The Longevity Lab Panel.

Standard reference: LabCorp 2.6–24.9 µIU/mL, derived from population distribution. Commonly targeted in longevity and functional practice: below 5 mIU/L, a practice convention representing highly insulin-sensitive status. Elevated fasting insulin precedes glucose abnormality by 10 or more years. HOMA-IR above 2.5 is widely used to define insulin resistance. In observational data, the highest vs. lowest insulin quartile carries approximately a 2.1-fold higher cardiovascular mortality risk, though insulin itself is a marker of metabolic state rather than a proven causal driver.

Standard reference: ADA below 5.7% as normal, 5.7–6.4% as prediabetes. Commonly targeted in longevity and functional practice: below 5.3%, a practice convention. Each 1% increase above 5.0% is associated with roughly 20–30% higher cardiovascular mortality in observational data, and metabolic dysfunction appears well before the 5.7% prediabetes threshold. The optimal target has no RCT Randomized controlled trial: people are assigned to the treatment or a comparison by chance, so the groups differ only in what they received. It is the design that can show cause and effect. basis in non-diabetic individuals.

Standard reference: ADA below 100 mg/dL as normal. Commonly targeted in longevity and functional practice: below 90 mg/dL, a practice convention. The relationship between glucose and cardiovascular risk extends below the diabetic threshold, as shown in the Emerging Risk Factors Collaboration (PMID 20801498). The longevity target has no RCT basis in normoglycemic individuals.

Standard reference: HOMA-IR below 2.5 is the widely used clinical cutoff for insulin resistance, though thresholds from 1.7 to 2.9 appear in the literature. Commonly targeted in longevity and functional practice: below 1.0, representing the highly insulin-sensitive range. Calculated as (fasting insulin × fasting glucose) / 405. In observational data, the highest vs. lowest HOMA-IR carries approximately 34% higher all-cause mortality and 2.1-fold higher cardiovascular mortality.

Standard reference: NCEP ATP III below 130 mg/dL. The ACC/AHA 2018 guidelines support below 80 mg/dL for high-risk and below 60 mg/dL for very high-risk patients in secondary prevention. Commonly targeted in longevity practice: below 60 mg/dL, a convention for primary prevention. ApoB is superior to LDL-C Low-density lipoprotein cholesterol, the cholesterol fraction most closely tied to plaque in the arteries. in 9 of 9 discordance studies because it counts atherogenic particles, not cholesterol mass. Two people with identical LDL-C can have meaningfully different ApoB and different risk.

Standard reference: EAS 2022 below 30 mg/dL or below 75 nmol/L as low risk, with risk rising continuously above it. Lp(a) Lipoprotein(a), a cholesterol-carrying particle whose level is set largely by genetics. is not routinely tested in standard panels despite affecting approximately 20% of the population. It is genetically determined and is an independent cardiovascular risk factor. Whether statins change Lp(a) is genuinely contested, and the two largest randomized analyses disagree by design: Tsimikas et al. (Eur Heart J, 2020; PMID 31111151), a subject-level meta-analysis of 5,256 patients across six randomized trials, found statins raised Lp(a) relative to placebo An inactive substitute made to look like the real treatment, so participants cannot tell which one they received. (ratio of geometric means 1.11, 95% CI 1.07 to 1.14, P<0.0001), while Xie et al. (Atherosclerosis, 2025; PMID 40618457), pooling 147 RCTs and 145,314 subjects, found statins did not affect it. The disagreement is methodological rather than a contradiction in the data: Tsimikas measured proportional change on log-transformed values, Xie measured absolute change in mg/dL, and because Lp(a) is heavily right-skewed a 10 to 20 percent proportional rise on a low baseline is a small absolute change that pools toward zero. EBL states this as unsettled rather than picking a side. Neither analysis supports any claim that statins lower Lp(a). Of the therapies Xie tested, PCSK9 monoclonal antibodies reduced Lp(a) by about 29 percent, inclisiran 22 percent, CETP inhibitors 46 percent and niacin 37 percent, while bempedoic acid, ezetimibe, omega-3 fatty acids and fibrates did not change it; whether any of those reductions produces cardiovascular benefit is untested. The EAS and ACC/AHA both recommend testing once in every adult's lifetime. A single measurement predicts MACE risk up to 30 years later.

