I most likely had a...
- 100% British & Irish parent, grandparent, or great-grandparent who was likely born between 1880 and 1940.
- 100% Scandinavian third-great-grandparent, fourth-great-grandparent, fifth-great-grandparent, or sixth-great-grandparent who was likely born between 1730 and 1820.
- 100% Sardinian third-great-grandparent, fourth-great-grandparent, fifth-great-grandparent, sixth-great-grandparent, or seventh-great- (or greater) grandparent who was likely born between 1700 and 1820.
- 100% West African third-great-grandparent, fourth-great-grandparent, fifth-great-grandparent, sixth-great-grandparent, or seventh-great- (or greater) grandparent who was likely born between 1700 and 1820.
- 100% Iberian fourth-great-grandparent, fifth-great-grandparent, sixth-great-grandparent, or seventh-great- (or greater) grandparent who was likely born between 1700 and 1790.
- 100% North African & Arabian fourth-great-grandparent, fifth-great-grandparent, sixth-great-grandparent, or seventh-great- (or greater) grandparent who was likely born between 1700 and 1790.
- 100% Native American fourth-great-grandparent, fifth-great-grandparent, sixth-great-grandparent, or seventh-great- (or greater) grandparent who was likely born between 1700 and 1790.
- 100% East African fourth-great-grandparent, fifth-great-grandparent, sixth-great-grandparent, or seventh-great- (or greater) grandparent who was likely born between 1700 and 1790.
- 100% Ashkenazi Jewish fourth-great-grandparent, fifth-great-grandparent, sixth-great-grandparent, or seventh-great- (or greater) grandparent who was likely born between 1700 and 1790.
Native American Detail
Many discover that there is a lack of details for AncestryDNA’s Native American results. 23andMe provides a greater dissection of populations. This is just one section, which displays my Native American results.
Ancestry Composition Chromosome Painting
These are your chromosomes; we’ve painted them with your Ancestry Composition results. The first 22 are called autosomes and come in pairs of two, each represented by one of the colored horizontal lines in the graphic below. Chromosomes have different lengths, and are named 1 through 22, when sorted by size (scientists are not very creative). Lastly, we also look at ancestry on your X chromosome: two copies like the autosomes if you are female, and only one copy if you’re male (that you got from mom).
How much of each ancestry did you inherit from your parents?
Connect a parent on 23andMe to see what ancestries you inherited from each parent. Or, connect with your children so they can see what you passed down to them. [This is too extensive to include to this page, but it is an option you can explore when adding your parents to your account.]
My maternal haplogroup is T1a1, which 1 of 75 participants share.
Paternal haplogroups are defined by sets of genetic variants on the Y chromosome. Although women inherit roughly 50% of their DNA from their fathers, they do not inherit Y chromosomes and as a result, do not have paternal haplogroups.
Haplogroup L 180,000 Years Ago
If every person living today could trace his or her maternal line back over thousands of generations, all of our lines would meet at a single woman who lived in eastern Africa between 150,000 and 200,000 years ago. Though she was one of perhaps thousands of women alive at the time, only the diverse branches of her haplogroup have survived to today. The story of your maternal line begins with her.
Haplogroup L3 65,000 Years Ago
Your branch of L is haplogroup L3, which arose from a woman who likely lived in eastern Africa between 60,000 and 70,000 years ago. While many of her descendants remained in Africa, one small group ventured east across the Red Sea, likely across the narrow Bab-el-Mandeb into the tip of the Arabian Peninsula.
Haplogroup N 59,000 Years Ago
Your story continues with haplogroup N, one of two branches that arose from L3 in southwestern Asia. Researchers have long debated whether they arrived there via the Sinai Peninsula, or made the hop across the Red Sea at the Bab-el-Mandeb. Though their exact routes are disputed, there is no doubt that the women of haplogroup N migrated across all of Eurasia, giving rise to new branches from Portugal to Polynesia.
Haplogroup R 57,000 Years Ago
One of those branches is haplogroup R, which traces back to a woman who lived soon after the migration out of Africa. She likely lived in southwest Asia, perhaps in the Arabian peninsula, and her descendants lived and migrated alongside members of haplogroup N. Along the way, R gave rise to a number of branches that are major haplogroups in their own right.
Haplogroup T 25,000 Years Ago
While some members of R traveled far and wide, some remained in the Middle East for tens of thousands of years. Haplogroup T arose among the latter group, from a woman who lived approximately 25,000 years ago. Its present-day geographic distribution is strongly influenced by multiple migrations out of the Middle East into Europe, India and eastern Africa within the last 15,000 years.
Origin and Migrations of Haplogroup T1a
Your maternal line stems from a branch of T1 called T1a. All the members of T1a can trace their maternal lines back to a woman who lived in the Middle East about 14,500 years ago. The world was just warming after the last great peak of the Ice Age, when the freezing climate had trapped much of the Earth’s moisture in the ice sheets that covered not only the poles but also reached far down into all but the most southern reaches of Eurasia. The dry cold also created extreme deserts in the Arabian peninsula, restricting humans to a limited range of hospitable pockets. Then, as the ice gradually melted over thousands of years, the land outside of these refuges became habitable once again, and communities began to grow and re-expand. Some of the women in these migrations carried T1a to far reaches of the Middle East, North Africa, and all the way into western Europe.
