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The Science

Where your numbers come from.

Every result in this app is measured against a range and read against your own baseline. This page explains each of those steps, names the evidence behind every Prime range, and defines the words the app uses. It is written to be checked: every source is linked, and a range with no source yet says so.

How it worksGlossary

On this page

  1. Three ranges, and which one you see
  2. How a Prime range is set
  3. How a result is scored
  4. Biological age and other calculations
  5. How a therapy is judged
  6. How your tests are chosen
  7. What this page does not claim
  8. Sources, marker by marker
  9. Reference list

1. Three ranges, and which one you see

A lab range answers “is this abnormal?”. A Prime range answers “where should I aim?”. They are different questions, and a result can be normal by the first and outside the second at the same time.

There are three ranges a marker can be read against, and they come from different places.

RangeIt answersIt comes from
Population percentileWhere do people like me actually sit?National survey data (NHANES), which samples everyone, healthy or not
Lab reference rangeIs this result abnormal?The laboratory that ran your sample, from a screened healthy group, on its own instrument
Prime rangeWhere should I aim?Prime Years, from published evidence, by the method in the next section

Only the third is a target. The first two describe; the third prescribes. They can sit far apart. HDL cholesterol is the clearest example on this page: a laboratory range has no ceiling, because a high HDL was long read as good, and the Copenhagen cohorts cited in the table below found mortality rising again at the highest values. A person at the top of the lab’s range is “completely normal” and outside the Prime range at once.

Which range you see beside a result

When your lab report carries its own reference range, that is the one shown beside the result, and the verdict on the results page is measured against it. When a report carries several ranges and does not say which applies to you, none is shown rather than a guess. The lab’s range is matched to the instrument that ran your sample on the day it ran, which is stronger than any static table. Your Prime range is still recorded on every result, and it is what the marker charts are measured against.

2. How a Prime range is set

A Prime range is set from the strongest evidence that exists for that marker, on a ladder of five evidence tiers, with a sixth label for a marker that has none. Every marker below carries its own entry: the step a range came from and what it cites, or, where that is still missing, which of the two is missing and why. Nothing is left blank for you to interpret.

A range is set from the highest tier that has evidence for that marker; lower tiers are not consulted once a higher one applies — and where no tier has evidence we defensibly believe, the judgment is to set no range, which is why 93 of the 116 carry none.

  1. Tier 1. Guideline threshold. A guideline body has set a target from hard outcomes such as heart attacks or kidney failure. The threshold is the zone boundary, unchanged.
  2. Tier 2. Risk inflection in cohort data. Published cohort data show where risk is lowest. The zone is that low point, not the whole span below a cut-off.
  3. Tier 3. Functional sufficiency. A level at which a body function stops failing or saturates. The zone starts at that level, and still needs a ceiling.
  4. Tier 4. Healthy-cohort reference interval, narrowed. No outcome evidence exists, but a properly screened healthy cohort has a published reference interval. The zone is drawn inside it, toward the end that is better for that marker.
  5. Tier 5. Population percentile, narrowed. Only population survey data exist. The zone is drawn inside the distribution, and is labelled as the weakest evidence tier.
  6. Tier 6. Reported, not evidence-tiered. The marker is shown with context and no evidence tier, usually because it is a device maker’s own composite score.

The rules every range must satisfy

  • Never looser than a guideline threshold. If a guideline says under 70 and the range says under 100, the range is wrong.
  • Never narrower than the test can measure. A range tighter than the assay’s own variation is scoring noise.
  • Never applied across methods where the method sets the scale. Free testosterone by equilibrium dialysis reads about ten times a direct immunoassay. A range must name its method.
  • Never stretched beyond the studied population. A range inherits the population its source measured.
  • Every range records its tier and its source. A range whose tier cannot be named is not ready.
  • Sufficiency is not a target to exceed. A level that is enough is a floor, not an invitation to go higher.
  • Where the Prime range and the lab range barely overlap, the page must say so. You are being told two contradictory-sounding things at once, and that deserves a sentence, not a footnote.

3. How a result is scored

Inside your Prime range a result scores 100. Outside it, the score falls in a straight line with distance. The same rule scores every marker, whichever direction is good for it, except that a range with no upper limit has no “too high”.

This curve is Prime Years’ own rule, not a published formula. The range it measures against is sourced; how fast the score falls outside it is a choice we made so results can be read at a glance.

Each result gets a score from 0 to 100 for how close it sits to the Prime range. Inside the range, 100. Just outside either edge, 85. From there the score falls in a straight line, reaching 0 at 1.5 range-widths beyond the edge. The rule is symmetric, so “lower is better” and “higher is better” are properties of the range, not of the scorer: a lower-is-better marker such as hs-CRP simply has no clinical floor, and the chart draws no “below” band for it. The mirror case is a range with no upper limit, where the evidence found no point past which more stopped helping: VO₂ max and Daily steps. Above the top of that range still scores 100, and the chart draws no “above” band.

The score is shown as one of three words.

  • Optimal: a score of 85 or more. Inside the range, or at its edge.
  • Watch: a score from 60 to 84. Outside the range, but not far.
  • Attention: a score under 60. Well outside the range.

