes chronic inflammation of the colon and rectum. There are similarities between ulcerative colitis and Crohn’s disease, but the two conditions are distinct. Symptoms of ulcerative colitis vary, with the most common being abdominal pain and diarrhea. About 2 people out of every 1,000 are affected. A higher incidence of the disease is seen in people with European or Jewish ancestry. The cause of ulcerative colitis is unknown and there is no cure. Treatments can, however, calm inflammation and reduce symptoms.

Joakim's
Genetic
Risk

What
is
my
risk
based
on?

1.1%
Joakim's risk of developing Ulcerative Colitis between the ages specified

0.8%
Chance that the average person will develop Ulcerative Colitis

0 - 79

Men

European ancestry 4 genetic markers
rs2395185 (HLA-DRA), rs9858542 (BSN), rs10883365 (NKX2-3), rs11209026 (IL23R)

compared to average

1.42x

Genes
vs.
Environment
The heritability of ulcerative colitis is unknown, but is thought to be less than that of another form of inflammatory bowel disease called Crohn's disease, which is 50-60% heritable. This means that environmental factors probably contribute more to differences in risk for ulcerative colitis than genetic factors. Genetic factors that play a role in ulcerative colitis include both unknown and known factors, such as the SNPs we describe here. The environmental factors that contribute to ulcerative colitis are currently unknown. Doctors do know that the condition is not caused by stress or sensitivity to certain foods or food products, although both of these can aggravate symptoms in some people.

Additional
Information
Screening
and
Risk
Assessment Talk to your health care provider if you experience symptoms. Certain medications and dietary changes may alleviate symptoms and promote healing should you have the disease. Environmental
Factors Environmental factors are believed to trigger onset of the disease and subsequent flares but few specifics are known.
View
the
full
report
online
for
links
to
resources,
references,
and
more
detailed
genetic
results
and
information.

https://www.23andme.com/user/report/health/

11/23

8/2/12

23andMe Printable Report

Carrier
status:
Congenital
Disorder
of
Glycosylation
Type
1a
(PMM2-CDG)
Congenital disorder of glycosylation type 1a, now officially called PMM2-CDG, is caused by mutations in the PMM2 gene, which encodes a PMM protein. PMM performs the very important function of attaching sugar molecules to other proteins, a process called glycosylation. Glycosylation is needed for normal functioning of many systems in the body, and mutations in PMM2, which impair this process, may cause a variety of symptoms ranging from neurological problems to multi-organ failure. PMM2-CDG is an autosomal recessive disorder and only occurs when a PMM2 mutation is inherited from each parent. About one out of 80,000 people with European ancestry is diagnosed with PMM2-CDG every year, with incidence being about four times higher in those with Dutch or Danish ancestry. The condition is believed to be underdiagnosed.

Joakim's
Genetic
Results
Variant Present

Has
one
mutation
in
the
PMM2
gene
linked
to
PMM2-CDG1a.
A
person
with
one
of
these mutations
typically
does
not
have
PMM2-CDG,
but
can
pass
the
mutation
to
offspring.
May have
other
mutations
in
the
PMM2
gene
(not
reported
here). Gene PMM2 Markers
tested: 2 Variant R141H DNA
change G to A Joakim's
genotype AG

Coverage: > 50% in individuals with European ancestry

What
does
this
test
cover?
More than 80 mutations in the PMM2 gene causing PMM2-CDG have been documented. 23andMe reports data for the two most common disease-causing mutations which account for more than 50% of the disease in individuals with European ancestry.

How
is
Congenital
Disorder
of
Glycosylation
Type
1a
(PMM2-CDG)
inherited?
PMM2-CDG is inherited in a recessive manner, meaning that only a child who receives two mutated copies of the PMM2 gene (one from each parent) will develop the disease.

How
common
is
this
condition?
Approximately one in 80,000 individuals with European ancestry is diagnosed with PMM2-CDG each year. Incidence is about four times higher in those with Dutch or Danish ancestry.

Additional
Information
View
the
full
report
online
for
links
to
resources,
references,
and
more
detailed
genetic
results
and
information.

https://www.23andme.com/user/report/health/

12/23

8/2/12

23andMe Printable Report

Drug
response:
Pseudocholinesterase
Deficiency
Choline esters are a class of drugs used in medical procedures that require a person's muscles to be temporarily relaxed, such as general anesthesia with insertion of a breathing tube. Examples include succinylcholine (Scoline®, Anectine® and Quelicin®) and mivacurium (Mivacron®). Once one of these drugs is administered a patient has no muscle control, including breathing, until the drug wears off. This usually takes only about five minutes, but for some people the drugs' effects last longer due to a deficiency of pseudocholinesterase, the enzyme that breaks down choline esters in the body.