Though not exceedingly common, shows a remarkable geographic spread. Members of this group have been found in the range from the west in Scandinavia and the Baltic to the south in Morocco and to the east in Central Asia.
Your maternal haplogroup, T1a1, traces back to a woman who lived approximately 7,000 years ago.
That’s nearly 280 generations ago! What happened between then and now? As researchers and citizen scientists discover more about your haplogroup, new details may be added to the story of your maternal line.
T1a1 is frequent among 23andMe customers.
Today, you share your haplogroup with all the maternal-line descendants of the common ancestor of T1a1, including other 23andMe customers.
Locations of Your DNA Relatives
Your 23andMe DNA Relatives live in 31 US states and 1 country.
(Unfortunately, 23andMe customers are based on shipping addresses.)
Ancestry Composition of Your DNA Relatives
Some of your DNA Relatives share aspects of your Ancestry Composition, while others have genetic ancestries that are distinct from your own. [Relatives that are also 23andMe participants, this does not include non-members data.]
Compared to the average 23andMe customer, your DNA Relatives are...
48% less likely to drink instant coffee
47% more likely to have red body or facial hair
36% less likely to like the taste of dark licorice
36% more likely to be able to do the side splits
35% more likely to own a dog
31% more likely to drink caffeinated soda
31% less likely to have sweaty feet
30% less likely to exercise by strength training
29% less likely to have perfect pitch
26% more likely to have lived near a farm when they were young
25% more likely to think that fresh cilantro tastes like soap
20% more likely to be able to do the forward splits
18% less likely to have learned a foreign language as an adult
17% less likely to drink espresso drinks
16% less likely to be able to do a backbend kickover
16% more likely to be able to do a cartwheel
14% more likely to be able to carry a tune
13% less likely to drink energy drinks
13% less likely to make new years resolutions
12% more likely to drink brewed coffee
12% less likely to have a gap between their two front teeth
12% less likely to be a vegetarian
10% more likely to sneeze when exposed to bright light
10% more likely to drink tea
87 Health Reports
Over the years 23andMe has provided additional reports, and do project to include more to the deluxe plan. Some of the medical reports, (specifically the BRCA results) will request your consent to reveal your results, even if you do not test positive. It is just a safeguard to ensure that you really want to learn of these risks.
Although, I do not have the genetic disposition for the following variants, I am sharing the list of tests that are available on the current list for the deluxe plan. As for the traits, I did find some of the results to counter my experience, … I love cilantro!
Click the caret ▶ for a partial explanation and a small portion of the scientific details.
27 Traits Reports
The genetics behind appearance and senses.
The genetic marker used in this report has been best studied in people of European descent. The results of this report may be less relevant for people of other ethnicities.Some people may see that they are less likely to be able to match a musical pitch, but also see a 50/50 percentage distribution. This can happen when there is just a slightly lower chance of being able to match pitch, but the percentage of 23andMe research participants who have the trait is displayed as a rounded 50%.
For this analysis, we used survey responses and genetic data from more than 660,000 23andMe research participants of European descent. We identified 529 genetic markers that were associated with the ability to match musical pitch. We used these markers together with non-genetic factors, specifically age and sex, to create a statistical model that predicts the ability to match musical pitch. The full statistical model used to calculate your result (which includes genetics, age, and sex) has an AUC value of 0.58. For comparison, models including genetics alone or demographics alone (age and sex) have AUC values of 0.58 and 0.53, respectively.
Your Chromosome 1, Genotype AG
What causes the asparagus odor in urine?
Scientists believe the asparagus odor in urine comes from molecules that are made by the body when asparagus is broken down. One of the molecules called “methanethiol,” contains sulfur and has an odor like cooked cabbage. Some bacteria that are used to make cheese produce methanethiol during the process, which gives cheeses like cheddar and Muenster their aromas.
Discovering the genetics behind asparagus-related odor detection
For decades scientists have been searching for a reason why some people can’t smell the asparagus-related odor in urine. Some studies have suggested that this trait can run in families, but the details of the genes involved remained a mystery until 2010. Genetic research at 23andMe identified, for the first time, a genetic marker that is linked to the likelihood of smelling the asparagus-related odor in urine.
The genetic marker is located near the OR2M7 gene. The OR2M7 gene contains instructions for a protein (an olfactory receptor) that detects odor molecules. But many questions still remain about how, exactly, this genetic marker influences smell detection.
Your Chromosome 7, CG Genotype
How did we calculate your result?
We looked at a place in your DNA (a genetic marker) that affects your chances of being able to detect a certain bitter chemical called “PTC.” Some vegetables like raw broccoli and brussels sprouts, contain bitter chemicals similar to PTC. Your combination of variants at this marker is usually found in people who are able to detect these bitter chemicals.