Every dot on a marker chart is scored the same way, and each one is scored against the Prime range recorded on that sample when it was taken. A range tightened on a later panel does not recolor your history, and the chart says so in words when it applies.

4. Biological age and other calculations

Biological age is a published measure, Phenotypic Age, worked out from your age and nine routine blood markers.

Your biological age is Phenotypic Age (Levine and others, 2018; Liu and others, 2018). It combines your age with nine routine blood markers: albumin, creatinine, fasting glucose, hs-CRP, lymphocyte percentage, mean corpuscular volume, red cell distribution width, alkaline phosphatase and white blood cell count. The result is the age at which an average American adult carries the same ten-year risk of death that your markers predict. It was built from one national US health survey and tested on another of more than 11,000 adults. It needs all nine markers from one blood test, within a month of each other; if one is missing, the app names it rather than guessing. It declines to answer outside ages 20 to 120. It is not an epigenetic clock.

Other calculated measures

Three more results are worked out from published formulas, each from results taken on the same blood draw. None is scored against a Prime range; each is shown with what its source says about it.

MeasureFormulaWhat it tells you
HOMA-IRfasting glucose (mg/dL) × fasting insulin (µIU/mL) ÷ 405How much insulin your body needs to hold blood sugar steady. Higher means more insulin resistance. Cut-offs differ between populations, so none is used. It needs a true overnight fast. From Matthews 1985.
TyG indexln(fasting triglycerides (mg/dL) × fasting glucose (mg/dL) ÷ 2)Insulin resistance without an insulin test, checked against the clamp, the reference method. Higher means more resistance. From Simental-Mendía 2008, Guerrero-Romero 2010.
FIB-4age × AST (U/L) ÷ (platelets (10⁹/L) × √ALT (U/L))The risk of advanced liver scarring. 1.30 or below makes it unlikely (2.0 from age 65); 2.67 or above is a reason for a doctor to look further; in between is indeterminate. Less reliable under 35. From Sterling 2006, Shah 2009, McPherson 2017, Rinella 2023.

5. How a therapy is judged

A therapy is judged against your own baseline, on the markers it is meant to move, while the markers it could disturb are watched. Nobody is compared with an average.

Each therapy Prime Years offers is tied to the markers it is meant to move (its targets) and the markers it could push the wrong way (its safety markers). That mapping is the same for everyone. What is yours is the comparison: each target’s latest reading against the reading you started with. This is the N-of-1 method, the same before-and-after logic a doctor uses, applied to your record automatically.

  • Too early to tell: fewer than six weeks since the therapy started. Most markers have not had time to move.
  • Working: every target has moved in its good direction by more than its normal variation, and at least one is Optimal.
  • Partial response: at least one target has moved in its good direction by more than its normal variation, but not every target has, or none has reached Optimal yet.
  • No response yet: no target has moved beyond its normal variation since baseline. Worth reviewing with your doctor.
  • No results yet: none of the therapy’s targets has a reading. The app says this rather than guessing.

When a change counts as real

Two results from the same person are never identical, even when nothing has changed. The lab’s instrument varies from run to run, and your body varies from day to day around its own set point. A change counts only when it is larger than both together. Laboratory medicine calls that threshold the reference change value (Fraser 2012).

It is worked out on the log scale, the form the database below uses in its own calculator (Fokkema 2006), so a fall needs a smaller move than a rise: rise = ek − 1 and fall = 1 − e−k, where k = 1.96 × √2 × √(σA² + σI²) and each σ = √ln(CV² + 1). CVA is the lab’s variation and CVI is a healthy person’s day-to-day variation, both from the European Federation of Clinical Chemistry and Laboratory Medicine’s biological variation database (EFLM database 2026). The lab’s variation is the database’s desirable figure for each test, half the day-to-day variation (Sandberg 2024). The 1.96 means a change this large happens by chance less than one time in twenty.

An example. Triglycerides vary about 20% from day to day in a healthy person, so a fall counts from about 46%. A fall from 228 to 118 mg/dL is 48%, and counts. A fall from 228 to 140 mg/dL is 39%: the right direction, but inside the normal variation, so it does not yet count toward a verdict.

MarkerDay-to-day variationLab variationA fall counts fromA rise counts from
ALT12.4%6.2%32%47%
ApoB6.3%3.2%18%22%
AST8.4%4.2%23%30%
Creatinine4.4%2.2%13%15%
Fasting glucose4.9%2.5%14%16%
Fasting insulin25.4%12.7%54%117%
GGT8.2%4.1%22%29%
HbA1c1.2%0.6%4%4%
HDL cholesterol5.7%2.9%16%19%
Hematocrit2.8%1.4%8%9%
hs-CRP34.7%17.4%65%186%
LDL cholesterol7.6%3.8%21%27%
Platelets7.2%3.6%20%25%
Total cholesterol5.4%2.7%15%18%
Total testosterone14.3%7.2%36%56%
Triglycerides19.8%9.9%46%84%

A marker with no published variation figure, such as resting heart rate or VO₂ max from a wearable, is judged by Prime Years’ own rule instead: a move of at least 5%. That rule is ours, not a published one.

A verdict is only ever written for a therapy actually recorded on your chart. The app never assumes you are on something because a marker happens to look like it.