Standard reference: AHA/CDC 2003 below 3.0 mg/L as the upper boundary of acceptable risk; above 3.0 = high risk. Commonly targeted in longevity practice: below 1.0 mg/L, in the low-risk tier. Inflammation is an independent cardiovascular risk factor. CANTOS proved reducing it reduces MACE Major adverse cardiovascular events: heart attack, stroke and cardiovascular death counted together as one trial outcome. events, but the RCT enrolled patients with hsCRP above 2.0 mg/L after a prior event: it tested the direction, not a specific low-end target.

Standard reference: ACC/AHA 2018 below 100 mg/dL for high-risk, below 70 mg/dL for very high risk. Commonly targeted in longevity practice: below 70 mg/dL as a primary prevention goal, below 55 mg/dL in high-risk or genetically elevated individuals. LDL-C is inferior to ApoB when the two disagree: LDL-C misses atherogenic particle burden in insulin-resistant individuals. Mendelian randomization shows lifelong lower LDL-C is associated with dramatically lower cardiovascular risk.

Standard reference: AHA below 150 mg/dL as normal. Commonly targeted in longevity practice: below 80 mg/dL, a convention reflecting insulin-sensitive metabolic status. TG above 100 mg/dL is an early signal of insulin resistance. The TG/HDL ratio is a stronger predictor of cardiovascular risk than total cholesterol and is computable from this and the HDL row.

Standard reference: ACC/AHA below 40 mg/dL (men) or below 50 mg/dL (women) as a risk-enhancing factor. Commonly targeted in longevity practice: above 60 mg/dL. Higher HDL-C is generally associated with lower cardiovascular risk in observational data, but HDL-raising drug trials failed, indicating HDL may be a marker of metabolic health rather than a causal driver. HDL function (cholesterol efflux capacity) matters more than HDL-C quantity alone.

Standard reference: Not routinely ordered. LipoScience reference intervals define borderline-high LDL-P at 1000–1300 nmol/L and small LDL-P above 527 nmol/L. Commonly targeted in longevity and functional cardiology practice: LDL-P below 1000, small LDL-P below 200, and pattern A (large buoyant particles). NMR measures particle number and size, not cholesterol mass. Small dense LDL is more atherogenic. Two people with identical LDL-C can have very different particle counts and correspondingly different cardiovascular risk.

Standard reference: LabCorp below 15 µmol/L. Commonly targeted in longevity practice: below 7 µmol/L, a practice convention. Elevated homocysteine is associated with impaired methylation, often driven by MTHFR variants or B-vitamin deficiency. It is linked to cardiovascular disease, stroke, and dementia in observational data. However, B-vitamin supplementation lowers homocysteine without reducing cardiovascular events in RCTs (HOPE-2), so lowering the number alone does not establish causal benefit. Responds to methylated B12, folate, and B6.

Standard reference: ACC/AHA 2018 Class IIa recommendation for CAC scoring at intermediate risk. CAC = 0 is guideline-supported as a basis for deferring statin therapy; any score above 0 supports initiating it. At roughly $100–300 cost, it reclassifies approximately 50% of intermediate-risk patients to low risk. The ACC/AHA recommends considering it from age 40–45 for baseline tracking. Any score above 0 indicates plaque is present regardless of conventional lipid values.

Standard reference: Westergren method below 20 mm/hr for younger adults, age-adjusted for older adults. Commonly targeted in longevity practice: below 10 mm/hr, a convention reflecting the low-inflammation range. ESR is a non-specific marker: elevated ESR with normal hsCRP can indicate autoimmune conditions. Low-grade elevation within the normal range carries clinical meaning when trended over time alongside more specific markers.

