Browse public phenotypes.

Mood instability measurement captures how frequently and intensely an individual’s emotional state fluctuates—ranging from periods of happiness to sudden shifts toward sadness, irritability, or anxiety. Research shows that variations near genes involved in neurotransmitter regulation and emotional processing (such as SLC6A4, BDNF, and CACNA1C) can influence individual differences in mood stability. Mood instability affects a significant portion of the population, with heritability estimates around 30–50%, reflecting a blend of genetic predisposition and environmental factors like stress and life events.

Neuroticism measurement captures a personality trait characterized by emotional instability, anxiety, and a tendency toward negative feelings like worry and irritability. Research shows that variations near genes involved in neurotransmission and stress response (such as SLC6A4, CRHR1, and BDNF) can influence individual differences in neuroticism. Neuroticism varies widely among individuals, with heritability estimates around 40–50%, reflecting a significant genetic contribution alongside environmental influences such as life stressors.

Non-word reading measures your ability to decode and pronounce unfamiliar letter combinations—testing phonological processing and early reading skills independent of vocabulary knowledge. Research shows that variations near genes involved in language and reading development (such as KIAA0319, DCDC2, and FOXP2) can influence individual differences in decoding ability. Performance in non-word reading varies across individuals, with heritability estimates around 40–60%, highlighting a meaningful genetic contribution alongside environmental factors like education and exposure.

Pain is your body’s warning system signaling injury, inflammation, or potential harm—ranging from sharp acute sensations to persistent chronic discomfort that affects daily life. Research shows that variations near genes involved in pain perception and nerve signaling (like SCN9A, OPRM1, and TRPV1) can influence individual differences in pain sensitivity and chronic pain risk. Pain experiences vary widely, with heritability estimates ranging from 30–50%, reflecting the complex interplay of genetic predisposition and environmental factors such as injury and psychological state.

Phoneme awareness measures your ability to recognize and manipulate individual sounds in spoken words—a foundational skill for learning to read and spell. Research shows that variations near genes involved in language development and auditory processing (such as KIAA0319, DCDC2, and FOXP2) can influence individual differences in phoneme awareness. Phoneme awareness varies across individuals, with heritability estimates around 40–60%, highlighting a meaningful genetic contribution alongside environmental factors like language exposure and education.

Puberty onset measurement captures the age at which an individual begins the biological transition from childhood to adolescence, marked by physical and hormonal changes. Research shows that variations near genes involved in hormonal regulation and reproductive development (like LIN28B, KISS1, and MKRN3) can influence differences in timing of puberty onset. The average age of puberty onset varies but typically occurs between 8–13 years in girls and 9–14 years in boys, with heritability estimates ranging from 50–80%, underscoring a strong genetic influence alongside environmental factors.

Some people tan golden brown with ease; others burn red within minutes. Our skin's reaction to sunlight isn’t a matter of toughness—it's a deeply wired trait shaped by millennia of adaptation to regional UV exposure. This sensitivity tells a story of ancestral geography, melanin protection, and cellular defense mechanisms. Knowing your own helps you make smarter choices—not just for beauty, but for long-term skin health. Genetically, sun sensitivity is largely influenced by variants in the MC1R, SLC24A5, and TYR genes, which regulate melanin type and skin pigmentation responses to UV light. Roughly 20–30% of Europeans carry MC1R variants associated with higher sun sensitivity. The heritability of skin sensitivity to sun is high—estimated between 60% and 90%—indicating that genetics plays a major role in how skin responds to ultraviolet radiation.

Sweet liking measures how much you enjoy sugary tastes—the simple pleasure that can brighten a moment or fuel a craving. This preference shapes your food choices and even your mood, balancing between delight and moderation. Understanding sweet liking helps reveal why some of us reach for desserts more often, while others keep their sweet tooth in check. Genetic variants in taste receptor genes like TAS1R2 and TAS1R3 influence how intensely sweetness is perceived and how much it’s enjoyed, affecting individual differences in sweet liking. Sweet liking varies across people, with heritability estimates ranging from 30% to 60%, showing that both genetics and environment—like culture and early exposure—play important roles in shaping this taste preference.