Joakim's
Genetic
Results
Increased

One
copy
of
one
of
the
BCHE
mutations
reported
by
23andMe.
Increased
risk
for
slightly extended
paralysis
and
apnea
after
treatment
with
choline
ester
drugs. Variants
detected:
Asp70Gly
(A) Gene BCHE BCHE BCHE Markers
tested: 3 Marker Asp70Gly (A) Thr243Met (F1) Gly390Val (F2) DNA
change T to C G to A C to A Joakim's
genotype CT GG CC

What
does
this
test
cover?
Mutations in the butyrylcholinesterase (BCHE) gene cause a deficiency in the enzyme that normally metabolizes choline ester drugs. 23andMe tests for three of the most common mutations in the BCHE gene linked to pseudocholinesterase deficiency, the "A" or "atypical" version (rs1799807), the "F1" version (rs28933389), and the "F2" version (rs28933390). Read more about the genetics.

Additional
Information
Symptoms Normally, the effects of choline ester drugs wear off in about five minutes. In people with pseudocholinesterase deficiency the recovery can take as long as several hours. During this time, they have no muscle control and cannot breathe on their own. Most people never know that they have pseudocholinesterase deficiency unless they are treated with a choline ester drug, although in some cases a personal or family history of adverse drug reactions to choline ester compounds can be suggestive. Read more about symptoms and management. Medications
and
Treatment People with known pseudocholinesterase deficiency may wear a medic-alert bracelet that will notify health care professionals of increased risk from administration of succinycholine. Because cocaine is a choline ester compound, mutations in BCHE may increase risk for adverse effects from cocaine use, including sudden cardiac death. Other
Risk
Factors Other variations in the BCHE gene not reported here can cause pseudocholinesterase deficiency. In addition, some variations also not reported here are associated with faster metabolism of choline ester drugs. People with these variations may be resistant to the muscle-relaxing effects of choline esters. Nongenetic factors contributing to pseudocholinesterase deficiency include pregnancy, malnutrition, chronic infections, cancer, liver disease, and other medications.
https://www.23andme.com/user/report/health/ 13/23

8/2/12

23andMe Printable Report
View
the
full
report
online
for
links
to
resources,
references,
and
more
detailed
genetic
results
and
information.

https://www.23andme.com/user/report/health/

14/23

8/2/12

23andMe Printable Report

Drug
response:
Warfarin
(Coumadin®)
Sensitivity
Each time a doctor writes a prescription for warfarin (Coumadin ®), a blood thinner given to about two million people each year in the United States, it's a guessing game. There is no "right" dose of the drug. Everyone is different and it can take weeks of adjustment to find a patient's optimal amount of the medication. Too much puts the patient at risk for bleeding. Too little can lead to clots and in turn, heart attack, stroke or even death. A patient's optimal dose depends not only on age, size, other medications and even diet, but also to a large extent on genetics.

Joakim's
Genetic
Results
Increased

Increased
warfarin
sensitivity.
May
require
decreased
warfarin
dose. Marker rs1799853 rs1057910 rs9923231 Markers
tested: 3 Joakim's
Genotype TT AA CC Genotype
combination: CYP2C9 *2/*2, VKORC1 -1639/3673 GG

What
does
this
test
cover?
Several genes involved in warfarin metabolism play prominent roles in the variable response to warfarin. 23andMe tests for two variants in the CYP2C9 gene (*2, defined using rs1799853, and *3, defined using rs1057910) that are associated with reduced ability to break down warfarin. 23andMe also tests for a variant near the VKORC1 gene (rs9923231) that is associated with increased sensitivity to the drug. Read more about the genetics.

