A lab reference range is a description of a population, and the population is not healthy. Its bounds are usually the middle 95% of whoever walked into the lab — which means 'normal' encodes the diseases of the people being measured. Everything below is split three ways: reference, optimal, and elite. Optimal is where the outcome curve actually bottoms. Elite is the score to beat. Nothing here is a diagnosis, and abnormal values belong in front of a doctor rather than a spreadsheet.
Research vintage · Q3 2026
The panel
Bloodwork
Quarterly. Fasted, same lab, same time of day — trend beats any single draw.
RCT / meta-analysisPrimary literature
Cardiovascular — the biggest killer, and the most measurable
Mechanism
Why ApoB is the number, not LDL-C
Atherosclerosis is a particle-driven disease. Every atherogenic lipoprotein — LDL, VLDL, IDL, Lp(a) — carries exactly one ApoB molecule, so ApoB is a direct particle *count* while LDL-C measures the cholesterol *cargo* those particles happen to be carrying. Two people with identical LDL-C can differ substantially in particle number, and it is the particles that penetrate the endothelium, get retained by proteoglycan binding, oxidise, and trigger the macrophage foam-cell cascade. The exposure is cumulative — particle-count multiplied by years — which is precisely why the number matters most when you are young and it seems irrelevant.
Marker
Lab 'normal'
Optimal
Elite — the score to beat
ApoB
< 130 mg/dL
< 80 mg/dL
< 60 mg/dL
LDL-C
< 130 mg/dL
< 70 mg/dL
< 50 mg/dL
Lp(a)
Rarely tested
< 30 mg/dL (~75 nmol/L)
Genetic — test once, ever. Unmodifiable by lifestyle; if high, everything else gets tighter
Triglycerides
< 150 mg/dL
< 80 mg/dL
< 60 mg/dL
HDL-C
> 40 mg/dL
50–80 mg/dL
Stop optimising this — Mendelian randomisation shows raising HDL pharmacologically does not reduce events. It is a marker, not a lever
hs-CRP
< 3.0 mg/L
< 1.0 mg/L
< 0.5 mg/L
Homocysteine
< 15 µmol/L
< 9 µmol/L
< 7 µmol/L
Lp(a) is worth a single lifetime test and almost nobody gets it. It is ~90% genetically determined, elevated in roughly one in five people, and independently multiplies cardiovascular risk. Knowing it changes how aggressive every other target should be.
RCT / meta-analysisPrimary literature
Metabolic — where 'normal' is most misleading
Marker
Lab 'normal'
Optimal
Elite
Fasting glucose
70–99 mg/dL
75–85 mg/dL
70–80 mg/dL
HbA1c
< 5.7%
4.9–5.3%
< 5.0%
Fasting insulin
2–25 µIU/mL
< 6 µIU/mL
< 4 µIU/mL
HOMA-IR
< 2.5
< 1.5
< 1.0
ALT
< 40 U/L
< 25 U/L
< 20 U/L (a proxy for hepatic fat)
Uric acid
< 7.0 mg/dL
< 5.5 mg/dL
4.0–5.0 mg/dL
Fasting insulin is the most under-ordered test in medicine
Glucose stays normal for years while insulin climbs to keep it there — the compensation *is* the disease process, and it is invisible on a glucose-only panel. By the time fasting glucose rises, beta-cell function has usually been declining for a decade. If one extra test gets added to a standard panel, make it this one.
Limited human dataPrimary literature
Hormonal, thyroid and micronutrient
Marker
Lab 'normal'
Optimal
Note
Total testosterone (male)
300–1,000 ng/dL
600–900 ng/dL
Free T and SHBG matter more than total; a healthy 17-year-old is usually near the top of range naturally
TSH
0.4–4.5 mIU/L
0.5–2.0 mIU/L
Interpret only alongside free T3 and free T4
25(OH) vitamin D
> 20 ng/mL
30–50 ng/mL
Above ~60 buys nothing and the supplementation trials in replete people are null
Ferritin
30–400 ng/mL
50–150 ng/mL
High ferritin is also an acute-phase reactant — read it against CRP before concluding iron overload
Vitamin B12
> 200 pg/mL
> 500 pg/mL
Check methylmalonic acid if borderline; serum B12 is an insensitive test
Omega-3 index
Not standard
> 8% of RBC fatty acids
One of the better-validated nutritional biomarkers; < 4% associates with the highest cardiovascular risk
Magnesium (RBC)
Serum is near-useless
> 5.5 mg/dL RBC
Serum magnesium is tightly buffered and stays normal during real deficiency
Composition
Body composition
RCT / meta-analysisPrimary literature
The numbers that actually track outcomes
Metric
Population
Optimal
Elite
Body fat % (male, DEXA) — see note
20–25%
12–18% under 20 · 12–15% adult
10–12% adult. Sub-12% year-round is NOT an appropriate target under ~20
Fat-free mass index (FFMI)
18–19
20–21
22–23; ~25 is the commonly cited drug-free ceiling — a rule of thumb, not a measured limit
Waist-to-height ratio
~0.50 — note 0.5 is the risk cutoff, not a population average
< 0.47
< 0.45
Visceral fat (DEXA)
< 1.0 kg
< 0.5 kg
< 0.25 kg — the depot that drives metabolic risk, distinct from subcutaneous
Grip strength (male, 17–25)
~46 kg
> 55 kg
> 62 kg — top 5%; one of the strongest single predictors of all-cause mortality
Bone mineral density (Z-score)
> −1.0
> +1.0
> +2.0 — built almost entirely by heavy loading and impact before ~30, then defended
Mechanism
Why FFMI and not weight
Fat-free mass index normalises lean mass to height squared — lean kg ÷ m² — which makes it comparable across body sizes in a way that bodyweight and BMI are not. The reason it matters beyond aesthetics: skeletal muscle is the primary site of insulin-stimulated glucose disposal, so lean mass is literally metabolic buffer capacity. It is also the single largest reservoir of amino acids available during illness, which is why lean mass predicts survival in almost every serious clinical setting studied.
