DNA can explain some variation. It does not choose a person’s path.
We review exercise, cognition, sleep and metabolism—separately from clinically actionable genetic conditions.
THE CORE LIMIT
A functional trait ≠ a talent test
There is no validated genetic test that reliably predicts an individual’s outcome in sport, intelligence, personality or career. The more complex the trait, the more development, environment, learning, health and observed function matter.
01 / TRAIT MAP
What people ask—and what can actually be inferred.
01Exercise and sport
Athletic ability
ACTN3 · ACE · PPARGC1A · thousands of variants
Question
Can DNA choose a sport for a child or adult?
Evidence
The trait is heritable, but individual variants explain too little of performance.
More useful
Observe actual skills, interest, health, training response and recovery.
Limit
Few-SNP panels are not validated for talent selection or training prescription, especially in children.
Does a genome predict gains in strength, endurance or injury risk?
Evidence
Group-level associations reproduce unevenly; environment and training design contribute strongly.
More useful
Functional assessment, history, movement technique and load tracking provide direct information for planning; consumer DNA panels have no validated individual prediction.
Limit
Do not use COL5A1, ACE or ACTN3 alone to predict injury or performance.
Not ‘every DNA test a child needs’, but tests with a clear benefit for the child.
Sports, intelligence, nutrition or personality panels are not necessary screening for a healthy child. Testing is justified when it answers a clinical question and can change care during childhood.
01
Newborn screening
When: For all newborns under the national programme in the relevant country.
How: Usually biochemical and physiological screening; DNA testing confirms selected findings.
Why: Early detection of conditions where timely action changes outcomes.
02
Diagnostic testing
When: For congenital anomalies, developmental delay, intellectual disability, seizures or another clinical suspicion.
How: Karyotype/CMA, targeted panel, exome or genome—selected for the phenotype.
Why: Can refine diagnosis, surveillance, treatment and family risk.
03
Familial variant actionable in childhood
When: When a pathogenic familial variant is known and surveillance or prevention begins before age 18.
How: Exact targeted confirmation of the familial variant after genetic counselling.
Why: An informative positive or true-negative familial result.
04
Medication-linked pharmacogenetics
When: When a child is receiving a specific medicine with an applicable guideline or label.
How: Validated testing of the relevant gene/allele, not a universal wellness panel.
Why: A clinician may refine choice or starting dose alongside clinical monitoring.
DO NOT USE AS A DECISION BASIS
Sports selection, educational restriction, intelligence prediction, career choice, symptom-free diets or personality labels based on a few DNA variants.
This register contains the high- and very-high-value tracks. Risk is assessed separately: the closer a feature comes to diagnosis, medication, children or reproductive decisions, the stricter its sources, stop rules and professional review.
01
Very high valueControlled risk
Local genetic-variant reference
Use
Checks a standardised designation and displays an exact record from a limited ClinVar snapshot without uploading a VCF or report.
Output
Source record, classification, review status, date and inference boundary.
Gate
Exact match; the query stays in browser memory; no match is not interpreted.
02
Very high valueMaximum clinical risk
Oncology clinical-evidence navigator
Use
Shows when a biomarker and clinical context match an exact regulatory source—and when context is insufficient.
Output
Not a prescription: a verifiable relationship for discussion with an oncologist and molecular tumour board.
Gate
Structured fields, exact indication, jurisdiction and source date only; no doses, ranking or VUS output.
03
Very high valueMaximum clinical risk
Medication-safety pharmacogenetics
Use
Matches an exact gene–medicine pair to a relevant professional guideline or official regulatory label without merging their statuses.
Output
Evidence status, required clarifications and clinician questions—not a personal dose.
Gate
Confirmed genotype/phenotype, exact medicine and clinical review; complex cases are blocked.
04
Very high valueHigh clinical risk
Inherited cardiometabolic pathways
Use
Separates familial hypercholesterolaemia, cardiomyopathies, arrhythmias and monogenic diabetes from weak wellness-risk claims.
Output
A pathway for checking the report, clinical phenotype and questions for family counselling.
Gate
Exact gene–condition validity, pathogenicity, phenotype and clinical assessment—not a generic polygenic score.
05
High valueControlled risk
Test audit and source freshness
Use
Helps evaluate intended use, method, coverage, limitations, privacy and clinical utility before purchase.
Output
A multi-axis transparency profile without a misleading universal quality score.
Gate
Versioned primary sources, review date and independent conflict disclosure.