Additional
Information
Other
Risk
Factors Many other clinical and demographic factors affect the optimal warfarin dose for an individual, including age, sex, weight, alcohol consumption, smoking status, ethnicity, vitamin K intake, and other medications. Other genetic variations in other genes (not reported here) can also impact a person’s response to warfarin. Only a medical professional can determine the optimal dose for an individual. Medications
and
Treatment Warfarin can interact with other medications, including some antibiotics, non-steroidal anti-inflammatory drugs, some antidepressants, cholesterol medications, and chemotherapy drugs. If you are taking one of these drugs, your health care provider can help devise appropriate treatment plans.
View
the
full
report
online
for
links
to
resources,
references,
and
more
detailed
genetic
results
and
information.

https://www.23andme.com/user/report/health/

15/23

8/2/12

23andMe Printable Report

Joakim
Jardenberg's
results
for
all
conditions
tested
by
23andMe
Conditions and diseases tested by 23andMe: This list is continually expanding as new genetic associations are discovered and reported. Please visit our website at https://www.23andme.com/health/all/ to view the most up-to-date list of conditions tested by 23andMe.
About
Risk
Estimates: 23andMe reports results as genotype-specific incidence, which is an estimate of how many individuals in a population composed of people with a customer's genotype are expected to be diagnosed with a condition given a specified ancestry and age range. These estimates are based on wellestablished genetic associations reported in the biomedical literature and do not account for non-genetic factors, family history, or additional genetic factors that may modify a customer's risk. The genotypespecific incidence estimate combines the odds for a condition for a customer's genotypes at a set of SNPs with data about disease incidence. For more information on how 23andMe calculates these estimates, please see our technical papers available at https://www.23andme.com/howitworks/.

Disease
risk
(29) Coronary Heart Disease Venous Thromboembolism Atrial Fibrillation Age-related Macular Degeneration Restless Legs Syndrome Ulcerative Colitis Celiac Disease Bipolar Disorder Scleroderma (Limited Cutaneous Type) Breast Cancer Chronic Kidney Disease Colorectal Cancer Gallstones Lung Cancer Lupus (Systemic Lupus Erythematosus) Melanoma Obesity Primary Biliary Cirrhosis

Your
risk 67.4% 41.8% 33.9% 11.9% 2.5% 1.1% 0.4% 0.2% 0.08%

Average risk 46.8% 12.3% 27.2% 6.5% 2.0% 0.8% 0.1% 0.1% 0.07%

Typical risk Typical risk Typical risk Typical risk Typical risk Typical risk Typical risk Typical risk Typical risk

Psoriasis Type 2 Diabetes Crohn's Disease Esophageal Squamous Cell Carcinoma (ESCC) Exfoliation Glaucoma Multiple Sclerosis Parkinson's Disease
https://www.23andme.com/user/report/health/

Typical risk Typical risk Decreased risk Decreased risk Decreased risk Decreased risk Decreased risk
16/23

8/2/12

23andMe Printable Report

Prostate Cancer Rheumatoid Arthritis Stomach Cancer (Gastric Cardia Adenocarcinoma) Type 1 Diabetes
About
Carrier
Status: 23andMe tests for specific genetic variants that are strongly linked to a number of inherited genetic conditions. These variants are typically the most common ones linked to the condition. Certain variants may be more common in certain populations than others. The absence of specific variants does not rule out the possibility that a customer may carry another variant linked to the condition.

Decreased risk Decreased risk Decreased risk Decreased risk

Carrier
status
(46) Congenital Disorder of Glycosylation Type 1a (PMM2-CDG) ARSACS Agenesis of the Corpus Callosum with Peripheral Neuropathy (ACCPN) Alpha-1 Antitrypsin Deficiency Autosomal Recessive Polycystic Kidney Disease Beta Thalassemia Bloom's Syndrome Canavan Disease Connexin 26-Related Sensorineural Hearing Loss Cystic Fibrosis D-Bifunctional Protein Deficiency DPD Deficiency Dihydrolipoamide Dehydrogenase Deficiency Factor XI Deficiency Familial Dysautonomia Familial Hypercholesterolemia Type B Familial Hyperinsulinism (ABCC8-related) Familial Mediterranean Fever Fanconi Anemia (FANCC-related) G6PD Deficiency GRACILE Syndrome Gaucher Disease Glycogen Storage Disease Type 1a Glycogen Storage Disease Type 1b Hemochromatosis (HFE-related) Hypertrophic Cardiomyopathy (MYBPC3 25bp-deletion) LAMB3-related Junctional Epidermolysis Bullosa Leigh Syndrome, French Canadian Type