Bone density has a closing window
Peak bone mass is essentially set by the late twenties and defended thereafter. Osteocytes sense mechanical strain through their dendritic processes in the lacuno-canalicular network and respond to fluid shear by downregulating sclerostin, which releases Wnt/β-catenin signalling and drives osteoblastic bone formation. The stimulus is high-magnitude, high-rate and novel-direction loading — heavy compounds, jumping, sprinting. Steady-state cardio does close to nothing for it. This is the one metric on this page where being 17 is a decisive and time-limited advantage.
Output
Performance benchmarks
What the body can actually do — the tests worth re-running quarterly.
RCT / meta-analysisPrimary literature
Aerobic
Test
Average (male, 18–25)
Excellent
Elite — the score to beat
VO₂max
40–45 ml/kg/min
55–60
65–70+ (world-class endurance: 80–90)
Resting heart rate
60–75 bpm
45–55
< 45
HRV (RMSSD, night avg)
40–60 ms
70–90 ms
> 100 ms — but compare only against your own baseline, never against another person
Heart-rate recovery (1 min post-max)
~20–25 bpm — ≤12 is the Cole abnormality threshold, not an average
> 35 bpm
> 45 bpm — a direct readout of parasympathetic reactivation. Strongly protocol-dependent, so only compare like with like
5k time
~28 min
20–22 min
< 18 min — a strong club standard. Genuinely elite is 13–14 min
VO₂max decline with age
−10%/decade
−5%/decade
≈ −2 to −3%/decade — the trajectory matters more than any single value
Mechanism
Why VO₂max is the single biggest lever on this page
Two results, often wrongly merged. Kodama et al. (JAMA, 2009) is the source of the per-unit figure: each 1-MET increase (~3.5 ml/kg/min) associated with roughly a 13% reduction in all-cause mortality. Mandsager et al. (JAMA Network Open, 2018, N=122,007) reported categorical comparisons — elite versus low fitness at a hazard ratio near 0.20, exceeding the mortality contribution of smoking, hypertension or diabetes in the same dataset — with no observed upper limit. Mechanistically it is a composite: stroke volume, oxygen-carrying capacity, capillary diffusion distance, and mitochondrial oxidative capacity. Nothing else on this scoreboard is simultaneously this predictive and this trainable.
Limited human dataOperator, verifiable record
Strength and power
Lift / test
Intermediate
Advanced
Elite (drug-free)
Bench press 1RM
1.0 × bodyweight
1.5 ×
2.0 ×
Back squat 1RM
1.5 ×
2.0 ×
2.5 ×
Deadlift 1RM
1.75 ×
2.5 ×
3.0 ×
Weighted pull-up 1RM
+20% BW
+50% BW
+80–100% BW
Overhead press 1RM
0.6 ×
0.9 ×
1.2 ×
Standing vertical jump
50–60 cm
70 cm
85–100 cm
Reactive Strength Index (drop jump)
1.5
2.5
> 3.0
30 m sprint (flying 10 m)
—
> 9.0 m/s
> 10.5 m/s
Strength standards are ratios to bodyweight and therefore get harder as lean mass climbs — that is intended. Note that a 125 kg bench at 78 kg bodyweight is ≈1.6×: past advanced, short of elite.
RCT / meta-analysisPrimary literature
Sleep
Metric
Typical
Optimal
Elite
Total sleep time (see note — age matters)
6.5 h
8–10 h under 18 · 7–9 h from ~18
9–10 h under 18, held seven days a week
Sleep efficiency
80–85%
> 90%
> 93%
Deep (SWS) as % of night
10–15%
16–20%
> 20% — the glymphatic clearance window
REM as % of night
15–20%
20–25%
22–25%
Sleep-onset latency
20–30 min
10–20 min
10–15 min (< 5 min consistently signals sleep debt, not skill)
Bedtime consistency (SD)
> 60 min
< 30 min
< 15 min — regularity predicts mortality better than duration does
Resting HR dip overnight
5–10%
> 12%
> 15% below daytime baseline
Sleep regularity outperforms sleep duration as a mortality predictor. A consistent 7.5 hours beats an average 8.5 hours assembled from a ragged, shifting schedule — which makes the fixed wake time the highest-leverage single decision in the whole protocol.
Research notes, not medical or financial advice. Every prescription or experimental item named here is named with its mechanism and its risk and without a dose, on purpose — several require physician supervision, several are unregulated, and several are inappropriate for a body that is still developing. Start from your own bloodwork and a doctor, never from someone else’s regimen.