What we crave on our plates isn’t random—it’s deeply personal, shaped by biology and memory alike. Whether you lean toward the sharpness of dark chocolate, the bitterness of coffee, or the creaminess of cheese, your taste preferences are more than habits—they’re reflections of how your brain interprets the world, and how your genes tune your senses to respond. Variants in genes like TAS2R38 (for bitter), TAS1R2/3 (sweet and umami), and OR6A2 (odor-related) influence not only how intensely we perceive certain tastes, but also how much we enjoy or avoid them. Taste liking varies widely between individuals, and studies suggest heritability estimates range from 20% to 70% depending on the specific taste category, showing strong genetic input but also large environmental influence from exposure, culture, and early dietary experiences.

Energy, clarity, and nerve function all quietly depend on something we rarely think about—vitamin B12. This essential nutrient fuels red blood cell production, DNA synthesis, and neurological health. Whether you're thriving on a balanced diet or navigating the risks of deficiency, your B12 levels say a lot about your internal balance, particularly if you're vegetarian, older, or managing gut issues. Genetic factors influencing B12 levels include variants in genes like FUT2, TCN2, and MTHFR, which affect B12 absorption, transport, and conversion into active forms. Vitamin B12 deficiency affects around 6% of people under 60 and up to 20% of those over 60 in developed countries. Heritability of B12 levels is estimated between 35–60%, reflecting a significant genetic role in determining individual needs and responses to supplementation.

Vitamin D amount is your sunlight-and-food snapshot — a measure of how much 25-hydroxyvitamin D circulates in your blood, reflecting time outdoors, diet, skin pigmentation, latitude, and season. It quietly tracks how your body captures light and turns it into support for bones, muscles, and everyday resilience. Research shows that common variants near genes governing synthesis, transport, and breakdown — including GC, CYP2R1, DHCR7, and CYP24A1 — contribute to individual differences in 25(OH)D levels. Population averages vary by season and region, often landing around 20–30 ng/mL (50–75 nmol/L), and twin and SNP-based studies estimate heritability at roughly 20–40%, indicating a measurable genetic signal atop environment and lifestyle.

Age at first sexual intercourse marks a significant milestone in personal development, influenced by a mix of cultural, social, and biological factors. This timing can impact future relationships, health outcomes, and emotional wellbeing, reflecting the complex interplay between individual readiness and environment. Genetic variations near genes such as CADM2, MSRA, and ESR1 have been linked to differences in the age individuals typically begin sexual activity, affecting traits like risk-taking and hormonal regulation. Across populations, the average age at first sexual intercourse ranges from the mid-teens to early twenties, with heritability estimates around 30–50%, highlighting the combined effects of genetics and social context.

Anxiety Measurement is your mind’s internal radar for stress and unease, dialed up when deadlines loom or uncertainties arise—capturing those racing thoughts, sweaty palms, and that knot in your stomach. Research shows that variations near genes regulating the stress‑response system (like CRHR1 and FKBP5) and those influencing neurotransmitter signaling (such as SLC6A4) can shape individual differences in anxiety levels. Between 15–20% of people experience clinically significant anxiety symptoms at some point, and twin studies estimate heritability of trait anxiety at around 30–50%, highlighting both genetic and environmental contributions.

Back pain is your body’s built‑in alert system when spinal structures get aggravated, turning a simple bend or twist into a sharp twinge or dull ache—a common reminder that even everyday movements can stress your lower back. Research shows that variations near genes regulating connective‑tissue integrity (like COL9A2 and COL11A1) and those influencing pain‑signal transmission (such as SCN9A) can increase susceptibility. Up to 80% of adults experience back pain at some point in their lives, and twin studies estimate heritability between 30–45%, highlighting both genetic and environmental contributions to chronic or recurrent pain.