The TAS2R38 gene contains instructions for a protein, or taste receptor, that can detect the bitter chemical called “PTC.” PTC isn’t usually found in the human diet, but it is similar to chemicals present in vegetables like broccoli and brussels sprouts. People with the G variant have a taste receptor that can detect these PTC-like chemicals. This means people with the G variant may taste bitterness in these foods and avoid them all together.
Why do cheek dimples exist?
Dimples might have no real purpose, or there might be more to the story. Some hypothesize that because dimples accentuate the smile they could provide a boost for communication. Primates evolved to live in complex social groups where cooperation is critical. Facial gestures like smiling are social signals, and primates — from macaques to chimpanzees to humans — use smile-like gestures to communicate things like submissiveness, friendliness, and playfulness.
Why would cilantro taste soapy?
Many people dislike cilantro (also known as coriander), describing the taste as “soapy.” 23andMe researchers identified two genetic markers associated with this aversion. These genetic markers are located near genes that help determine your sense of smell through proteins called olfactory receptors. Some of these receptors detect aldehydes, chemical compounds that are found in soap and thought to be a major component of cilantro aroma.
Your genotype at two tested markers
You have one genetic variant at these markers associated with higher odds of disliking cilantro. Since genetics is only part of the picture, you may still like cilantro. Overall, just 13% of 23andMe research participants think cilantro tastes “soapy.”
Why do we have chins anyway?
Humans are the only species that have chins — and no one knows why. But one possibility is that the chin is a holdover from ancient human ancestors that had larger jaws. When pre-humans began cooking with fire around a million years ago, their food became easier to chew, and they evolved smaller teeth and mouths to match. The bottom of the jawbone didn’t shrink as much, leaving us with a chin that sticks out from the rest of the face.
DNA differences could affect jawbone growth
We discovered the genetic variants in this report by looking for differences in the DNA of 23andMe research participants with and without cleft chins. Because these DNA differences are recent discoveries, we don’t yet know much about them. But our analysis suggests that many are in or near genes that play a role in the growth of bones in the face and skull. If genetic variants affect the function of these genes, they could make it more or less likely that the left and right jawbones will stop short of fusing all the way, leaving a cleft.
Spread the love, and the chins
Modern humans have some Neanderthal genetic variants because our ancestors interbred with Neanderthals over 40,000 years ago. But the sharing went both ways. In some Neanderthal fossils, you can see a hint of a chin. Scientists think they could have inherited this trait from their human ancestors.
No one knows why humans have earlobes at all, but that hasn’t stopped us from finding genetic variants linked to earlobe shape.
Because of the way earlobe shape is passed down through families, scientists initially proposed that this trait was controlled by just one gene. But 23andMe research suggests the genetics of earlobe shape are more complicated: we discovered 34 different genetic markers associated with earlobe type. We don’t know exactly how these markers may influence earlobe shape, but some are near genes known to play a role in development of the skin or other tissues, like WNT5A, SP5, PRRX1, and CUX1.
Your Chromosome 16 Genotype CC
Why do we have earwax anyway?
It may seem counterintuitive, but earwax helps your ears stay clean. It traps dirt and bacteria and slowly moves it up and out of the ear canal. Not only that, earwax also contains at least 10 compounds that help it prevent bacteria from growing inside your ear in the first place.
How your genes determine earwax type
Wet earwax is dark-colored and sticky, while dry earwax is light-colored and flaky. Both types are equally good at keeping dirt and bacteria at bay, but the difference between the two is determined by a single variant in the ABCC11 gene. The ABCC11 gene contains instructions for a protein that specializes in moving fat into, and out of, your cells. People who have 1 or 2 copies of the C variant in the ABCC11 gene have more fat in their earwax, making it dark-colored and sticky. People who have two copies of the T variant have less fat in their earwax, making it dry, light-colored, and flaky.
What your earwax says about your armpits
The same ABCC11 gene is involved in sweat production and body odor. Having more fat molecules in a person’s sweat is linked to more body odor. So the same genetic variant in the ABCC11 gene that determines the dry earwax type is also linked to lower levels of body odor.
Earwax in early human history
Dry earwax is found in 80-95% of people of East Asian descent, but in less than 3% of people of European or African descent. This distinct geographic distribution of earwax type provides clues about early human migration patterns. The variant that causes dry earwax likely arose in the group that migrated from Africa towards Asia. The group that migrated to Europe retained the wet earwax of their African ancestors.
Your Chromosome 15, Genotype AG
The ancient origins of eye colors
Early humans had brown eyes. But at some point in history, a baby was born with a genetic variant leading to a strange new eye color. Today, most light-eyed people carry that same genetic variant.
What gives your eyes their color?
The color of your eyes depends on how much eumelanin they have. Eumelanin is a brown pigment molecule. It looks dark because it absorbs the sunlight — so more eumelanin leads to darker eyes. It’s also the same molecule that colors your hair and skin, though different genetic factors can affect how much brown pigment you have in each place.
The genetic marker in this report is located near a gene called OCA2 that affects how much brown pigment your cells produce. People with 1 or 2 copies of the A variant of this marker tend to have more brown pigment in their eyes, so they are likely to have darker eyes.
