Lifestyle / Chronic-Disease / Drug-Risk Genes
Individual Test

Lifestyle / Chronic-Disease / Drug-Risk Genes

Regular price NT$ 8,800
Sale price NT$ 8,800 Regular price
Unit price

A blood-based genetic test gives a full read on your sleep, nutrient absorption, exercise performance, disease risk and drug response, providing a basis for health decisions that stays valid for the long term.

Worth testing if:

  • You want to understand why you are often tired, sleep badly, metabolise slowly, or get recurrent allergies
  • You take supplements without obvious effect and suspect poor absorption efficiency
  • Athletes, coaches and gym-goers wanting to plan training and recovery around their constitution
  • A family history of diabetes, cardiovascular disease, macular degeneration, fatty liver and similar conditions
  • You are on, or about to start, long-term medication and want to check metabolic risk and potential side effects

What this test is for

A blood-based genetic test gives a full read on your constitution across sleep, nutrient absorption, athletic performance, disease risk and medication response — a durable basis for long-term health decisions.

A health check tells you glucose 95, cholesterol 180, blood pressure normal. Those describe your body right now. What it can't answer is why your colleague eats the same meals and carries half your body fat; why three months of vitamin D supplementation still hasn't lifted your blood level; or why your mother takes a statin without trouble while the same drug leaves your muscles aching.

The answers to those questions sit in your genome. This report brings a decade of genome-wide association study (GWAS) findings together into one personalised summary — not to predict disease, but to show you clearly which aspects of your body start with a natural advantage, and which need more active management.

SampleBlood draw
Report reviewNot included

Test items

49 biomarkers · 14 groups

Category

Coagulation & blood vessels4
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 & fat4
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 density2
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 health2
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 & immunity4
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 response5
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 requirements6
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 sensitivity3
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 quality2
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 performance6
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
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
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
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 genes5
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.

Four steps to start your test

1

Order online, book a location

Choose your test and pick a blood-draw time and location that suits you as you order.

2

A 10-minute blood draw

When the time comes you just show up. A professional takes your sample — we handle the rest.

3

Accredited laboratory analysis

Samples are processed by accredited testing institutions and interpreted to standard protocols.

4

Digital report

Once complete, your report is uploaded to your personal account with values and reference ranges clearly marked.

Pair it with Body Decode for the full picture

This test isn't part of the core package. Build a whole-body baseline with Body Decode, then add this test on top for fuller health context

Body Decode + this add-on This test on its own
Number of biomarkers 68 + this test's 49 This test's 49 only
Biomarkers on this page
Cross-system interpretation
Full-system integrated report
Advisor report walkthrough
Personalized action plan
120-day check-ins
Explore the Body Decode core panel

Frequently asked questions

If a gene is 'bad' I can't change it anyway — so why test?

Genes don't change, but gene expression does. The same FTO obesity variant has only a third of the effect in people who exercise regularly; the same APOE cardiovascular risk gene halves its event rate in people who manage their diet. Genes tell you where your starting line is, so you know where to put your effort in lifestyle.

Genes are a tendency, not a destiny — and tendency is exactly what you should know when designing a lifestyle.

I'm healthy right now — why would I do a genetic test?

While you're healthy is precisely the right time. Genetic risk for chronic disease can usually be identified 10 to 20 years before symptoms appear, and by the time glucose, blood pressure and cholesterol start flashing amber you have lost the most valuable window for early intervention. Testing while healthy isn't about treating illness; it's about knowing what your body handles easily and what needs care starting now.

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

I have an annual health check — isn't that enough?

A health check and a genetic test look at different layers. A health check measures your current state: your glucose, your liver markers, whether any tumour markers show. A genetic test measures your built-in settings: why you're more prone to B12 deficiency, why certain drugs give you side effects more readily, why raising your vitamin D takes more effort than it does for others. Put together, they explain the why behind your health check numbers.

A health check answers "how are things now"; a genetic test answers "why are they like this" — complementary, not interchangeable.

Wouldn't knowing I'm high risk just make me anxious?

This is the most common misconception. Studies tracking the psychological state of people who received genetic testing found anxiety rose briefly in the week after the report, but six months later was actually lower than in an untested control group — because not knowing is the real source of anxiety. Once you can see the map, you'll find most results are simply average or advantageous, and the items genuinely needing management are usually far fewer than imagined.

Anxiety comes from uncertainty, not from information.

I'm only in my early thirties — isn't this too young?

Your genes were fixed at conception, so testing at 30 gives exactly the same result as testing at 60. The difference is how many years you have left to use it. Get the report at 30 and you have three decades to adjust diet, exercise and supplement strategy; get it at 60 and many tendencies may already have surfaced as real health problems. The report only needs doing once — and the earlier you do it, the longer it works for you.

The value of genetic testing is proportional to time — the earlier you know, the more time you have to use it.

If it's all hereditary, surely there isn't much I can do?

For most common diseases, genes account for only 20% to 40% of risk, with environment and lifestyle making up 60% to 80%. The report tells you explicitly which tendencies can be reversed through exercise (such as FTO and obesity), which can be reinforced through nutrition (such as MTHFR and folate), and which can be protected by avoiding specific drugs (such as MT-RNR1 and ototoxicity). Knowing where the risk comes from is what lets you apply effort precisely.

Genes set the starting line, but how you run from here decides the finish.