6. How your tests are chosen

Testing runs as a loop. It starts with one broad panel and gets smaller as your results settle, so that over time you need us less, not more.

The broad panel

44 tests for everyone and 46 for men, plus the tests your age, confirmed conditions and goals call for, each with its reason. It is a vein draw, at a lab or at home, because it needs more blood than a home kit can give.

How often you retest

After your plan, you choose 4, 3 or 2 tests a year, counting the broad panel: a retest every 3, 4 or 6 months. Until you choose, we recommend 3 on a protocol and 2 with none. No treatment sets its own testing schedule.

What comes off a retest

A retest carries only what needs another look: results that were outside the lab's range, what your protocol aims to move, and any test Marcus suggests and you add. Each comes off once it is inside the lab's range on two tests in a row. A retest with nothing left on it is skipped.

How a retest is collected

By home kit, a finger prick, only when every test on it is validated on a dried blood spot. Never by kit on a hormone applied to the skin, because the result reads falsely high. Otherwise a vein draw.

When the broad panel comes back

After 12 months, or 24 once your results settle: past the first year, no protocol, and nothing outside the lab's range since the last broad panel. Sooner whenever you ask, for example after a lifestyle change, a new symptom or a new medicine.

7. What this page does not claim

Prime ranges and the biological-age model are decision-support tools. They are not a diagnosis and do not replace your doctor’s judgment.

  • The ranges were drafted by the team building this app using the method in section 2.
  • The app tracks 116 markers and sets a Prime range for 23 of them. Every one of those 23 ranges has a verified source attached today. The other 93 markers are tracked with no Prime range at all — shown below as “Tracked, no PYM target”. That is a finding, not a review still outstanding: we looked and did not find a target we could defend, so the reading is judged against the range your lab printed, and shown but not scored if the lab printed none.
  • Few ranges are split by sex or age. 3 markers have ranges that change with age, shown against them in the table: PSA, VO₂ max, Daily steps. One marker carries a separate range for women, shown in the table: VO₂ max. Every other range applies to everyone, and the note beside a marker says when that matters. Where your lab report carries its own range, that one is matched to you and is the one shown beside the result.
  • Nothing here is a claim of treatment effect. Whether a therapy works for you is judged from your own readings, after the fact, by the method in section 5.

8. Sources, marker by marker

Every marker the app tracks — its Prime range where it has one, the evidence tier that range came from, and the sources it cites. “Under review” means a range exists but no verified source is attached yet, and the note says why. “No target found” means there is no Prime range to support.

Hormones

MarkerPrime rangeEvidenceBasis and sources
Free testosteroneTracked, no PYM targetNo target found
Total testosteroneTracked, no PYM targetNo target found
IGF-1120 to 160 ng/mLTier 2
Risk inflection in cohort data

Set on the range associated with the lowest all-cause mortality in a meta-analysis of 19 prospective cohorts covering 30,876 people. The relationship is U-shaped: compared with the middle of the distribution, low IGF-1 carries a 33% higher risk of death and high IGF-1 a 23% higher risk, so this is a band to stay inside rather than a number to push up. It is also the safety marker for sermorelin, which raises IGF-1 by design. Note that the range sits below the population: the reference median for men in their forties is around 199 ng/mL.

Sources: Rahmani 2022, Kim 2020

PSAUnder 2.5 ng/mL
18–49: under 2.5 ng/mL

50–59: under 3.5 ng/mL

60–69: under 4.5 ng/mL

70+: under 6.5 ng/mL
Tier 1
Guideline threshold

A screening ceiling, not a wellness target. Oesterling 1993 established the age-specific ninety-fifth percentiles that are standard in prostate screening — from 471 community men screened cancer-free by biopsy and ultrasound — at 2.5 ng/mL to age 49, 3.5 through the fifties, 4.5 through the sixties and 6.5 beyond. The prostate enlarges with age, so unlike most markers here the threshold genuinely belongs to the age rather than describing it. The trend matters more than any single value.

Sources: Oesterling 1993, Morgan 1996

Free PSA %25 to 100%Tier 1
Guideline threshold

A validated decision threshold, not an interval. Across 773 men at seven US medical centres, a free-PSA share at or below 25 percent was the point at which biopsy was recommended: it caught 95 percent of cancers while sparing a fifth of the biopsies that would otherwise have been done. Higher is better, so the zone is 25 percent and above. The scope is narrow and it matters — the figure was derived in men aged 50 to 75 whose total PSA sat between 4 and 10 ng/mL and whose prostate felt normal on examination. Outside that window this is not the test that was validated, and a reassuring percentage does not carry the meaning it carries inside it.

