best blood tests for longevity

The best blood tests for longevity are ApoB, Lp(a), fasting insulin, fasting glucose, HbA1c, hsCRP, a CMP with CBC, ferritin, and vitamin D. Most longevity panels try to sell you 80 markers you will never act on. The blood tests that carry the most actionable signal are this short list. If you only check those, you have covered the main blood-based levers that can be caught early and changed.

Buy the core set, not the 200-marker panel. ApoB, Lp(a), fasting insulin, fasting glucose, HbA1c, hsCRP, CMP/CBC, ferritin and vitamin D carry most of the signal you can act on before a doctor has to.

What are the best blood tests for longevity?

This table is educational, not diagnostic. Ranges are starting points for a clinician conversation, not treatment thresholds. Limitations and caveats are in the figure caption.

Why ApoB beats LDL-C, and what Lp(a) adds

LDL cholesterol is the mass of cholesterol inside LDL particles. ApoB is the number of LDL, VLDL and Lp(a) particles. There is exactly one ApoB molecule on each atherogenic particle. That is why ApoB is a closer match to plaque risk than LDL-C.

Two people can have the same LDL-C and different ApoB. Small dense LDL particles carry less cholesterol each, so LDL-C can look fine while particle number is high. On a lab report, this shows up as LDL-C under 100 mg/dL with ApoB above 90 mg/dL. That is the discordance case most worth knowing.

Guideline-based ApoB targets vary by risk category, region, and clinician judgment. As an illustrative example only, some prevention guidelines have used below 90 mg/dL for lower-risk people, below 70 mg/dL for higher-risk people, and below 60 or 55 mg/dL for people with established cardiovascular disease. These are examples, not universal optimal ranges.

Lp(a) is a different issue. It is an LDL particle with apolipoprotein(a) attached. It is associated with higher atherosclerotic risk and may have proatherogenic or prothrombotic properties. Elevated Lp(a) is common, but the percentage above a given risk threshold depends on the assay, cutoff, and ancestry. Diet and usual exercise barely move it, so the main reason to test it is to know how aggressive to be about ApoB. Measure it once, maybe twice. If it is high, the finding usually warrants a clinician conversation about overall risk and whether LDL or ApoB lowering should be more aggressive, rather than chasing the Lp(a) number itself.

The markers that catch hidden risk

Fasting insulin can catch insulin resistance before glucose or HbA1c move. When muscle and liver stop responding well to insulin, the pancreas may push out more insulin to hold glucose normal. This can go on for years. A single fasting insulin is noisy. Assays differ, and reference ranges are population-based, not metabolic-optimal ranges. HOMA-IR is calculated from fasting insulin and glucose, but the result and thresholds should be interpreted with the lab's assay and clinical context, not one universal cutoff. A high or rising fasting insulin is a reason to repeat testing and discuss with a clinician.

Fasting glucose and HbA1c are the standard metabolic pair. Fasting glucose catches the current fasting state, and HbA1c reflects average glucose over the prior two to three months. Together they are better than a single random or non-fasting glucose from a CMP. CMP glucose alone can be useful, but it depends on fasting state and may miss early dysglycemia.

hsCRP is a marker of immune activity, not a disease. The liver makes CRP in response to IL-6. In healthy people, hsCRP under 1 mg/L is low, 1 to 3 is average, and above 3 is high relative to cardiovascular risk. But a cold, poor sleep, a hard workout, obesity or an autoimmune flare can push it up. If it is high, rule out the obvious causes and repeat it after a quiet week before you treat it as your baseline.

CMP and CBC are less exciting but they catch the slow, silent stuff. Liver enzymes that rise year over year can be a clue, but AST/ALT alone are not diagnostic of fatty liver. They can rise from alcohol, medications, muscle injury, viral illness and other causes. An eGFR below 90 alone is not kidney strain. Age, trend over time, albuminuria and confirmatory testing matter. Hemoglobin, MCV, platelets and white cells catch anemia, B12 issues and bone marrow problems. You are not checking these to feel better tomorrow. You are checking them because liver, kidney and blood reserve are what fail in late life.

Ferritin is the one iron test worth doing first. Low ferritin means iron deficiency before anemia appears, which is common in menstruating women and can wreck endurance and sleep. High ferritin can mean inflammation, fatty liver, or hemochromatosis. A value above the lab-specific upper limit is worth working up, and that threshold varies by lab and context. Repeat it with CRP and transferrin saturation. The pattern matters: high ferritin with high CRP is often inflammation. High ferritin with low CRP and high transferrin saturation points toward iron overload. A raw DNA file can suggest an HFE variant, but it is not a diagnosis. If ferritin or transferrin saturation is abnormal, hereditary hemochromatosis should be confirmed with clinical testing.

Vitamin D is the most argued marker here. 25-hydroxyvitamin D is the storage form to measure. Most labs call anything above 20 ng/mL sufficient, many clinicians prefer 30 to 50 ng/mL. The strong evidence for vitamin D is in bone, muscle and severe deficiency. Trials supplementing vitamin D to prevent heart disease or death have mostly underperformed. Low vitamin D is often a marker of being indoors, older, sicker or carrying more fat mass, and it is not clear that giving the vitamin alone fixes those outcomes. Measure it once a year, correct genuine deficiency, and do not chase levels above 50.

Why your lab's normal is not the same as optimal

Reference ranges are usually the central 95% of a selected reference population, not a metabolic-optimal range. The population may include apparently healthy people, but that does not make the range a decision threshold. A value inside the reference range can still deserve action, and a value outside can sometimes be benign. Ferritin 15 ng/mL is low normal but can mean iron deficiency symptoms. ApoB often is not on the panel, so a normal LDL-C can hide high particle count. Read the number, not the flag.

Some markers need a true fast and a stable week. Fasting insulin and glucose need an 8 to 12 hour fast, water only. HbA1c does not require fasting. hsCRP can be high after a respiratory infection, a vaccination or a brutal workout. Vitamin D changes with season. A single abnormal result is a reason to repeat, not a diagnosis.

Where to get this drawn

You can get the core set several ways. Examples below may not be available in every location, and local rules determine who can order, manage or prescribe.

• Function Health and InsideTracker are examples of direct-to-consumer blood draw services. Availability and physician oversight vary by region.
• Marek Health is an example of a clinician-led service. If you expect abnormal results and might want medication, a clinician-led service may be able to order and manage follow-up where allowed.
• HealthOS /blood is for the lab PDF you already have. You upload it and see each result next to age- and sex-matched context, free. It does not diagnose or treat.

What the blood tests cannot tell you

Blood tests do not measure lifespan directly. They measure risk factors you can change. A perfect panel does not cancel a 20-year smoking habit, poor sleep, weak legs or a family history of early heart attack. And a bad panel does not mean you are doomed. The point is to catch the things that move slowly and give you time to act.

Someone with insulin resistance and high ApoB needs to change food, training and possibly medication. Someone with normal metabolism and high Lp(a) needs a different conversation. The lab panel is the start, not the end.

If you already have a lab PDF, upload it at HealthOS /blood and see the core set against your own numbers.