Heights and balance
While standing upright, the brain uses visual input from nearby objects to make tiny postural adjustments that help maintain balance. However, when standing at a high elevation relative to their surroundings — like at the edge of a tall building — most people feel somewhat off balance. This is because visual input from nearby objects is lacking, and the objects in view are too far away for the brain to use for balance control.
Fear of heights
Some scientists believe that people with an extreme fear of heights may depend more heavily on visual input for balance control than other people who can use physical sensations as well as visual input to keep their balance. As a result, they may feel especially unstable when standing at an elevation, triggering a fear response.
Palm readers believe the future is written in your hands, but some scientists believe the relative length of your fingers says a lot more about you — and your genetics.
Which finger is longer, your index finger or your ring finger? Everyone is a little different. Scientists have studied finger length ratio (index finger length divided by ring finger length) since the late 1800’s. The first discovery was that on average, men tend to have lower ratios than women. This means that, in general, men are more likely to have longer ring fingers relative to their index fingers, while women’s are often closer to equal in length.
Hormones in the womb
Scientists discovered that finger length ratio is influenced by the balance of testosterone and estrogen in the womb during early pregnancy. Higher testosterone exposure in the womb is linked to having a lower finger length ratio, while lower testosterone exposure is linked to having a higher finger length ratio. After birth, hands grow in perfect proportion to the size they were in the womb. So your finger ratio today is probably the same as it was when you were a baby.
Why do scientists study our hands?
Since finger length ratio is linked to fetal hormone exposure and stays constant throughout the lifetime, it can be used as an indicator of the conditions a person was exposed to in the womb during pregnancy. Some scientists gather finger length information from adults to study how conditions in the womb may have influenced things like their health and behavior later in life.
Why do some people get freckles?
Most of your skin cells don’t make their own pigment. Specialized skin cells called melanocytes manufacture little bags of pigment and hand them out to other skin cells. Pigment production gets ramped up in response to sunshine. If pigment is produced evenly across your skin, you end up with a tan — but if more pigment is produced in some areas than others, you get freckles. Scientist still aren’t sure what causes skin cells to behave differently when they’re located in freckles versus the paler areas between freckles.
We probably don’t have to tell you freckles are more common in people with lighter skin and hair. These traits share some, but not all, of their genetics in common. 23andMe research found 34 genetic markers associated with the likelihood of having freckles. Many of these markers are near genes we already know play a role in skin pigmentation, eye color, and/or hair color, like SLC45A2, OCA2, HERC2, and TYR.
For some people, frequent sun exposure can lighten their hair color. This happens when high-energy ultraviolet rays from the sun break down the hair’s pigment molecules, altering its color. While certain hair types are more susceptible to photobleaching than others, it’s important to keep in mind that all hair types are sensitive to the damaging effects of ultraviolet light on hair growth and hair strength. As such, reducing the amount of time spent in the sun is important for everyone’s overall hair health. And while we may not know exactly why certain hair types are more sensitive to photobleaching, 23andMe scientists identified 48 genetic markers associated with the trait.
For this analysis, we used survey responses and genetic data from more than 340,000 23andMe research participants of European descent. We identified 48 genetic markers that were associated with hair photobleaching. We used these markers together with non-genetic factors, specifically age and sex, to create a statistical model that predicts the likelihood of experiencing hair photobleaching. The full statistical model used to calculate your result (which includes genetics, age, and sex) has an AUC value of 0.61. For comparison, models including genetics alone or demographics alone (age and sex) have an AUC value of 0.58.
Scientists think the texture of your hair is created by the shape of your hair follicles. The curvier the follicle, the curlier the strand.
Your Traits Result
The combination of your genetics and other factors makes you most likely to have straight or wavy hair.
What gives your hair its texture?
Curved hair follicles build curly hairs. How might that happen? The building blocks of hair are hair cells, which are linked together by a tough protein called keratin. As new hair cells are born at the bottom of a follicle, they get added onto the growing strand of hair. Some research suggests that the shape of the bottom of the hair follicle affects how these building blocks are put together.
23andMe research found 75 genetic markers associated with hair texture. Though we don’t know exactly how all these markers may influence hair texture, many of them are linked to genes thought to be involved in hair follicle development. Interestingly, two of these genes, KRT71 and FGF5, have previously been associated with coat texture in dogs.
What makes hair thicker or thinner?
How thick or thin your individual strands of hair are depends on the size and shape of your hair follicles. Typically, people of East Asian descent have thicker hair strands than people of African or European descent.
Your genotype at one tested marker
One genetic marker seems to play a big role in determining the thickness of your hair strands. This genetic marker is in a gene called EDAR that is important for hair follicle development. Your genetic variants at this marker are associated with lower chances of having thick hair strands.
Pigment factories in your follicles
Deep within your hair follicles, specialized cells manufacture packets of pigment that they hand off to hair cells. More pigment leads to darker hair.
How hair gets its color
Hair cells don’t make their own pigment. Instead, specialized skin cells called melanocytes create pigment. Inside the hair follicle, melanocytes package pigment into bundles and transfer these bundles to developing hair cells. In mid-life, a gradual loss of melanocytes may lead to gray hair.