Sources: Catalona 1998

Free T3Tracked, no PYM targetNo target found
Total T3Tracked, no PYM targetNo target found
Total T4Tracked, no PYM targetNo target found
TPO antibodiesTracked, no PYM targetNo target found
Thyroglobulin antibodiesTracked, no PYM targetNo target found
ThyroglobulinTracked, no PYM targetNo target found
DHEA-STracked, no PYM targetNo target found
EstroneTracked, no PYM targetNo target found
ProgesteroneTracked, no PYM targetNo target found
FSHTracked, no PYM targetNo target found
LHTracked, no PYM targetNo target found
AMHTracked, no PYM targetNo target found
ProlactinTracked, no PYM targetNo target found
SHBGTracked, no PYM targetNo target found
EstradiolTracked, no PYM targetNo target found
Cortisol (morning)Tracked, no PYM targetNo target found
Testosterone:cortisol ratioTracked, no PYM targetNo target found
HematocritUnder 54%Tier 1
Guideline threshold

A testosterone-therapy safety ceiling, not a wellness target. The Endocrine Society clinical practice guideline directs stopping or reducing testosterone therapy if hematocrit climbs above 54%, and the zone is that stop threshold, ceiling only.

Sources: Bhasin 2018

TSHTracked, no PYM targetNo target found
Free T4Tracked, no PYM targetNo target found

Metabolic

MarkerPrime rangeEvidenceBasis and sources
Uric acidTracked, no PYM targetNo target found
AmylaseTracked, no PYM targetNo target found
LipaseTracked, no PYM targetNo target found
Selenium120 to 150 µg/LTier 3
Functional sufficiency

The only zone here whose two ends come from different kinds of evidence, and they agree. The floor is functional: in a randomised, placebo-controlled trial in 119 UK adults aged 50 to 64, the supplement dose that fully expressed selenoprotein P raised plasma selenium from 96 to 118 ng/mL, so below roughly 120 the body is still short of what its selenium-dependent enzymes need. The ceiling is a risk curve: across 13,887 US adults followed twelve years, mortality fell as selenium rose to about 130 ng/mL and then turned upward again above 150. More is not better with this one, which is unusual for a nutrient. Micrograms per litre and nanograms per millilitre are the same quantity written two ways, so both studies sit on this scale without conversion.

Sources: Hurst 2010, Bleys 2008

CalciumTracked, no PYM targetNo target found
Methylmalonic acidUnder 271 nmol/LTier 3
Functional sufficiency

Methylmalonic acid rises when a cell is functionally short of B12, which makes it the textbook sufficiency marker. The ceiling of 271 nmol/L is the NIH Office of Dietary Supplements Health Professional fact sheet’s own figure, cite-locked on 2026-09-15. Ceiling only — there is no floor a member should aim for. MMA also rises with age and with falling kidney function, so a raised value with a low eGFR is not automatically B12.

Sources: National 2024

ZincTracked, no PYM targetNo target found
CopperTracked, no PYM targetNo target found
LeptinTracked, no PYM targetNo target found
C-peptideTracked, no PYM targetNo target found
Creatine kinaseTracked, no PYM targetNo target found
HbA1cTracked, no PYM targetNo target found
Fasting insulinTracked, no PYM targetNo target found
Fasting glucoseTracked, no PYM targetNo target found
HOMA-IRTracked, no PYM targetNo target found
TyG indexTracked, no PYM targetNo target found
Vitamin B12Tracked, no PYM targetNo target found
FolateTracked, no PYM targetNo target found
Vitamin DTracked, no PYM targetNo target found
MagnesiumTracked, no PYM targetNo target found
RBC magnesiumTracked, no PYM targetNo target found

Liver

MarkerPrime rangeEvidenceBasis and sources
AlbuminTracked, no PYM targetNo target found
Total proteinTracked, no PYM targetNo target found
Total bilirubinTracked, no PYM targetNo target found
Alkaline phosphataseTracked, no PYM targetNo target found
ALTTracked, no PYM targetNo target found
ASTTracked, no PYM targetNo target found
FIB-4Tracked, no PYM targetNo target found
GGTTracked, no PYM targetNo target found

Kidney

MarkerPrime rangeEvidenceBasis and sources
Urine albumin/creatinine ratioUnder 30 mg/gTier 1
Guideline threshold

KDIGO places normal albumin excretion below 30 mg/g, moderately increased from 30 to 300, and severely increased above that. The ceiling is the first line and there is no floor. This one is deliberately NOT age-banded: more than a tenth of adults past fifty exceed 30 mg/g, and that is early kidney disease rather than a normal finding for their age, so an age band would hide the finding worth having.

Sources: KDIGO 2024

Sodium135 to 142 mmol/LTier 2
Risk inflection in cohort data

Set on a risk curve, and only on one side of it. Following 15,752 adults enrolled in middle age for twenty-five years, a serum sodium above 142 mmol/L carried a 39 percent higher risk of developing a chronic disease and a 50 percent higher chance of testing biologically older than chronological age; above 144, a 21 percent higher risk of dying early. The enrolment ages in that study are the ages of our own members. The ceiling is that 142. The floor is not from the same evidence and does not pretend to be: 135 is the bottom of the clinical normal range, below which low sodium is a problem in its own right, and the study says nothing about the low side. Read this as a hydration marker rather than a salt marker.

Sources: Dmitrieva 2023

Urine red blood cellsUnder 2 /hpfTier 1
Guideline threshold

A guideline definition with nothing inferred. Three or more red cells per high-power field on a single microscopic specimen is microhematuria under the 2020 AUA/SUFU guideline, so the target is two or fewer. It is an absolute threshold: not partitioned by age or sex, and deliberately not age-banded, for the same reason as the urine albumin ratio — blood in the urine becoming commoner with age does not make it normal. A dipstick positive for blood is a different test; the guideline rests the definition on microscopy.