Standard reference: solubility threshold below 7.0 mg/dL (men) and below 6.0 mg/dL (women); ACR gout target below 6.0 mg/dL. Commonly targeted in longevity practice: 3.0–5.5 mg/dL, a practice convention. Uric acid is tied to metabolic syndrome, insulin resistance, and fructose intake. A U-shaped mortality curve means both extremes elevate risk, making the mid-normal range the conventional target.

Calculated, not ordered: platelets × neutrophils ÷ lymphocytes, each in ×10⁹/L, taken from the CBC with differential that most routine bloodwork already includes. Standard reference: none. In 42,875 US adults (NHANES) followed for up to 20 years, the top quarter (above 655.56) carried higher all-cause mortality (HR 1.29) and cardiovascular mortality (HR 1.33) than the bottom quarter (below 335.36) after adjustment; the two middle quarters did not differ from the bottom one. A second NHANES analysis of 42,503 adults found the same direction by thirds (all-cause HR 1.24 for the top third, at or above 600.23). Acute infection, recent surgery or trauma, corticosteroids, pregnancy, smoking and hard exercise in the prior 24 to 48 hours all raise it, and anything that lowers the lymphocyte count inflates it, so a single value taken during any of these says little. No trial has shown that lowering SII changes any outcome.

Calculated, not ordered: neutrophils × monocytes ÷ lymphocytes, each in ×10⁹/L, from the same CBC with differential. Standard reference: none. In the 42,875-adult NHANES cohort, the top quarter (above 1.43) carried higher all-cause mortality (HR 1.39) and cardiovascular mortality (HR 1.39) than the bottom quarter (below 0.68) after adjustment. The 42,503-adult NHANES analysis found the same direction by thirds (all-cause HR 1.33, cardiovascular HR 1.42). In 85,154 adults of the Chinese Kailuan cohort followed for 10 years, the top quarter carried higher all-cause mortality (HR 1.39) and stroke risk (HR 1.19); the link with heart attack (HR 1.20) did not hold in those aged 60 and over. Acute infection, recent surgery or trauma, corticosteroids, pregnancy, smoking and hard exercise in the prior 24 to 48 hours all raise it, and anything that lowers the lymphocyte count inflates it, so a single value taken during any of these says little. No trial has shown that lowering SIRI changes any outcome.

VITAL (n=25,871) randomized 2000 IU/day for the prevention of cancer and cardiovascular disease. Neither primary endpoint was reduced: invasive cancer of any type and major cardiovascular events were both null. Death from cancer, a secondary endpoint, was lower. No randomized trial establishes an optimal concentration for longevity or disease prevention, so no optimal range is published here. The reference figure above is the National Academies sufficiency cutpoint; the 30 ng/mL target that circulates widely comes from the 2011 Endocrine Society guideline, which its own 2024 successor replaced while declining to set concentration thresholds for generally healthy people. How common low status actually is, and at which threshold, is set out under Nutrient Gaps.

Standard reference: most laboratories treat below 200 to 250 pg/mL as subnormal (NIH Office of Dietary Supplements). Commonly targeted in longevity and functional practice: above 600 pg/mL, a practice convention rather than a trial-derived threshold. Aroda 2016 found long-term metformin use associated with lower B12 in the Diabetes Prevention Program Outcomes Study; it addresses depletion A fall in a nutrient's level caused by a medication, for example through reduced absorption or increased loss., not where optimal begins.

Standard reference: WHO sets iron deficiency below 15 ng/mL and flags overload risk above 150 ng/mL in menstruating women and 200 ng/mL in men. Commonly targeted in longevity and functional practice: a floor of 50 ng/mL, which is a practice convention rather than a trial-derived threshold. Ferritin is also an acute-phase reactant, so inflammation raises it independently of iron stores, which is why WHO applies a higher 70 ng/mL deficiency threshold when infection or inflammation is present.

