Why we measure what we measure. And what we do not conclude from it.

Why we use it

ApoB counts atherogenic particles and captures cardiovascular risk more precisely than LDL cholesterol alone. Lp(a) is largely hereditary, stable for life, and almost never measured in routine care. European guidelines recommend measuring Lp(a) once in adult life.

What it cannot do

An elevated Lp(a) cannot currently be lowered directly with medication. The benefit lies in reclassifying overall risk and treating the remaining factors more consistently.

Why we use it

Cardiorespiratory fitness is among the strongest known predictors of all-cause mortality, and it responds to training. In a cohort of more than 122,000 people, higher measured fitness was consistently associated with lower mortality, with no observable upper limit of benefit.

What it cannot do

The test measures capacity, not the cause of a limitation. A poor result needs a work-up, not a training tip.

Why we use it

Colonoscopy, mammography, skin cancer screening, cervical screening and low-dose CT for heavy smokers are the procedures with proven benefit. They are the benchmark everything else has to be measured against, and they belong in the results conversation: if one of them is due for you, we say so.

What it cannot do

These procedures do not take place with us but with the relevant specialists. We do not replace them and we do not count them as part of our programs.

Why we use it

Visible plaque in the carotid or femoral artery shows that atherosclerosis has already begun. That moves a calculated risk estimate from a probability to a finding and regularly changes the treatment threshold.

What it cannot do

A normal ultrasound does not rule out coronary artery disease. The finding is a risk modifier, not a substitute for cardiac work-up when symptoms are present.

Why we use it

Monogenic findings such as BRCA1/2, Lynch syndrome or familial hypercholesterolaemia have clear consequences: tighter screening intervals, earlier treatment, relevance for family members. Pharmacogenetics changes concrete dosing. Predictive testing follows the German Genetic Diagnostics Act, with counselling before and after and your right not to know for each category of findings.

What it cannot do

An unremarkable genetic result does not rule out disease, because most conditions are not monogenic. We do not report polygenic risk scores without solid clinical validation, and no talent, personality or diet-type interpretations.

Why we use it

MRI shows structure where blood work and functional tests show nothing: aneurysms, masses, fatty liver, vascular anomalies. We run it at 3 Tesla, radiation-free and without contrast agent, read by a radiologist and then discussed with you by a physician. We use it in an explicitly research-adjacent context, because the longitudinal data we want to build does not yet exist.

What it cannot do

For whole-body MRI as screening in people without symptoms, no study with a mortality endpoint exists. A systematic review found critical or indeterminate incidental findings in around 32 percent of those examined and confirmed cancer in roughly one to two percent. Lung and colon are only partly assessable on MRI: low-dose CT and colonoscopy are not replaced by it.

Why we use it

The idea behind these tests is plausible: tumour cells and cell-free tumour DNA appear in blood early, long before symptoms. We use TruCheck, document the result and treat it as a research parameter, not a diagnosis.

What it cannot do

Published accuracy figures come mostly from case-control studies of known cancer cases, not from screening healthy people. In the only large randomised screening trial of a multi-cancer test, NHS-Galleri with more than 140,000 participants, the primary endpoint was missed. No procedure in this class has demonstrated a mortality benefit, and a positive result is not a cancer diagnosis.

Why we use it

Second- and third-generation clocks such as GrimAge and DunedinPACE show robust cohort-level associations with mortality and disease risk. As a longitudinal measure across years that is interesting, so we measure them from blood and disclose which model was used.

What it cannot do

No guideline recommends epigenetic clocks as a basis for decisions. For six widely used models, technical replicate measurements of the same sample differed by up to nine years; principal-component versions reduce that to around one and a half years. A single value means little for you personally, and it has not been shown that a lower value lowers disease risk.

Why we use it

These blood markers from Alzheimer research have substantially improved diagnostics in people with cognitive symptoms. We collect them in the Ultimate panel and flag them explicitly as experimental in the register.

What it cannot do

The test of this class cleared in the US in 2025 is explicitly indicated for people aged 55 and older with symptoms, not for screening people without symptoms. A value without symptoms permits no diagnosis, and outside clinical trials there is no treatment that would follow from it.

Why we use it

The composition of the gut flora is linked to metabolism, inflammation and immune function. As a longitudinal parameter and research variable it makes sense, and the sample goes into the biobank.

What it cannot do

For stool microbiome analysis there are no accepted reference ranges for healthy people and no guideline that ties treatment to it. We derive no probiotic protocols and no dysbiosis therapies from it.

Why we use it

Cryopreserved samples allow a question to be answered later that cannot be asked today: a marker that does not exist in 2026, measured on your 2026 sample. For the cohort, the biobank is the precondition for evaluating procedures retrospectively.

What it cannot do

Biobanking is infrastructure, not a treatment and not a promise. Whether and when stored cells become therapeutically usable is open. We do not present it as provision for any specific treatment.