Sources: Barocas 2020

Potassium4 to 4.9 mmol/LTier 2
Risk inflection in cohort data

Across 911,698 US medical records, death rates were lowest at 4.0 to just under 5.0 in people without heart failure, kidney disease or diabetes, and rose on both sides. A study of 9,651 community adults free of heart disease found the same above 5.0. Water pills and some blood-pressure drugs move potassium, so a result outside the zone is a question for your clinician before it is a target.

Sources: Collins 2017, Hughes-Austin 2017

ChlorideTracked, no PYM targetNo target found
Carbon dioxide23 to 30 mmol/LTier 2
Risk inflection in cohort data

The floor is a risk line: in 2,287 healthy adults in their seventies followed for ten years, bicarbonate below 23 carried a higher death rate, while high values did not. The ceiling is the top of the normal range derived from careful acid-base studies at sea level, 23 to 30, which is narrower than many labs print. It moves with breathing and altitude.

Sources: Raphael 2016, Kraut 2018

Urine white blood cellsTracked, no PYM targetNo target found
eGFR90 to 120 mL/minTier 1
Guideline threshold

KDIGO stage G1, normal kidney function, is an eGFR of 90 or above; the zone floor is that threshold. The ceiling is a scoring ceiling: a very high eGFR is not better and can reflect hyperfiltration.

Sources: KDIGO 2024

Cystatin CTracked, no PYM targetNo target found
CreatinineTracked, no PYM targetNo target found
BUNTracked, no PYM targetNo target found

Blood & immune

MarkerPrime rangeEvidenceBasis and sources
Red cell distribution widthUnder 13.4%Tier 2
Risk inflection in cohort data

In 8,175 US adults aged 45 and over, the risk of death rose steadily with RDW and was particularly high above 13.4 percent, even in people who were not anaemic and had no iron, folate or B12 deficiency. The zone is that ceiling, with no floor. Different lab machines read RDW slightly differently, so the trend on one lab matters more than a single number.

Sources: Patel 2009

Mean corpuscular volumeTracked, no PYM targetNo target found
Mean corpuscular hemoglobinTracked, no PYM targetNo target found
Mean corpuscular hemoglobin concentrationTracked, no PYM targetNo target found
Red blood cell countTracked, no PYM targetNo target found
Mean platelet volumeTracked, no PYM targetNo target found
NeutrophilsTracked, no PYM targetNo target found
LymphocytesTracked, no PYM targetNo target found
MonocytesTracked, no PYM targetNo target found
EosinophilsTracked, no PYM targetNo target found
BasophilsTracked, no PYM targetNo target found
LeadUnder 3.5 µg/dLTier 1
Guideline threshold

The ceiling is the level at which public health bodies say to act: 3.5 micrograms per decilitre, set for adults and children alike in 2022. Read it carefully, because it is not a safety line — it is the 97.5th percentile of the US population, a statement about how common a level is rather than about whether it harms. The National Toxicology Program found sufficient evidence of harm in adults and children below 10 and below 5. So the target is the span underneath the action line, and lower is better the whole way down; there is no lead level worth aiming to reach.

Sources: Council 2022, National 2012

MercuryUnder 5.8 µg/LTier 1
Guideline threshold

The ceiling of 5.8 micrograms per litre is the blood concentration matching the US environmental agency reference dose for methylmercury, which the CDC describes as an estimated level assumed to be without appreciable harm. That reference dose was derived to protect a developing fetus, the most sensitive endpoint rather than the one most of our members are at, so this is a deliberately conservative line. Note also what the test covers: blood mercury is mostly methylmercury from fish and falls over weeks once the diet changes, while elemental and inorganic mercury are measured in urine, which PYM does not test.

Sources: Centers 2004

CadmiumTracked, no PYM targetNo target found
Neutrophil countTracked, no PYM targetNo target found
Lymphocyte countTracked, no PYM targetNo target found
Monocyte countTracked, no PYM targetNo target found
Eosinophil countTracked, no PYM targetNo target found
Basophil countTracked, no PYM targetNo target found
HemoglobinTracked, no PYM targetNo target found
White blood cellsTracked, no PYM targetNo target found
PlateletsTracked, no PYM targetNo target found
FerritinTracked, no PYM targetNo target found
IronTracked, no PYM targetNo target found
TIBCTracked, no PYM targetNo target found
Transferrin saturation24 to 40%Tier 2
Risk inflection in cohort data

Set on the band with the lowest death rate in 15,823 US adults followed for up to eighteen years: risk was higher both below and above it, and the authors name 24 to 40 percent as the level associated with the greatest survival. The upper half is the weaker half, since the same study already saw higher risk above about 31 percent. Read with ferritin, it separates iron deficiency from overload.

Sources: Stack 2014

Inflammation

MarkerPrime rangeEvidenceBasis and sources
IgETracked, no PYM targetNo target found
Rheumatoid factorTracked, no PYM targetNo target found
hs-CRPUnder 1 mg/LTier 2
Risk inflection in cohort data

The CDC and American Heart Association statement grades cardiovascular risk by hs-CRP as low below 1 mg/L, average from 1 to 3, and high above 3. The zone is the low-risk grade, ceiling only, and is a risk grade rather than a wellness band. Draw twice if acute illness is suspected; above 10 mg/L reads as acute or inflammatory, not chronic cardiovascular risk.

