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Lifestyle/Chronic Disease/Drug Risk Genes GENO‑RISK

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You take an annual health screening, yet when the doctor says "let's monitor it," you still don't know what to do next. Genes aren't there to predict disease — they're the coordinates of how your body actually runs. Why some people react differently to the same medication, absorb the same vitamin to different levels, or take days longer to recover from the same workout. Predict Gene reads 14,000 genes and 236,000 loci from a single blood draw, weaving cardiovascular, metabolic, drug-response, nutritional, and exercise traits into one complete physiological map — showing you where you're naturally strong, and where you need to start managing from today.

Blood
Single blood draw
236K
Loci analyzed in parallel
14K
Genes cross-system mapped
14
Business days to report

SECTION 01

What is this test for?

Through blood gene testing, we can comprehensively analyze your sleep, nutrition absorption, exercise performance, disease risk and medication reaction constitution, providing a long-term and effective decision-making basis for health management.

49 markers · 14 groups
Coagulation & Vessels 4 items
Venous Thromboembolism (VTE) Integrates 12 coagulation-pathway genes including F5, F11, PROC, PROS, FGG, FGA, VWF, and ABO to evaluate venous thrombosis tendency. This pathway also informs risk assessment during long-haul flights, post-surgical recovery, and oral contraceptive use — and links downstream to vascular health via MTHFR/homocysteine metabolism. Hereditary Stroke NOTCH3 and CYBA influence small-vessel integrity and oxidative stress response. Shares mechanisms with atherosclerosis and blood pressure regulation — an early signal on the vascular-aging axis. Atherosclerosis IL-6 and JCAD assess the impact of chronic inflammation on vessel walls. The inflammation axis is shared with exercise recovery (IL6/TNF/CRP), influenza severity, and atopic dermatitis — a baseline indicator of your body's inflammatory reactivity. Familial Hypercholesterolemia (FH) APOB and LDLR directly determine LDL receptor clearance efficiency. Even with strict diet control, variants in these genes substantially shift the cholesterol metabolism ceiling — and modulate statin response in conjunction with SLCO1B1.
Glucose & Lipid Metabolism 4 items
Type 2 Diabetes Six genes — TCF7L2, UBE2E2, CDKAL1, HHEX, KCNQ1, SLC30A8 — collectively assess insulin secretion and glucose regulation. Also linked to weight management, fatty liver risk, and response to diabetes medications such as glimepiride and glipizide. Non-Alcoholic Fatty Liver (NAFLD) APOC3 and PNPLA3 are key regulators of hepatic fat accumulation. Even without alcohol intake, variants in these genes raise NAFLD progression risk — sharing a metabolic axis with insulin resistance and type 2 diabetes. Hyperuricemia ABCG2 is the major transporter for uric acid excretion. Variants lower clearance efficiency, elevate gout risk, and influence the response to urate-lowering drugs such as rasburicase. Obesity Predisposition FTO is a master regulator of fat storage. The same FTO variant simultaneously affects fat-burning capacity (exercise outcome), appetite regulation, and type 2 diabetes risk — a central node on the energy-balance axis.
Joints & Bone Density 2 items
Osteoarthritis TGFA, RUNX2, GDF5, and ALDH1A2 evaluate cartilage repair and inflammatory tendency. Shares genes with exercise injury risk (VDR/GDF5), allowing combined interpretation when designing training intensity and protective strategy. Osteoporosis Five genes — FGFR2, MPP7, JAG1, TNFRSF11B, ZBTB40 — assess bone density maintenance capacity. Best read alongside vitamin D metabolism (GC) and calcium absorption: genes set the ceiling, lifestyle determines how close you get to it.
Eye Health 2 items
Age-related Macular Degeneration (AMD) CFH, ARMS2, and C2 form the core gene panel for AMD risk. They link to the complement-system inflammation axis, which also drives macular pigment maintenance needs (e.g., the recommended intake intensity of lutein and zeaxanthin). Glaucoma GAS7, TMCO1, and FAM125B influence intraocular pressure regulation and optic nerve sensitivity, assessing predisposition to primary open-angle glaucoma.