Some of the 42 genetic markers in this report are near genes that are thought to play a role in creating melanin, including TYR, TYRP1, OCA2, and SLC45A2. You’ll see some of these genes in your Eye Color, Skin Pigmentation, and Freckles reports, too. These partly-overlapping genetics help explain why a person’s skin, hair, and eyes are often (but not always) all light or all dark.
What is misophonia?
Almost everyone hates noises like nails on a chalkboard, but for people with a condition called misophonia, everyday noises like the sound of chewing can cause a similar reaction, along with rage or panic. Some scientists speculate that misophonia could result from increased connections between the brain systems involved in hearing (the auditory cortex) and the “fight or flight” response (the limbic system and autonomic nervous system).
Your genotype at one tested marker
23andMe researchers identified one genetic marker associated with feeling rage at the sound of other people chewing. This genetic marker is located near the TENM2 gene which is involved in brain development. Your genetic variants at this marker are associated with slightly higher odds of having this trait.
Female mosquitoes have a complex olfactory system that lets them sniff out their food. As it turns out, mosquitoes have preferences! Mosquitoes are attracted to certain molecules in body odor and breath and depending on the proportions of these molecules, some people may appear more delicious than others. But keep in mind that anyone can get bitten by mosquitoes, which can carry disease. So to deter those itchy intruders, the Centers for Disease Control and the World Health Organization recommend using mosquito repellent, wearing protective clothing, and staying indoors during dawn and dusk when mosquitoes are most active.
For this analysis, we used survey responses and genetic data from more than 380,000 23andMe research participants of European descent. We identified 285 genetic markers that were associated with mosquito bite frequency, bite itchiness, or bite size. We used these markers together with non-genetic factors, specifically age and sex, to create a statistical model that predicts whether you would say you get bitten more or less often than people around you. The model was further recalibrated to be more accurate when applied to people of African American, Hispanic or Latino, East Asian, Middle Eastern, and Ashkenazi Jewish descent using data from more than 420,000 23andMe research participants. The full statistical model used to calculate your result (which includes genetics, age, and sex) has an R2 value of 6%. For comparison, models including genetics alone or demographics alone (age and sex) have R2 values of 2% and 4%, respectively.
Where did the lanugo go?
Babies are born with all the hair follicles they will need for their lifetime, about five million. Each of those follicles produces, and then sheds, one tiny strand of hair (called “lanugo”) in the uterus before the baby is born.
Baby hair and heartburn
An old wives’ tale predicts that if a mother has heartburn during pregnancy, the baby will be born with a full head of hair. In 2006, a group of scientists decided to put this folklore to the test. To their surprise, they found that the tale might be true. Mothers who experienced moderate to severe heartburn were more likely to have babies with thicker hair at birth, and vice versa.
Baby hair growth in the womb
Hair begins to grow around week 10 of pregnancy, and by week 20 the scalp is covered with hair. This first round of hair is called “lanugo” and it is shed in the uterus around 24-28 weeks of pregnancy. This means that any hair a baby is born with was likely grown during the last trimester of pregnancy.
Why do we sneeze?
Typically people sneeze as a result of irritation in our noses due to things like dust or viruses. In some people, however, sneezing seems to be a reaction to more unexpected stimuli like bright light, having a full bladder or even being very full after eating.
Discoveries in progress
Scientists are still trying to understand why light-induced sneezing happens. But that didn’t stop them from coming up with a clever name for it, “Autosomal Dominant Compelling Helio-Ophthalmic Outburst,” or “ACHOO Syndrome.” Although there is little research on this phenomenon, some studies suggest it runs in families. Research at 23andMe has identified 54 genetic markers associated with this quirky reaction to bright light.
Your Chromosome 16, Genotype CC CC GG
Redheads in ancient history
The red hair variants in this report likely first appeared in ancient humans ~30,000-80,000 years ago, around the time of early migrations out of Africa.
The genetics of red hair
Hair gets its color from pigment molecules. People with red hair have high levels of a red/yellow pigment called pheomelanin. Several variants in a single gene, MC1R, can cause red hair by increasing the amount of pheomelanin in your hair.
What about blond, brown, and black hair?
Hair color is determined by not just how much pigment you have, but also what kind. Whether you have red hair depends on your levels of red/yellow pigment (pheomelanin). But the lightness or darkness of your hair depends on your levels of a brown/black pigment called eumelanin. Since different genetic factors control how much of these two pigments you have, we split them into two different reports. See your Light or Dark Hair report to learn more.
Red hair may have appeared in Neanderthals even earlier than other ancient humans. Scientists sequenced the genes of Neanderthal remains found in Italy and Spain, and discovered a variant in the MC1R gene that is predicted to cause red hair. While different from the red hair variants in this report, this Neanderthal variant also affects how pigment is produced.
Your Chromosome 5, Genotype CG & Chromosome 15, Genotype AG
The original sunscreen
Though skin pigment is what gives us our diverse range of skin colors, it’s not just a matter of appearances: the real job of skin pigment is to protect us from the sun’s UV rays.