Sources: Pearson 2003

HomocysteineTracked, no PYM targetNo target found

Lipids & cardiovascular

MarkerPrime rangeEvidenceBasis and sources
Lipoprotein(a)Under 75 nmol/LTier 1
Guideline threshold

The National Lipid Association places low cardiovascular risk below 75 nmol/L, intermediate from 75 to 125, and high at or above 125, and the 2026 ACC/AHA guideline makes once-in-a-lifetime testing a Class 1 recommendation. The ceiling is the low-risk line. There is no floor — no amount of Lp(a) is too little. It is largely inherited and barely moves with diet or exercise, so it is read as risk stratification rather than as a target to chase.

Sources: Koschinsky 2024

NT-proBNPTracked, no PYM targetNo target found
Omega-3 totalTracked, no PYM targetNo target found
EPATracked, no PYM targetNo target found
DHATracked, no PYM targetNo target found
DPATracked, no PYM targetNo target found
Omega-6 totalTracked, no PYM targetNo target found
Arachidonic acidTracked, no PYM targetNo target found
Linoleic acidTracked, no PYM targetNo target found
ApoBTracked, no PYM targetNo target found
LDL cholesterolTracked, no PYM targetNo target found
HDL cholesterolTracked, no PYM targetNo target found
TriglyceridesUnder 150 mg/dLTier 1
Guideline threshold

The shipped 40 to 90 mg/dL half-band scored a member against the middle of the US population distribution rather than a guideline line, and is retired (Deliverable D §2b, 2026-09-15). Both NCEP ATP III and the 2019 ESC/EAS guideline treat a fasting triglyceride under 150 mg/dL as normal. The zone is that ceiling only, with no floor.

Sources: NCEP ATP III 2002, Mach 2020

Total cholesterolUnder 200 mg/dLTier 1
Guideline threshold

The shipped 120 mg/dL floor was invented — no guideline sets a total-cholesterol floor, and a member on a statin with a genuinely low total should not be scored against one — and is retired (Deliverable D §2b, 2026-09-15). NCEP calls a total cholesterol under 200 mg/dL desirable. The zone is that ceiling only, with no floor: ApoB and LDL carry the risk signal, not the total.

Sources: NCEP ATP III 2002

Recovery & fitness

MarkerPrime rangeEvidenceBasis and sources
Resting heart rateUnder 50 bpmTier 2
Risk inflection in cohort data

In the Copenhagen Male Study, 2,798 men without heart disease followed for 16 years, the risk of death rose steadily above a resting heart rate of 50, independent of fitness: about 16 percent per 10 beats a minute, and three times higher above 90. The zone is 50 or below, the study’s lowest-risk group, with no floor. The study measured men lying down on an ECG, not a wearable overnight. Women are scored on the same line: in 272,737 women in the UK Biobank, risk rose about 19 percent per 10 beats a minute with no sign of levelling off, but that study reported only the slope, not a lowest-risk group, so it sets no separate zone for women.

Sources: Jensen 2013, Raisi-Estabragh 2020

Heart-rate variabilityTracked, no PYM targetNo target found
VO₂ maxOver 43.75 mL/kg/min
Men · women, by age:

18–19: 49 · 45.5

20–29: 47.95 · 40.25

30–39: 45.5 · 38.15

40–49: 43.75 · 36.4

50–59: 39.9 · 35

60–69: 35 · 29.75

70–79: 29.75 · 24.5

80+: 25.55 · 22.05
Tier 2
Risk inflection in cohort data

In 122,000 patients tested on a treadmill, mortality fell with every step up in fitness and never levelled off, with the fittest group at a fifth of the risk of the least fit. The study grouped people against others of their own sex and decade of age, so the zone does too: it starts where the top quarter for your age and sex starts, and the top of the band is where the top 2.3 percent starts. Above that still scores fully, since more fitness was never worse. The study estimated fitness from treadmill speed and slope in people sent for a stress test; a watch’s VO₂ max is an estimate again.

Sources: Mandsager 2018

Respiratory rateTracked, no PYM targetNo target found
Sleep scoreTracked, no PYM targetNo target found
Sleep score (WHOOP)Tracked, no PYM targetNo target found
Daily stepsOver 8,000
18–59: over 8,000

60+: over 6,000
Tier 2
Risk inflection in cohort data

A meta-analysis of 15 cohorts and 47,471 adults found the risk of death kept falling with more daily steps until about 6,000 to 8,000 for adults aged 60 and over, and 8,000 to 10,000 for younger adults, then levelled off. So the zone starts at 6,000 from age 60 and 8,000 below it, judged at your age each week. Above 12,000 still scores fully: more steps are not worse. Counted from your wearable’s own daily total.

Sources: Paluch 2022

9. Reference list

Every PubMed entry below was fetched from PubMed and its title checked before it was cited. Links open the abstract on PubMed, or the publisher’s page for a source that is not a journal article.