Blood protein measurement is your bloodstream’s cargo manifest, revealing the concentration of key proteins—like albumin, globulins, and transport factors—that keep tissues nourished and immunity primed. Research shows that variations near genes regulating protein synthesis and turnover (such as ALB and SERPINA1) and those involved in immune‐related proteins (like C3) can influence your circulating protein levels. In healthy adults, total serum protein typically ranges from 60–80 g/L, and twin studies estimate heritability of total protein levels at around 50–60%, highlighting a substantial genetic contribution to these essential biomarkers.

Breast size is a visible, variable trait shaped by fat distribution, glandular tissue, and hormonal signaling — changing naturally through puberty, pregnancy, and weight fluctuation. Research shows that variations near genes involved in estrogen signaling, tissue development, and fat distribution (like ZNF703, ESR1, and IGF1) can influence individual differences in breast volume and shape. Breast size varies widely across individuals and populations, with moderate heritability estimates around 40–60%, highlighting a meaningful but not exclusive genetic contribution to this trait.

Cannabis dependence reflects a pattern of repeated use that becomes hard to control—where the line between casual and compulsive blurs, often tied to cravings, tolerance, and withdrawal symptoms. Research shows that variations near genes involved in endocannabinoid signaling and neural reward pathways (like CNR1, CADM2, and CHRNA2) can influence susceptibility to cannabis dependence. Cannabis dependence affects roughly 1–2% of the population globally, with higher rates among frequent users, and heritability estimates range from 50–70%, highlighting a substantial genetic contribution to risk.

Creatine measurement reflects the levels of creatine in your body, a molecule crucial for energy storage and supply—especially in muscles and the brain—supporting activities that require quick bursts of power. Research shows that variations near genes involved in creatine synthesis and transport (like GATM, CKB, and SLC6A8) can influence individual differences in creatine levels and metabolism. Creatine levels vary based on diet, muscle mass, and physiology, with heritability estimates around 40–60%, highlighting a meaningful genetic contribution to how your body manages this vital energy molecule.

Acne is your skin’s loudspeaker for oil and bacteria overload, showing up as stubborn spots or deep bumps—an all‑too‑familiar badge of teenage hormones (and sometimes adult stress). Research shows that variations near genes regulating sebum production (like TG and MC5R) and those involved in skin‑barrier function (such as FLG) can increase susceptibility. Acne affects up to 85% of adolescents—and persists into adulthood for about 12% of people—with heritability estimates around 75%, highlighting how much your DNA can shape breakout risk.

Appendicular lean mass is the measurable bulk of muscle in your arms and legs—your body’s built‑in strength reservoir that powers everything from lifting groceries to climbing stairs, and subtly shifts with age, activity, or injury. Research shows that variations near genes regulating muscle development (like MSTN and IGF1) and those involved in muscle metabolism (such as PPARGC1A) can influence how much limb muscle you maintain. In healthy adults, average appendicular lean mass ranges broadly (roughly 15–25 kg in women and 20–35 kg in men), and heritability estimates hover around 60–70%, highlighting a substantial genetic role in shaping your muscular frame.

Balding measurement is your scalp’s personal scoreboard for hair loss, tracking how far your hairline retreats or crown thins — an unspoken gauge of genetics, hormones, and the passage of time. Research shows that variations near genes regulating androgen signaling (like AR and EDA2R) and those involved in hair follicle cycling (such as WNT10A) can strongly influence individual differences in balding patterns. Male‑pattern baldness affects up to 80% of men by age 70 — and female hair thinning impacts about 40% of women by menopause — with heritability estimates often above 80%, underscoring a dominant genetic role in scalp hair retention.

BMI‑adjusted waist circumference is your body’s spotlight on where fat settles around your middle—capturing central adiposity independent of overall body size, and flagging risks that BMI alone can miss. Research shows that variations near genes regulating fat distribution and adipocyte biology (like LYPLAL1 and RSPO3) and those involved in lipid metabolism (such as HOXC13) can influence how much fat pools around your waist for a given BMI. Elevated central adiposity—reflected in high BMI‑adjusted waist circumference—affects roughly 30–40% of adults, and heritability estimates for this trait range from about 40–60%, underscoring a substantial genetic contribution to fat distribution.