Status Variant Present Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent

Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent
17/23

https://www.23andme.com/user/report/health/

8/2/12

23andMe Printable Report

(LSFC) Limb-girdle Muscular Dystrophy Maple Syrup Urine Disease Type 1B Medium-Chain Acyl-CoA Dehydrogenase (MCAD) Deficiency Mucolipidosis IV Neuronal Ceroid Lipofuscinosis (CLN5related) Neuronal Ceroid Lipofuscinosis (PPT1related) Niemann-Pick Disease Type A Nijmegen Breakage Syndrome Pendred Syndrome Phenylketonuria Primary Hyperoxaluria Type 2 (PH2) Rhizomelic Chondrodysplasia Punctata Type 1 (RCDP1) Salla Disease Sickle Cell Anemia & Malaria Resistance Tay-Sachs Disease Torsion Dystonia Tyrosinemia Type I Zellweger Syndrome Spectrum
About
Drug
Response: 23andMe displays your likely response to a number of drugs based on genetic variants associated with differences in response. These may be differences in sensitivity, in the likelihood or severity of side effects, or differences in disease risk tied to use of a drug. Only a medical professional can determine whether a drug is right for a particular patient. The information contained in this report should not be used to independently establish a drug regimen, or abolish or adjust an existing course of treatment.

Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Variant Absent Response Increased Increased Typical Typical Typical Typical Not Applicable

Drug
response
(8) Pseudocholinesterase Deficiency Warfarin (Coumadin®) Sensitivity Abacavir Hypersensitivity Alcohol Consumption, Smoking and Risk of Esophageal Cancer Clopidogrel (Plavix®) Efficacy Fluorouracil Toxicity Oral Contraceptives, Hormone Replacement Therapy and Risk of Venous Thromboembolism Response to Hepatitis C Treatment

Typical

https://www.23andme.com/user/report/health/

18/23

8/2/12

23andMe Printable Report

References
Coronary Heart Disease
Broadbent
HM
et
al.
(2008)
.
"Susceptibility
to
coronary
artery
disease
and
diabetes
is
encoded
by
distinct, tightly
linked
SNPs
in
the
ANRIL
locus
on
chromosome
9p."
Hum.
Mol.
Genet.
17(6):806-14 Preuss
M
et
al.
(2010)
.
"Design
of
the
Coronary
ARtery
DIsease
Genome-Wide
Replication
And
MetaAnalysis
(CARDIoGRAM)
Study:
A
Genome-wide
association
meta-analysis
involving
more
than
22
000 cases
and
60
000
controls."
Circ
Cardiovasc
Genet
3(5):475-83 Clarke
R
et
al.
(2009)
.
"Genetic
variants
associated
with
Lp(a)
lipoprotein
level
and
coronary
disease."
N. Engl.
J.
Med.
361(26):2518-28 Helgadottir
A
et
al.
(2007)
.
"A
common
variant
on
chromosome
9p21
affects
the
risk
of
myocardial infarction."
Science
316(5830):1491-3 Horne
BD
et
al.
(2008)
.
"Association
of
variation
in
the
chromosome
9p21
locus
with
myocardial
infarction versus
chronic
coronary
artery
disease."
Circ
Cardiovasc
Genet
1(2):85-92 Coronary
Artery
Disease
Consortium
et
al.
(2009)
.
"Large
scale
association
analysis
of
novel
genetic
loci for
coronary
artery
disease."
Arterioscler.
Thromb.
Vasc.
Biol.
29(5):774-80 Samani
NJ
et
al.
(2007)
.
"Genomewide
association
analysis
of
coronary
artery
disease."
N.
Engl.
J.
Med. 357(5):443-53 Wellcome
Trust
Case
Control
Consortium
(2007)
.
"Genome-wide
association
study
of
14,000
cases
of seven
common
diseases
and
3,000
shared
controls."
Nature
447(7145):661-78 Wang
F
et
al.
(2011)
.
"Genome-wide
association
identifies
a
susceptibility
locus
for
coronary
artery disease
in
the
Chinese
Han
population."
Nat.
Genet.
43(4):345-9 De
Bree
A
et
al.
(2002)
.
"Homocysteine
determinants
and
the
evidence
to
what
extent
homocysteine determines
the
risk
of
coronary
heart
disease."
Pharmacol.
Rev.
54(4):599-618 Kim
WY
et
al.
(2006)
.
"The
regulation
of
INK4/ARF
in
cancer
and
aging."
Cell
127(2):265-75 Do
R
et
al.
(2011)
.
"The
Effect
of
Chromosome
9p21
Variants
on
Cardiovascular
Disease
May
Be
Modified by
Dietary
Intake:
Evidence
from
a
Case/Control
and
a
Prospective
Study."
PLoS
Med
9(10):e1001106 Myocardial
Infarction
Genetics
Consortium
et
al.
(2009)
.
"Genome-wide
association
of
early-onset myocardial
infarction
with
single
nucleotide
polymorphisms
and
copy
number
variants."
Nat.
Genet. 41(3):334-41 Schunkert
H
et
al.
(2011)
.
"Large-scale
association
analysis
identifies
13
new
susceptibility
loci
for coronary
artery
disease."
Nat.
Genet.
43(4):333-8 Mehta
NN
et
al.
(2011)
.
"The
novel
atherosclerosis
locus
at
10q11
regulates
plasma
CXCL12
levels."
Eur. Heart
J.
32(8):963-71 Kathiresan
S
et
al.
(2008)
.
"Six
new
loci
associated
with
blood
low-density
lipoprotein
cholesterol,
highdensity
lipoprotein
cholesterol
or
triglycerides
in
humans."
Nat.
Genet.
40(2):189-97 Erdmann
J
et
al.
(2009)
.
"New
susceptibility
locus
for
coronary
artery
disease
on
chromosome
3q22.3." Nat.
Genet.
41(3):280-2 Chasman
DI
et
al.
(2009)
.
"Polymorphism
in
the
apolipoprotein(a)
gene,
plasma
lipoprotein(a), cardiovascular
disease,
and
low-dose
aspirin
therapy."
Atherosclerosis
203(2):371-6 Pennacchio
LA
et
al.
(2002)
.
"Two
independent
apolipoprotein
A5
haplotypes
influence
human
plasma triglyceride
levels."
Hum.
Mol.
Genet.
11(24):3031-8 Kamphaus
GD
et
al.
(2000)
.
"Canstatin,
a
novel
matrix-derived
inhibitor
of
angiogenesis
and
tumor growth."
J.
Biol.
Chem.
275(2):1209-15