  1. Rahmani J, Montesanto A, Giovannucci E, et al. Association between IGF-1 levels ranges and all-cause mortality: a meta-analysis. Aging Cell, 2022. PubMed 35048526
  2. Kim B, Cho Y, Ku CR, Lee SG, Lee KA, Kim JH. Establishment of reference intervals for serum insulin-like growth factor I in Korean adult population. Endocrinology and Metabolism, 2020. PubMed 33212546
  3. Koschinsky ML, Bajaj A, Boffa MB, et al. A focused update to the 2019 NLA scientific statement on use of lipoprotein(a) in clinical practice. Journal of Clinical Lipidology, 2024. PubMed 38565461
  4. Dmitrieva NI, Gagarin A, Liu D, Wu CO, Boehm M. Middle-age high normal serum sodium as a risk factor for accelerated biological aging, chronic diseases, and premature mortality. EBioMedicine, 2023. PubMed 36599719
  5. Hurst R, Armah CN, Dainty JR, et al. Establishing optimal selenium status: results of a randomized, double-blind, placebo-controlled trial. American Journal of Clinical Nutrition, 2010. PubMed 20181815
  6. Bleys J, Navas-Acien A, Guallar E. Serum selenium levels and all-cause, cancer, and cardiovascular mortality among US adults. Archives of Internal Medicine, 2008. PubMed 18299496
  7. Catalona WJ, Partin AW, Slawin KM, et al. Use of the percentage of free prostate-specific antigen to enhance differentiation of prostate cancer from benign prostatic disease: a prospective multicenter clinical trial. JAMA, 1998. PubMed 9605898
  8. Barocas DA, Boorjian SA, Alvarez RD, et al. Microhematuria: AUA/SUFU guideline. The Journal of Urology, 2020. PubMed 32698717
  9. Council of State and Territorial Epidemiologists; CDC/NIOSH. Blood lead level reference values for adults. CDC National Institute for Occupational Safety and Health, 2022. Source
  10. National Toxicology Program. NTP monograph on health effects of low-level lead. NTP Monograph, 2012. PubMed 23964424
  11. Centers for Disease Control and Prevention. Blood mercury levels in young children and childbearing-aged women, United States, 1999-2002. MMWR Morbidity and Mortality Weekly Report 53(43), 2004. Source
  12. Oesterling JE, Jacobsen SJ, Chute CG, et al. Serum prostate-specific antigen in a community-based population of healthy men. Establishment of age-specific reference ranges. JAMA, 1993. PubMed 7688054
  13. Morgan TO, Jacobsen SJ, McCarthy WF, Jacobson DJ, McLeod DG, Moul JW. Age-specific reference ranges for prostate-specific antigen in black men. New England Journal of Medicine, 1996. PubMed 8663870
  14. Soffer DE, Marston NA, Maki KC, et al. Role of apolipoprotein B in the clinical management of cardiovascular risk in adults: An Expert Clinical Consensus from the National Lipid Association. Journal of Clinical Lipidology, 2024. PubMed 39256087
  15. Januzzi JL, van Kimmenade R, Lainchbury J, et al. NT-proBNP testing for diagnosis and short-term prognosis in acute destabilized heart failure: an international pooled analysis of 1256 patients: the International Collaborative of NT-proBNP Study. European Heart Journal, 2005. PubMed 16293638
  16. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology & Metabolism, 2018. PubMed 29562364
  17. Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice. A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation, 2003. PubMed 12551878
  18. Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. European Heart Journal, 2020. PubMed 31504418
  19. National Cholesterol Education Program Expert Panel. Third report of the National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III): final report. Circulation, 2002. PubMed 12485966
  20. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney International, 2024. PubMed 38490803
  21. Jensen MT, Suadicani P, Hein HO, Gyntelberg F. Elevated resting heart rate, physical fitness and all-cause mortality: a 16-year follow-up in the Copenhagen Male Study. Heart, 2013. PubMed 23595657
  22. Mandsager K, Harb S, Cremer P, et al. Association of cardiorespiratory fitness with long-term mortality among adults undergoing exercise treadmill testing. JAMA Network Open, 2018. PubMed 30646252
  23. Raisi-Estabragh Z, Cooper J, Judge R, et al. Age, sex and disease-specific associations between resting heart rate and cardiovascular mortality in the UK BIOBANK. PLOS ONE, 2020. PubMed 32470091
  24. Paluch AE, Bajpai S, Bassett DR, et al. Daily steps and all-cause mortality: a meta-analysis of 15 international cohorts. The Lancet Public Health, 2022. PubMed 35247352
  25. Stack AG, Mutwali AI, Nguyen HT, Cronin CJ, Casserly LF, Ferguson J. Transferrin saturation ratio and risk of total and cardiovascular mortality in the general population. QJM, 2014. PubMed 24599805
  26. Patel KV, Ferrucci L, Ershler WB, Longo DL, Guralnik JM. Red blood cell distribution width and the risk of death in middle-aged and older adults. Archives of Internal Medicine, 2009. PubMed 19273783