Why do people have different skin colors?
All early humans had dark skin. Genetic variations causing lighter skin probably appeared at least twice in human history, during two separate migrations out of Africa: one to Europe, and one to Asia. This is likely because higher amounts of pigment make darker skin more effective at sun protection, but less efficient at using sunlight to make vitamin D. As people began living in northern latitudes, having lighter skin helped them make more vitamin D using less sunlight.
Health tradeoffs of light and dark skin
It’s important to both protect your skin from the sun and to get adequate vitamin D. But the lighter your skin is, the more important it is to protect your skin from even brief sun exposure to reduce the risk of skin cancer. And if you have darker skin and live in northern latitudes where there is less sun, you may have more trouble getting enough vitamin D. That makes it especially important to get plenty of vitamin D from dietary sources like fish and fortified dairy.
The genetic variants in this report, in two genes named SLC45A2 and SLC24A5, are associated with variation in skin color in people of European and African descent. These variants affect how much of a brown/black pigment, called eumelanin, is produced by your skin cells. But there are likely different genetic variants that help explain skin color variation in people of Asian and Native American descent.
The brain and taste preference
There’s no taste map on your tongue. But there is a vast taste network in your brain. Genetics may influence how your brain judges and responds to tastes.
How the brain judges tastes
Many areas of your nervous system work together to influence your taste preferences. The tongue detects the molecules present in foods you eat and sends signals to a brain area, the “primary gustatory cortex”, that helps identify their tastes. Another area, the “orbitofrontal cortex”, then helps judge whether you like these tastes. And several other brain areas help determine your responses to pleasant flavors — like deciding to eat more.
Like almost all traits, taste preference is partly shaped by genetics, and partly by environment. 23andMe research identified 43 genetic markers where people can have variants that make them more likely to prefer sweet snacks or salty/savory snacks. A few of these 43 genetic markers are in or near genes involved in brain development or function (like CDH8, ELAVL2, AUTS2, and KCNA3). But most are near genes with a broad range of functions, perhaps reflecting the complexity of this trait.
Footprints left behind by some of our early human ancestors, including Australopithecus afarensis, show a longer second toe.
Skeleton bones and mummy feet, oh my!
In 1864, noticing that many Roman statues had longer second toes, a British anthropologist named James Park Harrison was inspired to perform one of the earliest studies on human toe length. Harrison found that toe length ratio varied from country to country. He even measured the toes of old skeletons displayed in museums, and at least one Egyptian mummy.
Fingers, toes and hormones
Like finger length, toe length may be influenced by the balance of testosterone and estrogen present in the womb during early pregnancy. Fingers and toes form at the same time during pregnancy, and both finger and toe length ratios may tend to differ between men and women. Because of this, some scientists study how finger and toe lengths relate to hormone-linked diseases and behaviors later in life.
Not much is known about the genetics of eyebrow hair distribution. But initial findings offer some clues. Two of the genetic variants in this report are common variations in or near genes, called PAX3 and EDAR, that have been previously associated with unibrow growth.
PAX3: This gene plays an important role in the development of pigment-producing skin cells.
EDAR: This gene controls the development of hair follicles, along with sweat glands and teeth.
Why do we have eyebrows?
Eyebrows contribute to many facial expressions, communicating messages from greetings to surprise to anger. One study also found that people have trouble recognizing faces that are missing their usual eyebrows. This suggests the shape of our eyebrows may also help others recognize us.
When does your internal alarm clock ring?
Our biological sleep rhythms affect when we naturally prefer to fall asleep and wake up. We looked at data from 23andMe research participants and discovered genetic associations with being a morning person or a night person. Fittingly, self-described morning people tend to wake up earlier than self-described night people.
How age changes hairline shape
Children usually start out with a smooth, flat hairline. Starting in adolescence, many people’s hairlines begin to recede. In people with a widow’s peak, the hairline recedes everywhere except a small point at the center of the forehead. With more time, many men and some women also start to thin at the temples. This can create a hairline similar to a widow’s peak.
8 Wellness Reports
Discover out how your DNA may affect your body’s response to diet, exercise, and sleep.
What causes the alcohol flush reaction?
In people who experience the alcohol flush reaction, a toxic substance called acetaldehyde builds up after drinking. Acetaldehyde causes tiny blood vessels in the face to temporarily expand and fill with more blood — similar to what happens when people blush. But acetaldehyde can also cause other effects, like nausea, headaches, and sleepiness. Studies have found that people who flush are less likely to drink alcohol because this reaction is so uncomfortable.
A genetic bottleneck in alcohol breakdown
Before alcohol molecules can be cleared from the body, they have to be broken down into smaller molecules. Acetaldehyde is one of the molecules created during this process. For people who don’t have the alcohol flush reaction, acetaldehyde is quickly broken down further into another, harmless substance. But for people who have one or two copies of the alcohol flush variant, the enzyme responsible for breaking down acetaldehyde is less efficient, so acetaldehyde builds up in the body faster than it can be cleared away.