Venous Thromboembolism
Rosendaal
et
al.
(1995)
.
"High
risk
of
thrombosis
in
patients
homozygous
for
factor
V
Leiden
(activated protein
C
resistance)."
Blood
85(6):1504-8
https://www.23andme.com/user/report/health/ 19/23

8/2/12

23andMe Printable Report

Smith
et
al.
(2007)
.
"Association
of
genetic
variations
with
nonfatal
venous
thrombosis
in
postmenopausal women."
JAMA
297(5):489-98 Emmerich
et
al.
(2001)
.
"Combined
effect
of
factor
V
Leiden
and
prothrombin
20210A
on
the
risk
of venous
thromboembolism--pooled
analysis
of
8
case-control
studies
including
2310
cases
and
3204 controls.
Study
Group
for
Pooled-Analysis
in
Venous
Thromboembolism."
Thromb
Haemost
86(3):809-16 Bertina
et
al.
(1994)
.
"Mutation
in
blood
coagulation
factor
V
associated
with
resistance
to
activated
protein C."
Nature
369(6475):64-7 Lane
et
al.
(2000)
.
"Role
of
hemostatic
gene
polymorphisms
in
venous
and
arterial
thrombotic
disease." Blood
95(5):1517-32 Poort
et
al.
(1996)
.
"A
common
genetic
variation
in
the
3'-untranslated
region
of
the
prothrombin
gene
is associated
with
elevated
plasma
prothrombin
levels
and
an
increase
in
venous
thrombosis."
Blood 88(10):3698-703. Colucci
et
al.
(2004)
.
"Hyperprothrombinemia
associated
with
prothrombin
G20210A
mutation
inhibits plasma
fibrinolysis
through
a
TAFI-mediated
mechanism."
Blood
103(6):2157-61 Wolberg
et
al.
(2003)
.
"Elevated
prothrombin
results
in
clots
with
an
altered
fiber
structure:
a
possible mechanism
of
the
increased
thrombotic
risk."
Blood
101(8):3008-13 Kyrle
et
al.
(1998)
.
"Clinical
studies
and
thrombin
generation
in
patients
homozygous
or
heterozygous
for the
G20210A
mutation
in
the
prothrombin
gene."
Arterioscler
Thromb
Vasc
Biol
18(8):1287-91 Heit
JA
et
al.
(2011)
.
"Genetic
variation
within
the
anticoagulant,
procoagulant,
fibrinolytic
and
innate immunity
pathways
as
risk
factors
for
venous
thromboembolism."
J.
Thromb.
Haemost.
9(6):1133-42 Trégouët
DA
et
al.
(2009)
.
"Common
susceptibility
alleles
are
unlikely
to
contribute
as
strongly
as
the
FV and
ABO
loci
to
VTE
risk:
results
from
a
GWAS
approach."
Blood
113(21):5298-303 Germain
M
et
al.
(2011)
.
"Genetics
of
venous
thrombosis:
insights
from
a
new
genome
wide
association study."
PLoS
ONE
6(9):e25581 O'Donnell
J
et
al.
(2002)
.
"Amount
of
H
antigen
expressed
on
circulating
von
Willebrand
factor
is
modified by
ABO
blood
group
genotype
and
is
a
major
determinant
of
plasma
von
Willebrand
factor
antigen
levels." Arterioscler.
Thromb.
Vasc.
Biol.
22(2):335-41 Miñano
A
et
al.
(2008)
.
"AB0
blood
group
and
risk
of
venous
or
arterial
thrombosis
in
carriers
of
factor
V Leiden
or
prothrombin
G20210A
polymorphisms."
Haematologica
93(5):729-34