06
High valueHigh clinical risk
Rare-disease diagnostic pathway
Use
Explains when a panel, CMA, exome, genome or familial-variant test fits the clinical question.
Output
A map of method, possible results, limitations and next step with a genetics professional.
Gate
No diagnosis from a web form; phenotyping and method selection remain clinician-led.
07
High valueMaximum clinical risk
Carrier, reproductive and newborn pathways
Use
Separates couple carrier screening, prenatal screening, diagnosis and national newborn screening.
Output
Purpose, residual-risk, confirmation and genetic-counselling explanation.
Gate
Separate child and reproductive ethics; no automated recommendation.
08
High valueHigh clinical risk
GDC tumour-cohort research context
Use
Shows alteration frequency and research context in de-identified cancer cohorts.
Output
Aggregate research visualisation kept separate from clinical actionability.
Gate
Never used for individual treatment selection, prognosis or bypassing controlled-access data.
04 / IN DEVELOPMENT
A living register of the next modules—from clinical pathways to research boundaries.
This is an editorial roadmap, not a promise of personal prediction. Before publication, every topic receives an exact relationship, measurement method, evidence, clinical actionability and an inference boundary.
01Question-dependent
Appearance and senses
Skin, hair and iris pigmentation
Hair texture and androgenetic hair loss
Freckles, sun sensitivity and phototype
Taste, smell, colour vision and selected hearing phenotypes
Common appearance traits stay separate from monogenic vision, hearing or pigmentation disorders.
02Question-dependent
Sleep, rhythms and the nervous system
Chronotype, sleep duration and regularity
Rare familial circadian-rhythm disorders
Restless legs and narcolepsy—only in clinical context
Migraine, pain and sensory sensitivity
A polygenic signal does not replace a sleep diary, examination or diagnostic testing.
03Question-dependent
Exercise, recovery and sports safety
Aerobic adaptation, strength and muscle-fibre composition
Bone, tendon, ligament and injury traits
Recovery, inflammatory response and thermoregulation
Rhabdomyolysis, cardiomyopathies and anaesthetic risk
SNPs do not determine talent or a training plan; clinical red flags receive a separate pathway.
04Question-dependent
Nutrition and metabolism
Lactase, caffeine, alcohol and taste receptors
Lipids, glucose, uric acid and iron
Coeliac disease: HLA as an exclusion aid, not a diagnostic test
Vitamins and nutrients without ‘DNA diet’ promises
Genotype does not calculate a universal diet or a safe substance dose.
05Clinical pathway
Cardiometabolic traits
Familial hypercholesterolaemia and Lp(a)
Inherited cardiomyopathies and arrhythmias
Monogenic diabetes and rare metabolic disorders
Polygenic risks for blood pressure, diabetes and body weight
Monogenic diagnoses, measurable biomarkers and polygenic risks are shown separately.
06Question-dependent
Immunity and inflammation
HLA relationships with autoimmune conditions
Pharmacogenetic HLA alleles
Rare primary immunodeficiencies
Allergy and infection susceptibility—without consumer promises
An HLA risk association is not a diagnosis or a general ‘immunity test’.
07Clinical pathway
Reproductive health and life course
Carrier screening and couple-level risk
Genetic causes of infertility and premature ovarian insufficiency
Prenatal screening and diagnostic testing
Newborn screening and early diagnosis
Screening, diagnosis and prediction for a healthy person must not be conflated.
08Not for personal prediction
Cognition and behaviour
Memory, attention and educational outcomes
Personality, risk-taking and addictions
Neurodevelopment in the presence of clinical symptoms
Neurodegenerative risks and the right not to know
We do not create talent, personality or schooling scores, especially for children.
09Clinical pathway
Medicines and adverse reactions
CPIC/DPWG relationships for exact gene–drug pairs
Oncology toxicity: DPYD, TPMT, NUDT15 and UGT1A1
Antiplatelets, statins, immune reactions and anaesthesia
Limits of combinatorial psychiatric PGx panels
Every recommendation is tied to a medicine, indication, guideline and clinician-led decision.
10Research zone
Ageing and lifespan
APOE, FOXO3 and population longevity associations
Cardiovascular and cancer contributors to long-term risk
Clonal haematopoiesis as an acquired, not inherited, signal
Epigenetic clocks as a separate biomarker, not a genomic forecast
A group-level association is never converted into a promise of extra years.
This register is not an exhaustive list of human traits and will expand only where a verifiable source and clear use boundary exist.
05 / NEXT STEP
Question first. Method second. Genetic test third.