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Lifestyle / Chronic-Disease / Drug-Risk Genes

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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 & blood vessels 4 items
Venous thromboembolism (VTE) Combines 12 coagulation-pathway genes including F5, F11, PROC, PROS, FGG, FGA, VWF and ABO to assess your tendency to form venous clots. The same pathway extends into risk judgement around long-haul flights, post-operative recovery and oral contraceptive use, as well as vascular health downstream of MTHFR homocysteine metabolism. Hereditary stroke NOTCH3 and CYBA affect small-vessel integrity and the oxidative stress response. They share some mechanisms with atherosclerosis and blood pressure control pathways, making them an early signal along the vascular ageing axis. Atherosclerosis IL-6 and JCAD assess the impact of chronic inflammation on vessel walls. This inflammatory axis shares the same gene set as exercise recovery capacity (IL6/TNF/CRP), influenza severity and atopic dermatitis — the underlying gauge of how strongly your body mounts inflammation. Familial hypercholesterolaemia (FH) APOB and LDLR directly determine how efficiently LDL receptors clear cholesterol. Even with good dietary control, variants in these two genes substantially shift the ceiling on cholesterol metabolism and affect response to statins (linked with SLCO1B1).
Glucose metabolism & fat 4 items
Type 2 diabetes TCF7L2, UBE2E2, CDKAL1, HHEX, KCNQ1 and SLC30A8 jointly assess insulin secretion and blood sugar regulation. They also bear on weight management, fatty liver risk and response to diabetes medications (glimepiride, glipizide). Non-alcoholic fatty liver disease (NAFLD) APOC3 and PNPLA3 are key regulators of fat deposition in the liver. Even without alcohol, variants in these genes raise the risk of fatty liver progression and share a metabolic axis with insulin resistance and type 2 diabetes risk. Hyperuricaemia ABCG2 is the main transporter for uric acid excretion. Variants reduce clearance efficiency, raising gout risk and affecting response to urate-lowering drugs such as rasburicase. Obesity predisposition FTO is the key gene for fat storage. The same FTO variant simultaneously affects fat-burning potential (how well exercise works), appetite regulation and type 2 diabetes risk — the central node on the energy balance axis.
Joints & bone density 2 items
Osteoarthritis TGFA, RUNX2, GDF5 and ALDH1A2 assess cartilage repair and inflammatory tendency. They share some genes with exercise injury risk (VDR/GDF5), so both can be read together when setting training intensity and protective strategy. Osteoporosis FGFR2, MPP7, JAG1, TNFRSF11B and ZBTB40 assess your capacity to maintain bone density. Best read alongside vitamin D metabolism (the GC gene) and calcium absorption — genes set the ceiling, lifestyle decides how close you get to it.
Eye health 2 items
Age-related macular degeneration (AMD) CFH, ARMS2 and C2 form the core gene combination for AMD risk. They also connect to the complement inflammation axis, which influences how strongly you need to maintain macular pigment density (and therefore your lutein and zeaxanthin intake). Glaucoma GAS7, TMCO1 and FAM125B affect intraocular pressure regulation and optic nerve sensitivity, assessing your tendency toward primary open-angle glaucoma.
Respiratory & immunity 4 items
Asthma risk GSTP1 and GSDMB assess airway inflammatory tendency. GSDMB also relates to inflammatory cell death pathways, influencing cold severity and the risk of dust-mite-triggered asthma. Atopic dermatitis RTEL1 and RTEL1-TNFRSF6B assess skin barrier function and the tendency toward immune over-reaction. They share part of the immune axis with asthma and dust mite allergy — scoring high on all three suggests an overall allergic constitution. Dust mite allergy LY86-AS1 and LY86 assess how strongly immune cells recognise dust mite antigens. Part of the IgE allergy axis, so it can be cross-read with asthma and atopic dermatitis risk. Traffic pollutant sensitivity SAMSN1, RARS2 and BMP8A-PPIEL influence how strongly your body mounts inflammation against particulates such as PM2.5 and exhaust. Those who are more sensitive carry higher risk of triggered asthma and cardiovascular events — particularly worth noting for city commuters.
Viral infection & vaccine response 5 items
Influenza infection risk LGALS1 and IL1B assess your tendency to catch influenza. IL1B is a core inflammatory cytokine, and variants also affect the severity of other infections and the fever response. Influenza severity IL10 and LTA influence the risk of complications after infection. IL10 is the main anti-inflammatory axis and also bears on how strongly you react with fever to influenza vaccination. Influenza vaccine protection MBL-2 and IL-1RN assess how efficiently you generate antibodies after vaccination. The same gene set also affects the likelihood of a fever response, so the two can be read together to see whether you are "well protected with low reaction" or "well protected but fever-prone". Influenza vaccine fever response MBL-2 and IL10 assess whether you are prone to fever after vaccination. Knowing in advance lets you prepare antipyretic measures, or schedule vaccination away from important commitments. Common cold severity ORMDL3, GSDMB, CCR5, IL-13 and SCGB1A1 jointly assess the risk of developing asthma or bronchitis after a cold. They share some genes with asthma and dust mite sensitivity — anyone sensitive on all three should pay particular attention to respiratory protection.