Atrial Fibrillation
Kääb
et
al.
(2009)
.
"Large
scale
replication
and
meta-analysis
of
variants
on
chromosome
4q25
associated with
atrial
fibrillation."
Eur.
Heart
J.
30(7):813-9 Gudbjartsson
et
al.
(2007)
.
"Variants
conferring
risk
of
atrial
fibrillation
on
chromosome
4q25."
Nature 448(7151):353-7

Age-related Macular Degeneration
Maller
et
al.
(2006)
.
"Common
variation
in
three
genes,
including
a
noncoding
variant
in
CFH,
strongly influences
risk
of
age-related
macular
degeneration."
Nat
Genet
38(9):1055-9 Johnson
et
al.
(2006)
.
"Individuals
homozygous
for
the
age-related
macular
degeneration
risk-conferring variant
of
complement
factor
H
have
elevated
levels
of
CRP
in
the
choroid."
Proc
Natl
Acad
Sci
U
S
A 103(46):17456-61 Laine
et
al.
(2007)
.
"Y402H
polymorphism
of
complement
factor
H
affects
binding
affinity
to
C-reactive protein."
J
Immunol
178(6):3831-6 Skerka
et
al.
(2007)
.
"Defective
complement
control
of
factor
H
(Y402H)
and
FHL-1
in
age-related
macular degeneration."
Mol
Immunol
44(13):3398-406 Conley
et
al.
(2006)
.
"CFH,
ELOVL4,
PLEKHA1
and
LOC387715
genes
and
susceptibility
to
age-related maculopathy:
AREDS
and
CHS
cohorts
and
meta-analyses."
Hum
Mol
Genet
15(21):3206-18 Sofat
R
et
al.
(2012)
.
"Complement
factor
H
genetic
variant
and
age-related
macular
degeneration:
effect size,
modifiers
and
relationship
to
disease
subtype."
Int
J
Epidemiol
41(1):250-262
https://www.23andme.com/user/report/health/ 20/23

8/2/12

23andMe Printable Report

Maller
et
al.
(2006)
.
"Common
variation
in
three
genes,
including
a
noncoding
variant
in
CFH,
strongly influences
risk
of
age-related
macular
degeneration."
Nat
Genet
38(9):1055-9 Gold
et
al.
(2006)
.
"Variation
in
factor
B
(BF)
and
complement
component
2
(C2)
genes
is
associated
with age-related
macular
degeneration."
Nat
Genet
38(4):458-62 Yates
et
al.
(2007)
.
"Complement
C3
variant
and
the
risk
of
age-related
macular
degeneration."
N
Engl
J Med
357(6):553-61 Spencer
et
al.
(2007)
.
"Protective
effect
of
complement
factor
B
and
complement
component
2
variants
in age-related
macular
degeneration."
Hum
Mol
Genet
16(16):1986-92 Kanda
et
al.
(2007)
.
"A
variant
of
mitochondrial
protein
LOC387715/ARMS2,
not
HTRA1,
is
strongly associated
with
age-related
macular
degeneration."
Proc
Natl
Acad
Sci
U
S
A
104(41):16227-32 Chen
W
et
al.
(2010)
.
"Genetic
variants
near
TIMP3
and
high-density
lipoprotein-associated
loci
influence susceptibility
to
age-related
macular
degeneration."
Proc.
Natl.
Acad.
Sci.
U.S.A.
107(16):7401-6 Neale
BM
et
al.
(2010)
.
"Genome-wide
association
study
of
advanced
age-related
macular
degeneration identifies
a
role
of
the
hepatic
lipase
gene
(LIPC)."
Proc.
Natl.
Acad.
Sci.
U.S.A.
107(16):7395-400 Park
KH
et
al.
(2009)
.
"Complement
component
3
(C3)
haplotypes
and
risk
of
advanced
age-related macular
degeneration."
Invest.
Ophthalmol.
Vis.
Sci.
50(7):3386-93 McKay
GJ
et
al.
(2010)
.
"Complement
component
3:
an
assessment
of
association
with
AMD
and
analysis of
gene-gene
and
gene-environment
interactions
in
a
Northern
Irish
cohort."
Mol.
Vis.
16(None):194-9