Respiratory & Immune 4 items
Asthma Risk GSTP1 and GSDMB assess airway inflammation tendency. GSDMB also participates in inflammatory cell-death pathways, influencing both common cold severity and dust-mite-induced asthma risk. Atopic Dermatitis RTEL1 and RTEL1-TNFRSF6B evaluate skin barrier function and immune hyperreactivity. Shares immune axes with asthma and dust mite allergy — when all three score high, an overall allergic constitution is likely. Dust Mite Allergy LY86-AS1 and LY86 assess immune-cell recognition intensity against dust mite antigens. Sits on the IgE-mediated allergy axis and can be cross-interpreted with asthma and atopic dermatitis risk. Traffic Pollutant Sensitivity SAMSN1, RARS2, and BMP8A-PPIEL govern the inflammatory response to PM2.5 and traffic exhaust particles. Higher sensitivity elevates the risk of asthma and cardiovascular events — particularly relevant for urban commuters.
Viral Infection & Vaccine Response 5 items
Influenza Risk LGALS1 and IL1B assess susceptibility to influenza infection. IL1B is a core inflammatory cytokine — its variants also modulate other infection severity and fever response. Influenza Severity IL10 and LTA influence post-infection complication risk. IL10 anchors the anti-inflammatory axis and also modulates the intensity of post-vaccine fever. Flu Vaccine Efficacy MBL-2 and IL-1RN assess antibody production efficiency after vaccination. The same gene set also modulates post-vaccine fever likelihood — useful for distinguishing 'high protection + low reaction' from 'high protection + likely fever' profiles. Flu Vaccine Fever Response MBL-2 and IL10 assess the likelihood of fever after vaccination. Knowing this in advance lets you prepare antipyretics or schedule the shot away from important commitments. Common Cold Severity Five genes — ORMDL3, GSDMB, CCR5, IL-13, SCGB1A1 — jointly assess the risk of post-cold asthma or bronchitis. Shared with asthma and dust mite sensitivity genes — when all three are elevated, extra airway protection is warranted.
Vitamin Demand 6 items
Vitamin A RBP4 governs vitamin A transport in the bloodstream. Linked to macular health and night vision function. Vitamin B6 NBPF3 modulates B6 metabolic clearance rate. B6 sits with folate and B12 on the homocysteine metabolism axis — together influencing cardiovascular risk. Folate MTHFR is the central enzyme for folate metabolism and a key node in homocysteine handling. Variants simultaneously affect cardiovascular risk (VTE axis), neurotransmitter synthesis, and DNA methylation (aging axis) — one of the most cross-domain loci in this panel. Vitamin B12 Five genes — MS4A3, CLYBL/LOC101927437, FUT6, PRELID2 — jointly assess B12 absorption and utilization. Particularly relevant for vegetarians and long-term users of acid-suppressing medications. Vitamin D The GC gene controls vitamin D binding protein activity, dictating the bioavailable D concentration in blood. Connected to osteoporosis, immune modulation, and glucose metabolism — among the most cross-system vitamins in this panel. Vitamin E CYP4F2 and ZPR1 regulate vitamin E metabolism rate. As a core fat-soluble antioxidant, vitamin E status links to macular health, skin aging, and cardiovascular oxidative stress.
Dietary Sensitivity 3 items
Lactose Intolerance MCM6 controls adult lactase expression. Approximately 85% of Taiwanese carry the lactase non-persistence genotype, though symptom severity varies widely between individuals. Gluten Sensitivity HLA-DQA1 and HLA-DQB1 are the core risk genes for celiac disease. Sitting on the immune axis, they correlate with other autoimmune tendencies. Alcohol Sensitivity ALDH2 is the key enzyme for acetaldehyde metabolism. About 47% of Taiwanese carry the ALDH2 variant; slow metabolizers experience facial flushing and dizziness with alcohol — and the same variant is associated with increased risk of oral and esophageal cancers.
Sleep Quality 2 items
