Overview
A snapshot across every section of this analysis. Nothing here is a diagnosis, it's information to understand and to discuss with a clinician.
Genotype-backed reads across metabolism, sleep, diet response and caffeine sensitivity.
Carrier for two recessive conditions. Not expected to affect you; relevant for family planning.
Altered metabolism for three common drug classes, see the pharmacogenomics table.
Above-average polygenic lipid score; pairs with your uploaded LDL of 165 mg/dL.
Max Plan: ask the Health AI about anything in this report. It reads these results alongside the labs you upload. Open the assistant ›
Traits
How your genotype shapes a selection of observable traits.
You clear caffeine slowly. Late-day intake is more likely to affect your sleep.
The variant associated with endurance performance over raw power.
Likely able to digest lactose into adulthood.
A slight lean toward an evening chronotype ("night owl").
Carrier status
Recessive variants you carry. A carrier is typically unaffected, but two carrier parents can pass a condition to a child.
Heterozygous H63D. One copy only, not expected to cause iron overload, but relevant with your low ferritin.
Carrier for one CF-associated variant. Partner screening is informative for family planning.
Pharmacogenomics
How your genetics may affect your response to common medications. Never change a prescription without your clinician.
| Medication class | Gene | Metaboliser | Note |
|---|---|---|---|
| Statins | SLCO1B1 | Normal | Standard metabolism; no increased myopathy-risk variant. |
| Clopidogrel | CYP2C19 | Intermediate | Reduced activation; discuss alternatives if prescribed. |
| SSRIs | CYP2D6 | Poor | Slower clearance; lower starting doses may be considered. |
| Warfarin | VKORC1 | Sensitive | Lower dose requirement predicted. |
| NSAIDs | CYP2C9 | Normal | Standard metabolism. |
Cardiovascular markers
Genetic contributors to cardiovascular health, scored against population distributions.
Above-average genetic tendency toward higher LDL. Your uploaded lipid panel shows LDL 165 mg/dL, consistent.
One ε4 allele, associated with higher LDL clearance resistance.
Typical polygenic blood-pressure tendency.
Hereditary disease risk
Assessments for heritable conditions. A clear result reduces but does not eliminate risk.
Moderately elevated polygenic risk. Lifestyle factors remain the largest lever.
Neither high-risk haplotype detected, coeliac disease is unlikely.
Population-typical risk at CFH and ARMS2.
Oncological markers
Variants associated with heritable cancer risk. These are screening flags, not diagnoses, confirm clinically significant findings with a validated test.
No pathogenic variant detected in the screened positions.
No pathogenic MMR variant detected.
Monoallelic carrier. Low personal risk; relevant for relatives and family planning.
Gene integration
Max Plan only: how multiple variants interact across systems, rather than one gene at a time.
Your elevated LDL polygenic score, APOE ε4 allele, and above-median type 2 diabetes score point in the same direction. Individually each is modest; together they compound a cardiometabolic tendency. Paired with your measured LDL of 165 mg/dL, this is the most actionable theme in your report, a good one to take to your clinician.
This report provides genetic information for education and discussion. It is not a medical diagnosis and does not replace professional care. Always consult a qualified healthcare professional before acting on any result.