Restless Legs Syndrome
Stefansson
et
al.
(2007)
.
"A
genetic
risk
factor
for
periodic
limb
movements
in
sleep."
N
Engl
J
Med 357(7):639-47 Winkelmann
et
al.
(2007)
.
"Genome-wide
association
study
of
restless
legs
syndrome
identifies
common variants
in
three
genomic
regions."
Nat
Genet
39(8):1000-1006 Collins
et
al.
(2001)
.
"All
in
the
family:
the
BTB/POZ,
KRAB,
and
SCAN
domains."
Mol
Cell
Biol 21(11):3609-15

Ulcerative Colitis
Silverberg
et
al.
(2009)
.
"Ulcerative
colitis-risk
loci
on
chromosomes
1p36
and
12q15
found
by
genomewide
association
study."
Nat.
Genet.
41(2):216-20 Franke
et
al.
(2008)
.
"Sequence
variants
in
IL10,
ARPC2
and
multiple
other
loci
contribute
to
ulcerative colitis
susceptibility."
Nat.
Genet.
40(11):1319-23 Franke
et
al.
(2008)
.
"Replication
of
signals
from
recent
studies
of
Crohn's
disease
identifies
previously unknown
disease
loci
for
ulcerative
colitis."
Nat.
Genet.
40(6):713-5 Parkes
et
al.
(2007)
.
"Sequence
variants
in
the
autophagy
gene
IRGM
and
multiple
other
replicating
loci contribute
to
Crohn's
disease
susceptibility."
Nat.
Genet.
39(7):830-2 Wellcome
Trust
Case
Control
Consortium
(2007)
.
"Genome-wide
association
study
of
14,000
cases
of seven
common
diseases
and
3,000
shared
controls."
Nature
447(7145):661-78 Fisher
et
al.
(2008)
.
"Genetic
determinants
of
ulcerative
colitis
include
the
ECM1
locus
and
five
loci implicated
in
Crohn's
disease."
Nat.
Genet.
40(6):710-2 Hashida
et
al.
(1998)
.
"Cloning
and
mapping
of
ZNF231,
a
novel
brain-specific
gene
encoding
neuronal double
zinc
finger
protein
whose
expression
is
enhanced
in
a
neurodegenerative
disorder,
multiple
system atrophy
(MSA)."
Genomics
54(1):50-8 Weersma
et
al.
(2008)
.
"ATG16L1
and
IL23R
are
associated
with
inflammatory
bowel
diseases
but
not
with celiac
disease
in
the
Netherlands."
Am.
J.
Gastroenterol.
103(3):621-7

Congenital Disorder of Glycosylation Type 1a (PMM2-CDG)
Matthijs
G
et
al.
(2000)
.
"Mutations
in
PMM2
that
cause
congenital
disorders
of
glycosylation,
type
Ia (CDG-Ia)."
Hum.
Mutat.
16(5):386-94 Kjaergaard
S
et
al.
(1998)
.
"Absence
of
homozygosity
for
predominant
mutations
in
PMM2
in
Danish
https://www.23andme.com/user/report/health/ 21/23

8/2/12

23andMe Printable Report

patients
with
carbohydrate-deficient
glycoprotein
syndrome
type
1."
Eur.
J.
Hum.
Genet.
6(4):331-6 Schollen
E
et
al.
(2000)
.
"Lack
of
Hardy-Weinberg
equilibrium
for
the
most
prevalent
PMM2
mutation
in CDG-Ia
(congenital
disorders
of
glycosylation
type
Ia)."
Eur.
J.
Hum.
Genet.
8(5):367-71

Pseudocholinesterase Deficiency
Yen
et
al.
(2003)
.
"Butyrylcholinesterase
(BCHE)
genotyping
for
post-succinylcholine
apnea
in
an Australian
population."
Clin.
Chem.
49(8):1297-1308 Maiorana
et
al.
(2003)
.
"Heterozygous
pseudocholinesterase
deficiency:
a
case
report
and
review
of
the literature."
J
Oral
Maxillofac.
Surg.
61(7):845-847