Drinking, smoking, and health
For people with the alcohol flush variant in this report, drinking alcohol carries additional health risks because their bodies can’t break down the toxic substance acetaldehyde normally. Acetaldehyde is also one of many toxic substances in cigarette smoke. Just like with alcohol, when people with the alcohol flush variant smoke, acetaldehyde builds up in their system. That means it’s especially unhealthy for them to smoke, too.
The role of ancient human migration
Scientists believe that the variant in this report first appeared in ancient China due to a random genetic mutation, and spread to neighboring regions as people migrated. It’s very rare for people who don’t have East Asian ancestry to carry the variant, though it does happen. For example, some Iranian individuals have the alcohol flush variant, possibly because millennia ago, traders traveling along the Silk Road brought the variant from China to the Middle East.
This report is based on genetic variants near two genes that play a role in how your body handles caffeine. The first gene, CYP1A2, contains instructions for an enzyme that breaks down 95% of the caffeine you consume. The second gene, AHR, contains instructions for a protein that ramps up production of the CYP1A2 enzyme. Variants in these genes may affect how quickly the body breaks down and clears away caffeine.
Other factors that affect caffeine consumption
The genetic variants in this report are associated with a difference of up to about two thirds of a cup of coffee per day. But there are other factors that also affect how much and what types of caffeine people choose to drink:
Other genetic factors: Scientists are still discovering genetic variants that may help account for differences in caffeine consumption.
Culture and history: Caffeine has been consumed for thousands of years in the form of coffee, tea, chocolate, and mate. Coffee originally became popular in Africa and the Middle East, tea in China, and chocolate drinks and mate in Central and South America.
Several studies have linked a genetic variant in the ADA gene to differences in a certain type of brain activity that characterizes deep sleep, called delta waves. People with your genetic result have delta waves that are about as strong as average, and also tend to feel less sleepy than deep sleepers after a night of missed sleep.
What is deep sleep?
Deep sleep is the phase of sleep when it’s hardest to wake up. When you enter deep sleep, your brain cells communicate with each other in a specific pattern that produces slow waves of electrical activity called delta waves. This pattern of activity is very different from when you’re awake, when brain activity is mostly composed of faster waves called alpha waves. Scientists think that the brain uses deep sleep to transfer memories of the day’s events from temporary to longer-term storage.
The biology of sleep pressure
The longer we stay awake, the sleepier we get. This accumulating need for sleep is sometimes called “sleep pressure.” A molecule called adenosine builds up in the brain the longer we stay awake, increasing sleep pressure and causing us to feel sleepy. Mid-day naps can help us feel more alert because they reduce adenosine levels and relieve the sleep pressure that has built up during the day.
The genetic marker in this report is in the ADA gene, which contains instructions for an enzyme that helps control adenosine levels. Scientists think that adenosine builds up more quickly in people with one or two copies of the T variant at this marker. This extra adenosine increases sleepiness, leading to stronger delta waves. Because of this stronger sleep pressure, people with the T variant also report feeling sleepier than other people after a night of missed sleep. However, one study found that taking naps eliminated this difference in sleepiness.
Your genes predispose you to weigh about average.
This doesn’t mean your weight will definitely be average. While your genes don’t appear to be strongly influencing your weight in either direction, your lifestyle and environment have just as much impact, if not more.
How did we calculate your result?
We determined your result by looking at DNA variants associated with weight based on our research. Some variants have a stronger effect on weight than others, which our analysis took into account. Because of this, your proportion of higher to lower weight variants may not exactly align with your overall predisposition. Keep in mind that other variants may also affect your weight.
Growing out of milk
Just about everybody is born with the ability to digest lactose, and this allows babies to live and grow by drinking their mothers’ milk. But as children grow older and begin to eat different foods, many of them lose that ability. People become lactose intolerant because their bodies stop producing lactase, the enzyme that digests lactose. The ability to continue producing lactase after childhood has evolved multiple times in different populations across the world, whenever a group of people depended on milk and dairy products as important sources of nutrition.
Evolution in action
Your DNA determines whether you can produce lactase after childhood, a trait known as “lactase persistence.” Research suggests that ancient humans were lactose intolerant, and different genetic variants associated with lactase persistence evolved at different times in different parts of the world. This report is based on a genetic variant associated with lactase persistence that evolved in Europe within the last 20,000 years.
Your genetic muscle composition is common in elite power athletes.
Studies have found that almost all elite power athletes (including sprinters, throwers, and jumpers) have a specific genetic variant in a gene related to muscle composition. You have the same genetic variant as these elite athletes.
Muscles and genetics
This report is based on a genetic marker in the ACTN3 gene. This marker controls whether muscle cells produce a protein (called alpha-actinin-3) that’s found in fast-twitch muscle fibers. While some people don’t produce this protein at all, almost all of the elite power athletes who have been studied have a genetic variant that allows them to produce the protein. This suggests that the protein may be beneficial at least at the highest levels of power-based athletic competition.