BMI‑adjusted waist‑hip ratio is your body’s map for fat distribution, revealing whether excess weight settles around your waist versus your hips—insights that BMI alone can miss when assessing cardiometabolic risk. Research shows that variations near genes regulating adipose tissue patterning (like LYPLAL1, RSPO3, and TBX15) and those involved in hormonal control of fat storage (such as PPARG) can shape individual differences in how fat is allocated between waist and hips. Elevated BMI‑adjusted waist‑hip ratio is seen in roughly 25–35% of adults, and twin studies estimate its heritability at about 50–60%, underscoring a substantial genetic influence on body‑fat distribution.

Body fat distribution is your body’s custom landscape for where extra energy stores settle—whether they pool around your midsection, hug your hips, or pad your thighs—shaping both your silhouette and your metabolic health. Research shows that variations near genes regulating adipocyte development and fat‐cell differentiation (like FTO and MC4R) and those involved in hormone signaling (such as ESR1) can influence how and where fat is deposited. Central versus peripheral fat patterns differ across individuals—abdominal fat accumulation impacts roughly 30–40% of adults—and twin studies estimate heritability of body‐fat distribution at about 50–60%, highlighting a substantial genetic role.

Body mass index (BMI) is your body’s basic weight‑to‑height ratio—a quick, if imperfect, snapshot of overall body composition that flags underweight, overweight, or obesity risk. Research shows that variations near genes regulating appetite, energy balance, and fat storage (like FTO, MC4R, and TMEM18) can influence individual differences in BMI. BMI varies widely across populations, with global averages ranging from 22 to 28, and heritability estimates between 40–70%, highlighting a strong genetic influence on body weight regulation.

Educational attainment measures the highest level of formal education completed, reflecting a combination of cognitive abilities, motivation, and social factors shaping learning success. Research shows that variations near genes involved in brain development and cognitive function (like FOXP2, KIAA0319, and DRD2) can influence differences in educational achievement. Educational attainment varies widely across populations, with heritability estimates ranging from 40–60%, indicating a significant genetic influence alongside environmental and socioeconomic factors.

Executive function measurement captures your brain’s ability to plan, organize, control impulses, and adapt to new situations—skills essential for goal-directed behavior and problem-solving. Research shows that variations near genes involved in prefrontal cortex activity and neurotransmission (such as COMT, DRD4, and BDNF) can influence individual differences in executive function. Executive function varies widely among individuals, with heritability estimates ranging from 40–60%, reflecting a meaningful genetic contribution alongside environmental influences like education and stress.

Feeling emotionally hurt measurement captures how deeply individuals perceive and respond to emotional pain—reflecting sensitivity to rejection, criticism, or loss that can shape mental well-being. Research shows that variations near genes involved in emotional regulation and stress response (like OXTR, SLC6A4, and FKBP5) can influence individual differences in emotional sensitivity. Emotional hurt sensitivity varies widely, with heritability estimates around 30–50%, highlighting a blend of genetic predisposition and environmental influences like upbringing and life experiences.

Growth rate attribute measures how quickly an individual’s body or specific tissues increase in size over time—reflecting developmental speed during childhood and adolescence. Research shows that variations near genes involved in cell proliferation and hormonal regulation (like IGF1, GH1, and GHR) can influence individual differences in growth rate. Growth rates vary widely across individuals and stages of development, with heritability estimates around 60–80%, underscoring a strong genetic influence on how quickly people grow.

Head circumference measures the size of the skull around its widest part—an important indicator of brain growth and development, especially in infancy and early childhood. Research shows that variations near genes involved in brain growth and cranial development (like HMGA2, EFEMP1, and SOX9) can influence individual differences in head size. Head circumference varies with age and sex, and heritability estimates range from 70–90%, highlighting a strong genetic contribution to this physical trait.