Warfarin (Coumadin®) Sensitivity
International
Warfarin
Pharmacogenetics
Consortium
et
al.
(2009)
.
"Estimation
of
the
warfarin
dose
with clinical
and
pharmacogenetic
data."
N.
Engl.
J.
Med.
360(8):753-64 Budnitz
et
al.
(2007)
.
"Medication
use
leading
to
emergency
department
visits
for
adverse
drug
events
in older
adults."
Ann.
Intern.
Med.
147(11):755-65 Rieder
et
al.
(2005)
.
"Effect
of
VKORC1
haplotypes
on
transcriptional
regulation
and
warfarin
dose."
N. Engl.
J.
Med.
352(22):2285-93 Wadelius
et
al.
(2007)
.
"Association
of
warfarin
dose
with
genes
involved
in
its
action
and
metabolism." Hum.
Genet.
121(1):23-34 Zhu
et
al.
(2007)
.
"Estimation
of
warfarin
maintenance
dose
based
on
VKORC1
(-1639
G>A)
and
CYP2C9 genotypes."
Clin.
Chem.
53(7):1199-205 Aquilante
et
al.
(2006)
.
"Influence
of
coagulation
factor,
vitamin
K
epoxide
reductase
complex
subunit
1, and
cytochrome
P450
2C9
gene
polymorphisms
on
warfarin
dose
requirements."
Clin.
Pharmacol.
Ther. 79(4):291-302 Gage
et
al.
(2008)
.
"Use
of
pharmacogenetic
and
clinical
factors
to
predict
the
therapeutic
dose
of warfarin."
Clin.
Pharmacol.
Ther.
84(3):326-31 Aithal
et
al.
(1999)
.
"Association
of
polymorphisms
in
the
cytochrome
P450
CYP2C9
with
warfarin
dose requirement
and
risk
of
bleeding
complications."
Lancet
353(9154):717-9 Peyvandi
et
al.
(2004)
.
"CYP2C9
genotypes
and
dose
requirements
during
the
induction
phase
of
oral anticoagulant
therapy."
Clin.
Pharmacol.
Ther.
75(3):198-203 Hillman
et
al.
(2004)
.
"Relative
impact
of
covariates
in
prescribing
warfarin
according
to
CYP2C9 genotype."
Pharmacogenetics
14(8):539-47 Veenstra
et
al.
(2005)
.
"CYP2C9
haplotype
structure
in
European
American
warfarin
patients
and association
with
clinical
outcomes."
Clin.
Pharmacol.
Ther.
77(5):353-64 Wang
et
al.
(2008)
.
"Genetic
factors
contribute
to
patient-specific
warfarin
dose
for
Han
Chinese."
Clin. Chim.
Acta
396(1-2):76-9 Limdi
et
al.
(2008)
.
"VKORC1
polymorphisms,
haplotypes
and
haplotype
groups
on
warfarin
dose
among African-Americans
and
European-Americans."
Pharmacogenomics
9(10):1445-58 Oldenburg
et
al.
(2007)
.
"VKORC1:
molecular
target
of
coumarins."
J
Thromb
Haemost.
5
Suppl
1:1-6 Yuan
et
al.
(2005)
.
"A
novel
functional
VKORC1
promoter
polymorphism
is
associated
with
inter-individual and
inter-ethnic
differences
in
warfarin
sensitivity."
Hum.
Mol.
Genet.
14(13):1745-51 Takeuchi
et
al.
(2009)
.
"A
genome-wide
association
study
confirms
VKORC1,
CYP2C9,
and
CYP4F2
as principal
genetic
determinants
of
warfarin
dose."
PLoS
Genet.
5(3):e1000433

https://www.23andme.com/user/report/health/

22/23

8/2/12

23andMe Printable Report

About the 23andMe Personal Genome Service®
23andMe's Personal Genome Service provides customers with data on nearly 1,000,000 single nucleotide polymorphisms (SNPs) in their genome using a microarray-based genotyping assay. Customers provide saliva samples, which are analyzed by a CLIA-certified laboratory. Results are viewable on the 23andMe website at https://www.23andme.com/you/ where reports are considered Established or Preliminary Research reports depending on the amount of evidence supporting the associations reported. We currently provide more than 60 Established Research reports on various disease risk, drug response, and carrier status topics, as well as Preliminary Research reports on more than 150 conditions and traits.

https://www.23andme.com/user/report/health/

23/23