Sleep Effectiveness ADA modulates adenosine metabolism rate, determining post-sleep alertness restoration. Partially overlaps with the caffeine metabolism axis. Sleep Continuity FABP7 affects sleep continuity. Those prone to fragmented sleep may need to pay closer attention to their sleep environment.
Exercise Performance 6 items
Recovery Capacity Three core inflammation genes — IL6, TNF, CRP — assessed together. Shared with the atherosclerosis and chronic inflammation gene set: 'fast recovery after exercise' also signals 'well-controlled inflammatory response.' Oxygen Uptake (VO₂) VEGFA governs angiogenesis and oxygen delivery. Also relevant to cardiovascular health and wound healing. Fat Burning Capacity FTO doubles as the key gene for obesity predisposition — a single locus tells you two things: your fat storage tendency, and the ceiling of your exercise-induced fat burning efficiency. Injury Risk VDR and GDF5 assess ligament and tendon strength. VDR is also the vitamin D receptor, sharing an axis with osteoporosis and osteoarthritis — those flagged as injury-prone may also need to attend to long-term bone health. Muscle Power ACTN3 is the so-called 'sprinter gene,' determining fast-twitch muscle fiber composition. AGT modulates blood pressure response to exercise. Endurance ADRB3 and BDKRB2 assess aerobic endurance-related physiological response. Cross-read with VO₂ to determine whether you're better suited to short-burst or long-distance disciplines.
Hepatic Metabolism (CYP450) 4 items
NSAIDs CYP2C9 dictates the metabolism rate of six common NSAIDs including ibuprofen, celecoxib, and meloxicam. Slow metabolizers face elevated hepatic burden and GI bleeding risk with long-term use. CYP2C9 also processes warfarin, phenytoin, and several other prescription drugs. Antidepressants & Antiepileptics CYP2C19 governs metabolism of citalopram, escitalopram, sertraline (antidepressants), clobazam (antiepileptic), and clopidogrel (antiplatelet). A single metabolic pathway spanning four major drug classes — exemplifying the core value of pharmacogenomic testing. Anti-infective (Efavirenz) CYP2B6 modulates efavirenz metabolism. Intermediate metabolizers are advised to adjust the starting dose to reduce neurotoxicity risk. Immunosuppressants CYP3A5 modulates tacrolimus metabolism — a critical gene in organ transplantation. It also influences the metabolism of corticosteroids and certain chemotherapy agents.
Oxidative Stress (G6PD) 1 items
G6PD-related Drugs G6PD is far more than the 'favism' label — it is the central antioxidant enzyme in red blood cells. The same gene drives hemolysis risk across more than ten drug categories: certain antibiotics (ceftriaxone, nalidixic acid), diabetes medications (glimepiride, glipizide), antimalarials, anesthetics, antidotes, and more. A truly cross-class critical gene.
Mitochondrial (MT-RNR1) 1 items
Aminoglycoside Antibiotics MT-RNR1 encodes the mitochondrial ribosome. Carriers of the variant face substantially elevated ototoxicity risk (permanent hearing loss) with six aminoglycoside antibiotics: amikacin, gentamicin, neomycin, streptomycin, tobramycin, and paromomycin. A textbook example of 'one gene = one life-saving warning.'
Other Metabolic Genes 5 items
TPMT (Immunosuppressants/Chemotherapy) TPMT controls the metabolism of thiopurine drugs such as azathioprine and mercaptopurine. Slow metabolizers receiving standard doses face severe bone marrow suppression. NAT2 (Antitubercular/Sulfonamides) NAT2 affects the metabolism of isoniazid (antitubercular) and sulfamethoxazole/sulfasalazine. Slow metabolizers face increased hepatotoxicity risk. UGT1A1 (Chemotherapy) UGT1A1 governs the metabolism of three chemotherapy agents: irinotecan, nilotinib, and pazopanib. Variant carriers receiving standard doses face heightened risk of serious adverse effects. SLCO1B1 (Statins) SLCO1B1 is the key transporter delivering statins into hepatocytes. Variant carriers using simvastatin are prone to myopathy — directly relevant to familial hypercholesterolemia management. IFNL3/IL28B (Hepatitis C) Predicts response to peginterferon Alfa-2a and ribavirin in hepatitis C treatment — favorable genotypes correlate with higher sustained virological response (SVR) rates.