Vitamin requirements 6 items
Vitamin A RBP4 affects how efficiently vitamin A is transported in the blood. Relevant to macular health and night vision. Vitamin B6 NBPF3 affects how quickly B6 is metabolised and cleared. B6 sits on the homocysteine metabolism axis alongside folate and B12 — together the three shape cardiovascular risk. Folate MTHFR is the core enzyme in folate metabolism and a key node in homocysteine metabolism. MTHFR variants simultaneously bear on cardiovascular risk (the VTE axis), neurotransmitter synthesis and DNA methylation (the ageing axis) — one of the loci most worth reading across categories. Vitamin B12 MS4A3, CLYBL/LOC101927437, FUT6 and PRELID2 jointly assess how efficiently B12 is absorbed and used. Particularly worth reviewing for vegetarians and long-term users of acid-suppressing medication. Vitamin D The GC gene affects the activity of vitamin D binding protein, determining how much usable D circulates in your blood. Relevant to osteoporosis, immune regulation and glucose metabolism alike — one of the widest cross-system influences in this test. Vitamin E CYP4F2 and ZPR1 affect how quickly vitamin E is metabolised. E is a core fat-soluble antioxidant, relevant to macular health, skin ageing and cardiovascular oxidative stress.
Dietary sensitivity 3 items
Lactose intolerance MCM6 controls how much lactase is expressed in adulthood. Roughly 85% of people in Taiwan carry the genotype for declining lactase activity, though the strength of symptoms varies widely between individuals. Gluten intolerance HLA-DQA1 and HLA-DQB1 are the core risk genes for coeliac disease. They sit on the immune axis and relate to other autoimmune tendencies. Alcohol sensitivity ALDH2 is the key enzyme for acetaldehyde metabolism. Around 47% of people in Taiwan carry an ALDH2 variant, and slow metabolisers flush and feel dizzy when drinking — the same variant is also associated with increased oral and oesophageal cancer risk.
Sleep quality 2 items
Sleep effectiveness ADA affects the speed of adenosine metabolism, determining how mentally restored you feel on waking. Shares part of its axis with caffeine metabolism. Sleep quality FABP7 affects sleep continuity. People who wake repeatedly through the night may need to pay closer attention to their sleep environment.
Athletic performance 6 items
Exercise recovery capacity Assessed jointly through the three major inflammatory marker genes IL6, TNF and CRP. They share the same gene set as atherosclerosis and chronic inflammation risk — recovering quickly after exercise also means controlling inflammation well. Oxygen uptake efficiency VEGFA affects blood vessel formation and oxygen delivery. Also relevant to cardiovascular health and wound healing. Fat-burning potential FTO is also the key gene for obesity predisposition — the same locus tells you two things: your tendency to store fat, and the ceiling on how efficiently exercise burns it. Exercise injury risk VDR and GDF5 assess ligament and tendon strength. VDR is also the vitamin D receptor, sharing an axis with osteoporosis and osteoarthritis — people who injure easily may also need to watch long-term bone health. Muscle strength (power) ACTN3 is the so-called athlete gene, determining your proportion of fast-twitch muscle fibres. AGT affects how blood pressure responds to exercise. Endurance ADRB3 and BDKRB2 assess physiological responses related to aerobic endurance. Cross-read with oxygen uptake efficiency to judge whether you are better suited to short bursts or long distances.
Hepatic metabolism (CYP450 series) 4 items
NSAID painkillers CYP2C9 determines how quickly six commonly used NSAIDs — including ibuprofen, celecoxib and meloxicam — are metabolised. Slow metabolisers taking them long term face increased liver burden and gastrointestinal bleeding risk. CYP2C9 also metabolises warfarin, phenytoin and various other prescription drugs. Antidepressants & antiepileptics CYP2C19 affects the metabolism of citalopram, escitalopram and sertraline (antidepressants), clobazam (antiepileptic) and clopidogrel (antiplatelet). A single metabolic pathway spanning four drug classes — this is the core value of genetic testing. Anti-infective drugs CYP2B6 affects efavirenz metabolism. Intermediate metabolisers are advised to adjust the starting dose to reduce neurotoxicity risk. Immunosuppressants CYP3A5 affects tacrolimus metabolism and is a critical gene for transplant patients. It also affects the metabolism of corticosteroids and certain chemotherapy drugs.
Oxidative stress related (G6PD) 1 items
G6PD-related drug group G6PD is more than a favism label — it is the core antioxidant enzyme in red blood cells. The same gene simultaneously affects haemolysis risk across more than a dozen drugs: certain antibiotics (ceftriaxone, nalidixic acid), diabetes drugs (glimepiride, glipizide), antimalarials, anaesthetics and antidotes. A genuinely cross-class key gene.
Mitochondria related (MT-RNR1) 1 items
Aminoglycoside antibiotics MT-RNR1 is a mitochondrial ribosomal gene. Carriers of the variant face substantially increased ototoxicity risk (permanent hearing loss) from six aminoglycoside antibiotics: amikacin, gentamicin, neomycin, streptomycin, tobramycin and paromomycin. The classic case of one gene equalling one life-saving warning.
Other metabolic genes 5 items
TPMT (immune / anticancer drugs) TPMT affects the metabolism of thiopurines such as azathioprine and mercaptopurine. Slow metabolisers on standard doses can suffer severe bone marrow suppression. NAT2 (anti-TB / sulfonamides) NAT2 affects the metabolism of isoniazid (anti-TB) and sulfamethoxazole/sulfasalazine. Slow acetylators face increased hepatotoxicity risk. UGT1A1 (anticancer drugs) UGT1A1 affects the metabolism of three chemotherapy drugs: irinotecan, nilotinib and pazopanib. Carriers of the variant on standard doses face increased risk of severe side effects. SLCO1B1 (lipid-lowering drugs) SLCO1B1 is the key transporter carrying statins into liver cells. Carriers of the variant are prone to myopathy on simvastatin — directly relevant to treating familial hypercholesterolaemia. IFNL3/IL28B (hepatitis C treatment) Predicts response to peginterferon alfa-2a and ribavirin in treating hepatitis C — favourable genotypes have a higher sustained virological response rate.

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