Standard laboratory reference interval: 3.7–7.0 mg/dL (LabCorp Test 080283). Commonly targeted in longevity and functional practice: 5.0–6.5 mg/dL, a practice convention used by multiple longevity clinicians and functional medicine sources, not a trial-derived threshold. No randomized outcome trial has established that treating RBC magnesium to 5.0–6.5 mg/dL improves clinical endpoints. RBC magnesium reflects intracellular magnesium more reliably than serum, but neither measure has been validated against hard clinical outcomes in an RCT. The Zhang 2016 meta-analysis of 34 RCTs (PMID 27402922) established that magnesium supplementation reduces blood pressure (systolic -3.6 mmHg, diastolic -2.3 mmHg), it did not validate RBC magnesium as a monitoring target. Serum magnesium below 0.75 mmol/L is useful for detecting frank deficiency; within normal ranges, the assay is a poor index of body stores.

Standard reference: WHO sets possible serum deficiency below 10 nmol/L, about 4.4 ng/mL, and prefers red-cell folate as the status biomarker. Commonly targeted in longevity and functional practice: above 15 ng/mL serum, a practice convention rather than a trial-derived threshold. Wald 2002 established the homocysteine to cardiovascular risk relationship and the folate to homocysteine link; it does not establish where a folate level should sit.

Standard reference: no established range. Harris and Von Schacky 2004 defined risk zones: above 8% associated with greatest cardioprotection; below 4% with least. Commonly targeted in longevity practice: above 8%. The index reflects EPA+DHA incorporation into red blood cell membranes, which turns over approximately 90 days and is not subject to the daily variation of plasma omega-3 measurements. The REDUCE-IT trial (n=8,179) showed icosapentaenoic acid at 4 g/day reduced cardiovascular events in high-risk patients, but enrolled patients with low omega-3 status and did not test targeting the index to 8%.

Standard reference: LabCorp below 65 U/L (men) and below 45 U/L (women), though ranges vary by lab. Commonly targeted in longevity practice: below 20 U/L, a convention reflecting low hepatic and oxidative stress burden. GGT rises before ALT and AST and is an independent marker of cardiovascular risk in a dose-response relationship with all-cause mortality. Also associated with metabolic syndrome, fatty liver, and alcohol intake.

Standard reference: most labs below 45 U/L (men) and below 35 U/L (women), but Prati 2002 (PMID 12093239) showed the true normal in healthy adults is substantially lower. Commonly targeted in longevity practice: below 25 U/L, a midpoint between the Prati-derived normal and the conventional permissive range. Current lab ranges are too permissive because their reference populations include individuals with subclinical fatty liver and metabolic dysfunction.

Standard reference: ATA 0.4–4.5 mIU/L, derived from a population that includes individuals with undiagnosed thyroid disease. Commonly targeted in longevity and functional practice: 1.0–2.5 mIU/L. In thyroid-antibody-negative, iodine-sufficient adults, TSH above 2.5 mIU/L exceeded the 97.5th percentile in NHANES III data, suggesting the upper conventional limit captures early thyroid dysfunction. TSH in the 2.5–4.5 range may represent early thyroid dysfunction in many people, though no RCT has tested treating euthyroid adults to the lower portion of the range.

Standard reference: LabCorp 2.3–4.2 pg/mL, highly assay-dependent. Optimal range: not established. EBL previously published 3.0–4.0 pg/mL as an optimal range and removed it in July 2026 because no randomized trial has shown that targeting any particular Free T3 concentration in euthyroid individuals changes a clinical outcome. Free T3 is the biologically active thyroid hormone; most standard panels omit it. If a clinical reason exists to check it, interpret it in the context of TSH and Free T4, not in isolation.

Standard reference: LabCorp 0.8–1.8 ng/dL, highly assay-dependent. Optimal range: not established. EBL previously published 1.0–1.5 ng/dL as an optimal range and removed it in July 2026. No RCT establishes a Free T4 target in euthyroid individuals. Free T4 reflects the circulating hormone that is converted to active Free T3 in peripheral tissues; the conversion ratio varies by individual and tissue, making Free T4 alone an incomplete picture.

Any elevation = immune attack on thyroid. Hashimoto's present 5-10 years before TSH abnormality. If nobody checks antibodies, nobody catches it.