Section 02 — Why Trust This Test

Your genome isn't 236,000 isolated answers — it's a single interwoven map

Cross-system reading

One gene moves several physiological dials at once

FTO doesn't only decide obesity tendency — it also sets your fat-burning ceiling. MTHFR doesn't only affect folate — it links to cardiovascular and neurological pathways. G6PD isn't just a "favism" label — it's the shared origin of hemolysis risk across more than ten drug categories. Predict Gene gathers these cross-system links into one report, so what you see isn't a list of points, but a network.

Polygenic risk scoring

236,000 loci, approaching genome-wide array resolution

Instead of checking a few popular genes, Predict Gene analyzes 14,000 genes across 236,000 loci in parallel. Every risk score is calculated as a polygenic risk score (PRS) — for example, type 2 diabetes integrates 6 genes; venous thromboembolism integrates 12. This is the modern standard for genomic medicine, not a single-gene snapshot.

Clinical-grade pharmacogenomics

Drug guidance follows CPIC, FDA, and DPWG standards

The pharmacogenomic section isn't speculative — it follows clinical-grade recommendations from the U.S. FDA drug label, the Clinical Pharmacogenetics Implementation Consortium (CPIC), and the Dutch Pharmacogenetics Working Group (DPWG). A single report archived once becomes a lifelong reference for any future physician — particularly valuable for chemotherapy, immunosuppression, and antidepressant dosing.

236Kloci
High-resolution genotyping array

14,000 genes analyzed in parallel across four domains: health risk, nutrition, exercise performance, and drug response.

13drug classes
Full pharmacogenomic (PGx) coverage

Spans NSAIDs, antibiotics, antidepressants, chemotherapy, immunosuppressants, and 50+ commonly prescribed medications.

Resolution depth comparison
Predict Gene
Standard SNP panel
Single-gene test
Compared by number of loci analyzed; interpretive value depends on cross-gene analytical capability.

Section 03 — Who It's For

Not just for the unwell — for anyone who wants to see their genetic baseline clearly

🧬
Family-history conscious

Parents or siblings with cardiovascular disease, diabetes, or cancer history

Family history isn't destiny, but it does raise your baseline. With polygenic scoring, you see your actual risk tier — possibly higher than you expected, possibly milder — and gain a 10-to-20-year window to act on it before symptoms emerge.

💊
Complex medication users

On long-term medication, managing chronic conditions, or preparing for major treatment

If a painkiller doesn't work for you, the answer might be in your genes; certain antibiotics that "sometimes affect hearing" may carry specific risk for you. The report covers metabolism guidance for 50+ commonly prescribed drugs — archived once, available for any future physician.

🥗
Nutrition & training investors

For those who spend on supplements, coaches, and structured nutrition plans

The same vitamin D works for one person and not another; the same training plan suits power athletes for some, endurance work for others. Your genes reveal the underlying configuration — so every health investment lines up with how your body is actually wired.

🔍
Preventive health mindset

Healthy now, but want to see the underlying physiology

Annual screenings reveal your current status; genetic testing reveals your inherited tendencies. Layered together, you can see which patterns are accumulating over time and which require dedicated lifelong management. This map is drawn once — and used for a lifetime.

Section 04 — Why You Need to Know Now

Health screenings show what's happening now. Genes explain why.

"Same diet, same exercise, same environment — so why do some people gain weight more easily, tire faster, or get less benefit from the same medication?"

A health screening tells you your blood sugar is 95, your cholesterol is 180, your blood pressure is normal — snapshots of where your body is right now. What it can't tell you is why your colleague eats the same meals and has half the body fat, why three months of vitamin D supplementation hasn't moved your serum level, or why your mother takes statins without issue while you develop muscle pain.

The answers sit in your genome. Predict Gene synthesizes a decade of genome-wide association studies (GWAS) into a single personalized report — not to predict disease, but to clarify where your body has natural advantages and where you need a more deliberate management strategy.

This is a genetic predisposition assessment intended to inform lifestyle and health management decisions. It does not replace clinical diagnosis or treatment recommendations. Pharmacogenomic information is intended for clinician reference during prescribing.

10–20 yrs

Window between genetic risk and symptom onset

Most chronic disease tendencies become genetically identifiable 10 to 20 years before symptoms appear. Knowing early means you have two decades to change the trajectory.

Nature Reviews Genetics, 2018
7%

Prescriptions affected by pharmacogenomics

Studies estimate that roughly 7% of prescriptions have efficacy or safety modulated by genotype. An archived PGx record reduces the risk of major adverse drug reactions.

Clin Pharmacol Ther, 2021 — CPIC Guidelines

Discriminative power of polygenic scoring

For coronary artery disease, type 2 diabetes, and other common conditions, polygenic risk scores (PRS) can identify individuals with 5× the population risk — reshaping decisions about early intervention.