About endurance athletes
Most of the elite power athletes who have been studied have a genetic variant that allows them to produce the alpha-actinin-3 protein in their muscles. Does that mean that people who don’t produce this protein are more likely to be endurance athletes? Studies in mice suggest that the answer may be yes: young mice who don’t make any of this protein are able to run farther without getting tired. But studies in humans have not consistently shown an endurance advantage for people who don’t produce the alpha-actinin-3 protein.
Your weight is likely to be similar on diets high or low in saturated fat with the same number of total calories.
People with your genetic result tend to have a similar BMI on diets with greater or less than 22 grams of saturated fat per day, as long as they consume the same number of total calories.
However, diets high in saturated fat have been associated with increased LDL (“bad”) cholesterol, which is a risk factor for heart disease.
In addition to diet and exercise, genetics plays a role in determining your body weight. People with two copies of the variant in this report tend to weigh more on a high saturated fat diet. This variant is near a gene called APOA2, which contains instructions for making a protein called apolipoprotein A-II (apo A-II). People with two copies of the variant produce less apo A-II protein than people with zero or one variant. Scientists are working to understand how apo A-II affects our body’s response to saturated fat.
Based on your genetics, you’re likely to move less than average during sleep.
Several studies have shown that a genetic variant is associated with how much people move their arms and legs in their sleep. One of these studies found that people with your genetic result tend to move about 7 times an hour during sleep. On average, people move about 13 times an hour.
This report looks at a genetic marker in the BTBD9 gene. There are two possible versions of this marker, the A variant and the G variant. For each copy of the A variant a person has, they’re likely to move their limbs an additional 4-5 times per hour while sleeping, relative to people with two copies of the G variant. But scientists still don’t fully understand how this variant influences sleep movements.
The biology of sleep movements
Some evidence suggests that the BTBD9 protein affects how the body stores iron, which could influence how the brain regulates sleep movements. Some of the brain areas that store the most iron are also involved in regulating movements. The brain uses iron for many functions, including building molecules that brain cells use to communicate with each other.
9 Genetic Health Risk Reports
Learn whether you have specific genetic variants that can influence your risk for certain health conditions.
Age-Related Macular Degeneration
Alpha-1 Antitrypsin Deficiency
BRCA1/BRCA2 (Selected Variants)
Hereditary Hemochromatosis (HFE‑Related)
Late-Onset Alzheimer’s Disease
43 Carrier Status Reports
Learn whether you have specific genetic variants that may not affect your health, but could affect your children’s health.
Agenesis of the Corpus Callosum with Peripheral Neuropathy
Autosomal Recessive Polycystic Kidney Disease
Beta Thalassemia and Related Hemoglobinopathies
Congenital Disorder of Glycosylation Type 1a (PMM2-CDG)
D-Bifunctional Protein Deficiency
Dihydrolipoamide Dehydrogenase Deficiency
Familial Hyperinsulinism (ABCC8-Related)
Fanconi Anemia Group C
Gaucher Disease Type 1
Glycogen Storage Disease Type Ia
Glycogen Storage Disease Type Ib
Hereditary Fructose Intolerance
Herlitz Junctional Epidermolysis Bullosa (LAMB3-Related)
Leigh Syndrome, French Canadian Type
Limb-Girdle Muscular Dystrophy Type 2D
Limb-Girdle Muscular Dystrophy Type 2E
Limb-Girdle Muscular Dystrophy Type 2I
Maple Syrup Urine Disease Type 1B
Mucolipidosis Type IV
Neuronal Ceroid Lipofuscinosis (CLN5-Related)
Neuronal Ceroid Lipofuscinosis (PPT1-Related)
Niemann-Pick Disease Type A
Nijmegen Breakage Syndrome
Nonsyndromic Hearing Loss and Deafness, DFNB1 (GJB2-Related)
Pendred Syndrome and DFNB4 Hearing Loss (SLC26A4-Related)
Phenylketonuria and Related Disorders
Primary Hyperoxaluria Type 2
Rhizomelic Chondrodysplasia Punctata Type 1
Sickle Cell Anemia
Tyrosinemia Type I
Usher Syndrome Type 1F
Usher Syndrome Type 3A
Zellweger Syndrome Spectrum (PEX1-Related)
Tools and Research
23andMe has recently added a podcast named Spit, available on iHeartRadio, featuring conversations with scientists and celebrities, sharing insight on family lore, society, identity, and genetics.
23andMe also offers a Tool section which includes:
- DNA Relatives – Find your genetic relatives to make connections and compare DNA. You can learn about relationships, shared ancestors and family history, plus see what segments you share to discover even more.
- GrandTree – Trace the flow of DNA from grandparents to grandchildren in your family.
- Share and Compare – Share your reports with close family and friends to view your genetic similarities and differences.
- Your Connections – Connecting with friends and family allows you to share reports and activate comparison tools.
- DNA Comparison – Identical or overlapping DNA segments indicate a common ancestor and can help identify relationships across multiple relatives.
Lastly, there is a Research section which includes:
- Surveys – Customers who consented may contribute their data which may be published in scientific journals.
- Health Communities – Learn about health conditions that affect 23andMe customers and explore treatments they’ve tried.
- Publications – Since 2010, there are 112 published.