  27. Collins AJ, Pitt B, Reaven N, et al. Association of serum potassium with all-cause mortality in patients with and without heart failure, chronic kidney disease, and/or diabetes. American Journal of Nephrology, 2017. PubMed 28866674
  28. Hughes-Austin JM, Rifkin DE, Beben T, et al. The relation of serum potassium concentration with cardiovascular events and mortality in community-living individuals. Clinical Journal of the American Society of Nephrology, 2017. PubMed 28143865
  29. Raphael KL, Murphy RA, Shlipak MG, et al. Bicarbonate concentration, acid-base status, and mortality in the Health, Aging, and Body Composition Study. Clinical Journal of the American Society of Nephrology, 2016. PubMed 26769766
  30. Kraut JA, Madias NE. Re-evaluation of the normal range of serum total CO2 concentration. Clinical Journal of the American Society of Nephrology, 2018. PubMed 29339355
  31. Rupprecht M, Wagenpfeil S, Schöpe J, Vieth R, Vogt T, Reichrath J. Meta-Analysis of European Clinical Trials Characterizing the Healthy-Adult Serum 25-hydroxyvitamin D Response to Vitamin D Supplementation. Nutrients, 2023. PubMed 37764770
  32. Kavyani Z, Musazadeh V, Fathi S, Hossein Faghfouri A, Dehghan P, Sarmadi B. Efficacy of the omega-3 fatty acids supplementation on inflammatory biomarkers: An umbrella meta-analysis. International Immunopharmacology, 2022. PubMed 35914448
  33. AbuMweis S, Jew S, Tayyem R, Agraib L. Eicosapentaenoic acid and docosahexaenoic acid containing supplements modulate risk factors for cardiovascular disease: a meta-analysis of randomised placebo-control human clinical trials. Journal of Human Nutrition and Dietetics, 2018. PubMed 28675488
  34. Zhao JV, Huang X, Zhang J, Chan YH, Tse HF, Blais JE. Overall and Sex-Specific Effect of Berberine on Glycemic and Insulin-Related Traits: a Systematic Review and Meta-Analysis of Randomized Controlled Trials. The Journal of Nutrition, 2023. PubMed 37598753
  35. Jovanovski E, Yashpal S, Komishon A, et al. Effect of psyllium (Plantago ovata) fiber on LDL cholesterol and alternative lipid targets, non-HDL cholesterol and apolipoprotein B: a systematic review and meta-analysis of randomized controlled trials. American Journal of Clinical Nutrition, 2018. PubMed 30239559
  36. Sohouli MH, Almuqayyid F, Alfardous Alazm A, et al. A comprehensive review and meta-regression analysis of randomized controlled trials examining the impact of vitamin B12 supplementation on homocysteine levels. Nutrition Reviews, 2024. PubMed 37495210
  37. National Institutes of Health, Office of Dietary Supplements. Vitamin B12 — Health Professional Fact Sheet. NIH Office of Dietary Supplements, 2024. Source
  38. Fraser CG. Reference change values. Clinical Chemistry and Laboratory Medicine, 2012. PubMed 21958344
  39. Fokkema MR, Herrmann Z, Muskiet FA, Moecks J. Reference change values for brain natriuretic peptides revisited. Clinical Chemistry, 2006. PubMed 16873298
  40. Sandberg S, Coskun A, Carobene A, et al. Analytical performance specifications based on biological variation data - considerations, strengths and limitations. Clinical Chemistry and Laboratory Medicine, 2024. PubMed 38501489
  41. European Federation of Clinical Chemistry and Laboratory Medicine. EFLM Biological Variation Database, meta-analysis estimates (updated 8 October 2026). biologicalvariation.eu, 2026. Source
  42. Sterling RK, Lissen E, Clumeck N, et al. Development of a simple noninvasive index to predict significant fibrosis in patients with HIV/HCV coinfection. Hepatology, 2006. PubMed 16729309
  43. Shah AG, Lydecker A, Murray K, Tetri BN, Contos MJ, Sanyal AJ. Comparison of noninvasive markers of fibrosis in patients with nonalcoholic fatty liver disease. Clinical Gastroenterology and Hepatology, 2009. PubMed 19523535
  44. McPherson S, Hardy T, Dufour JF, et al. Age as a confounding factor for the accurate non-invasive diagnosis of advanced NAFLD fibrosis. American Journal of Gastroenterology, 2017. PubMed 27725647
  45. Rinella ME, Neuschwander-Tetri BA, Siddiqui MS, et al. AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology, 2023. PubMed 36727674
  46. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia, 1985. PubMed 3899825
  47. Simental-Mendía LE, Rodríguez-Morán M, Guerrero-Romero F. The product of fasting glucose and triglycerides as surrogate for identifying insulin resistance in apparently healthy subjects. Metabolic Syndrome and Related Disorders, 2008. PubMed 19067533
  48. Guerrero-Romero F, Simental-Mendía LE, González-Ortiz M, et al. The product of triglycerides and glucose, a simple measure of insulin sensitivity. Comparison with the euglycemic-hyperinsulinemic clamp. Journal of Clinical Endocrinology & Metabolism, 2010. PubMed 20484475

Questions about a range, or a source you think is missing: email support@primeyearsmedical.com.

Prime ranges, therapy checks and the biological-age model are decision-support tools, not a diagnosis. They do not replace your provider’s clinical judgment.

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