Nature Genetics, 2018 — Khera et al.

Section 05 — Common Myths

Is genetic testing worth it? Most people get stuck on these questions.

Common myth

"If my genes are bad, knowing won't change anything. Why test?"

Your genes don't change — but how they express does. The same FTO obesity variant has only one-third the impact on regular exercisers; the same APOE cardiovascular risk gene cuts event rates by half in those with disciplined diets. Your genes show where your starting line is, so you know exactly where lifestyle effort earns the highest return.

Genes are tendencies, not verdicts — and tendencies are exactly what you should know before designing your lifestyle.

Common myth

"I'm healthy. Why would I test now?"

Healthy is exactly the right time. Most chronic disease risk becomes genetically identifiable 10 to 20 years before symptoms appear. Once blood sugar, blood pressure, or cholesterol start drifting, you've already lost the most valuable window for early intervention. Testing while healthy isn't about treating illness — it's about knowing which parts of your body handle stress easily and which need attention starting today.

Genetic testing isn't for patients — it's for people who still have time to decide.

Common myth

"I get an annual health screening. Isn't that enough?"

Health screenings and genetic testing look at different layers. Screenings show current status — blood glucose, liver enzymes, tumor markers. Genetic testing shows your inherited configuration — why you're prone to B12 deficiency, why certain medications hit you harder, why your vitamin D level lags despite consistent supplementation. The two together explain the "why" behind every screening result.

Screenings answer "what's happening now." Genetic testing answers "why it's happening." They complement, not replace.

Common myth

"Knowing my risks will just make me anxious. Better not to know."

This is one of the most common misconceptions. Longitudinal studies tracking the psychological state of people who've taken genetic tests show anxiety briefly rises in the first week — and then, six months later, sits lower than in the untested control group. "Not knowing" is the real source of anxiety. Once you see the map, most results turn out to be "normal" or "advantageous," and the items requiring active management are typically fewer than expected.

Anxiety comes from uncertainty, not from information.

Common myth

"I'm only in my early 30s. Isn't this too early?"

Your genes were set at conception — the result of testing at 30 is identical to the result at 60. The difference is how many years you have left to act on it. At 30, you've got three decades to adjust diet, training, and supplementation. At 60, many tendencies may have already materialized into actual health problems. The test only needs to happen once — but the earlier, the more years it serves you.

The value of genetic testing scales with time. The earlier you know, the more time it gives you.

Common myth

"It's all genetic. There's probably not much I can do."

For most common conditions, genes account for only 20–40% of the risk. Environment and lifestyle account for the remaining 60–80%. The Predict Gene report tells you exactly which tendencies are reversible through exercise (such as FTO obesity), which can be addressed through targeted nutrition (such as MTHFR folate), and which simply require avoiding specific medications (such as MT-RNR1 ototoxicity). Knowing the source of risk is what makes precision possible.

Genes set the starting line. How you run the race decides the finish.

Section 06 — Upgrade

An inherited map, or a continuously updated health coordinate?

Standalone purchase

Predict Gene Comprehensive Analysis

236,000 loci / 14,000 genes / 13 drug classes — a single complete read of your genome.

NT$ 12,800/ one-time
  • Full genetic report (health risk + lifestyle + medication safety)
  • Cross-system interpretation with link notes on every marker
  • Pharmacogenomic record archived for lifelong reference
  • Cannot show how your tendencies are expressing right now
  • No data on current nutrition, metabolism, or inflammation
  • No personalized lifestyle adjustment guidance
Recommended
Complete decoding

Body Decoded

Genetic + functional medicine testing — layering your inherited configuration over how it's actually expressing today.

NT$ 13,800starting
  • Full genetic analysis (entire Predict Gene panel included)
  • Functional medicine blood panel (actual nutrient concentrations)
  • Gut microbiome, inflammation, and oxidative stress markers
  • Cross-reading of genetic tendencies against current data
  • Personalized nutrition, training, and supplement guidance
  • One-on-one report interpretation with a health consultant
  • Follow-up tracking and ongoing adjustment

"Predict Gene tells you your body's inherited configuration. Body Decoded tells you how that configuration is performing today — and which layer to start adjusting first."

Explore Body Decoded