Standard reference: LabCorp age-specific ranges; DHEA-S declines approximately 2–3% per year after age 25–30. Commonly targeted in longevity practice: upper quartile for age, a convention based on epidemiological associations between higher DHEA-S and lower all-cause and cardiovascular mortality. Lower DHEA-S is independently associated with cardiovascular mortality and biological aging. Supplementation RCTs have not confirmed causal benefit, so this is a monitoring target, not a proven intervention target.

Standard reference: LabCorp age-specific ranges. Commonly targeted in longevity practice: 100–180 ng/mL, the nadir of the U-shaped mortality curve. Too high increases cancer risk; too low is associated with frailty and cardiovascular disease. This is not a 'lower is better' biomarker. It is read in the context of age, body composition and cancer history, and it is measured before any peptide or growth hormone protocol begins.

Standard reference: LabCorp 0.56–1.00 mg/L; KDIGO defines CKD by eGFR derived from cystatin C. Commonly targeted in longevity practice: below 0.8 mg/L, a convention reflecting below-median renal and vascular function. Cystatin C is more accurate than creatinine-based eGFR in older adults and those with low muscle mass because it is not influenced by muscle mass. It independently predicts cardiovascular mortality and all-cause mortality in large prospective cohorts.

Standard reference: No single cutoff; fitness is continuous. AHA/ACSM percentile categories by age and sex are the reference framework. Commonly targeted in longevity practice: top quartile for age and sex, derived from observational data showing the lowest mortality in the highest-fitness stratum. In 122,007 adults undergoing treadmill testing, the least-fit had approximately 5-fold higher mortality than elite performers. No RCT randomizes people to a VO2max target; the association is prognostic, but the magnitude of benefit from improving fitness is as large as or larger than any pharmacologic longevity intervention.

Standard reference: EWGSOP2 2019 sarcopenia diagnostic cutpoints (below 7.0 kg/m² men, below 5.5 kg/m² women). Commonly targeted in longevity practice: above the EWGSOP2 cut-point, with higher being better. Low appendicular lean mass predicts incident fractures, falls, and mortality independently. DEXA is a measurement, not a treatment: the goal is to track lean mass trajectory and ensure resistance training is preventing the age-related decline that begins in the fourth decade.

Standard reference: EWGSOP2 2019 cutpoints for sarcopenia diagnosis. Commonly targeted in longevity practice: above the EWGSOP2 cut-point, with more being better. Grip strength is the simplest, lowest-cost longevity test available and among the strongest predictors of all-cause mortality across large cohorts. EWGSOP2 makes it the primary defining parameter of sarcopenia. A hand dynamometer costs under $30 and a test takes 30 seconds.

Standard reference: no clinical standard. CDC and WHO specify 150 minutes per week of moderate-intensity activity, not steps. Commonly targeted in longevity practice: 7,000–8,000 steps per day, the level at which Paluch 2022 (meta-analysis of 15 cohorts, n=47,471) found the mortality-reduction plateau. Above this threshold, additional steps were not associated with additional mortality benefit in that analysis. The 10,000-step target has no evidence basis. No RCT tests a step-count target: this is prognostic epidemiological evidence.

Standard reference: no established range. Reports contextualize results against each company's reference population. Optimal range: not established. Epigenetic clocks A test that estimates biological age from chemical marks on DNA (DNA methylation). are among the most promising longevity biomarkers, but commercial precision is not yet sufficient for confident clinical decision-making. Intraclass correlations of 0.86–0.99 sound high but translate to meaningful variation in absolute age estimates. Most useful as a tracking tool over time within the same individual using the same assay, not as a single-point comparison.

Standard reference: no established range. Telomere length associates with age and with several diseases. Optimal range: not established. Telomeres shorten with cell division and oxidative stress. The UK Biobank association (n=472,174) is prognosticly real, but commercial testing reproducibility remains too variable for reliable individual guidance. Most appropriate as a research tool or for longitudinal tracking within a single individual using the same laboratory methodology.