Longevity blood test: 8 biomarkers, and why 'normal' is not the same as lowest risk
A lab 'normal' range shows where most people sit or where a diagnosis starts, not your lowest-risk value. Here are eight markers, what the studies say about lower-risk values, where those targets are only practitioner conventions, and where 'optimizing' does nothing. We sell neither tests nor supplements.
Updated 23 min read46 sources
The short answer
A longevity blood test usually covers eight markers: fasting insulin, HOMA-IR, hs-CRP, homocysteine, HbA1c, the Omega-3 Index, ferritin and vitamin D (25-OH-D). The 'normal' range on your lab report shows where most healthy people sit or where a diagnosis starts, not your lowest-risk value.[3][5] Several 'optimal' targets you will see online, such as a fasting insulin of 2 to 6, are practitioner conventions with no outcome trials behind them.[4] In Germany, glucose, fasting insulin, HbA1c, hs-CRP, ferritin and vitamin D cost about 100 euros together at GOÄ rates (as of October 2026), and the lab prices homocysteine and the Omega-3 Index on top.[45]
This content is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making changes to your diet, exercise routine, or supplement regimen.
Which blood tests matter for longevity, and why is 'normal' not 'optimal'?
There is no single official longevity panel, but most include the same eight markers: fasting insulin, HOMA-IR, hs-CRP, homocysteine, HbA1c, the Omega-3 Index, ferritin and vitamin D (25-OH-D). Between them they cover blood sugar, inflammation, B-vitamin status, omega-3 intake, iron stores and vitamin D. The two most causal lipid markers, ApoB and Lp(a), get a guide of their own. Here they only appear as a row in the table at the end.
Around those eight, a complete panel also adds a few cheap basics that this guide does not cover in depth. They are creatinine and eGFR for the kidneys, the liver enzymes ALT and GGT, and a blood count. The statutory Check-up 35, whose markers are listed in the Check-up 35 guide, measures none of these extras (as of October 2026).
Each of the eight core markers comes with a 'normal' range on your lab report, and those ranges are built in two different ways. Some are statistical: the middle 95% of healthy people, which is how reference intervals for fasting insulin and HOMA-IR work.[3] Others are decision limits set by guidelines, such as the cutoffs for HbA1c,[5] hs-CRP,[2] ferritin.[12] and vitamin D[22][24] Neither kind is built to show the value with the lowest risk of disease and death. That is why 'normal' and 'optimal' can come apart. Each section below therefore says whether a tighter target comes from a study, a guideline or simply a practitioner habit.
We sell neither lab tests nor supplements and earn no commission on panels, so none of those targets is an upsell. Before any of them matter, though, the numbers have to be measured cleanly. Four steps before the blood draw take care of most of that:
- Fast for glucose and fasting insulin, because the HOMA formula is built on fasting values.[1] Follow your lab's instructions on how long, which usually means overnight. HbA1c, the Omega-3 Index,[17] ferritin, hs-CRP and vitamin D are usually measured without fasting. Homocysteine needs no strict fast for a routine check either, but the blood has to be spun down within an hour or kept cold, so follow your lab's instructions.[6]
- Tell your lab about supplements. High-dose biotin, the vitamin B7 common in hair and nail products, can distort some antibody-based lab tests (immunoassays).[41] The effect differs by test and manufacturer, so ask the lab how long to pause it.[41]
- If your panel includes serum iron or transferrin saturation (how full the blood's iron carrier is), skip iron tablets and iron-rich foods for at least 24 hours and have the blood drawn in the morning, as the US sleep medicine society AASM advises for iron work-ups.[27] For ferritin on its own, follow your lab's instructions.
- For a routine check, wait until you have fully recovered from an infection, injury or surgery before testing hs-CRP and ferritin, because inflammation pushes both up.[2][12]
That last step does not make ferritin worthless while you are ill. If your doctor is looking for iron deficiency during an infection, WHO uses a higher cutoff of below 70 micrograms per liter in adults.[12] It then reads ferritin alongside an inflammation marker such as CRP.[12] For a routine check, though, waiting is the better choice, because the hs-CRP and ferritin ranges below are meant for values measured without an infection.[2][12]
HOMA-IR and fasting insulin: How do I catch insulin resistance before blood sugar slips?
HOMA-IR is a simple calculation from fasting insulin and fasting glucose. It estimates how insulin-resistant you are, meaning how poorly your cells still respond to the hormone insulin, and it earns its place because blood sugar is a late signal. In the Whitehall II study of British civil servants, insulin sensitivity fell steeply during the 5 years before a diabetes diagnosis.[31] Fasting glucose, by contrast, rose steeply only in the last 3, so insulin gives you a head start of a couple of years.[31]
The formula behind that head start comes from the original HOMA paper from 1985.[1] You multiply fasting insulin (in micro-units per mL) by fasting glucose (in mg/dL) and divide by 405, or by 22.5 if your glucose is in mmol/L.[1] Our HOMA-IR calculator handles both unit systems and interprets the result, so you do not have to do the arithmetic yourself.
The harder question is what counts as too high. Published cutoffs for insulin resistance vary with population, age and the lab's insulin test, so no single number works everywhere.[3] German data make a better anchor than imported US or Asian values. The population-based Gutenberg Health Study looked at 1,065 strictly healthy adults aged 35 to 74, and their median HOMA-IR was 1.09.[3] Only 2.5% of them sat above 2.35, which makes 2.35 the statistical upper limit of 'normal' in healthy Germans.[3] That figure is tied to the insulin test the study used, and other tests can read higher or lower.[3]
A median of 1.09 describes healthy people; it is not an outcome-tested target. You will often read that an 'optimal' HOMA-IR sits below 1 to 1.5. No study has shown, though, that pushing it that low extends life.[3][4] What the research does show is a link with risk. In a meta-analysis of non-diabetic adults, the highest HOMA-IR group had about a third higher risk of dying from any cause than the lowest.[4]
That third comes with two limits. The same analysis found a roughly doubled risk of death from heart disease, but that figure rests on only two studies.[4] And both results come from observational cohorts, which follow people rather than test a treatment. So they mark risk without proving that lowering HOMA-IR adds years.[4]
Fasting insulin on its own is a weaker guide still. Its reference ranges are wide and depend on the lab's test, so use the range printed on your report.[3] Metabolic-health writers often cite an optimal window of about 2 to 6 micro-units per mL, or about 12 to 36 pmol/L. That window is a practitioner convention with no backing from outcome trials.[4] The meta-analysis also found the mortality link for HOMA-IR, not for fasting insulin in isolation.[4] So HOMA-IR is the number to watch for the early signal, while HbA1c shows the later one.
hs-CRP: What level is good, and what does a high value mean?
hs-CRP (high-sensitivity C-reactive protein) is the same inflammation marker as standard CRP. It is measured with a test that can resolve the low range below 10 mg/L.[2] That low range shows the quiet background inflammation that tracks with atherosclerosis, the slow build-up of plaque in your arteries. For heart risk, the AHA/CDC statement sorts values into three bands.[2]:
- Below 1 mg/L: low risk
- 1 to 3 mg/L: average risk
- Above 3 mg/L: high risk
That low-risk band below 1 mg/L is a risk category rather than a treatment target[2] No trial has shown that pushing a healthy person's hs-CRP below 1 extends life. Some practitioners aim for below 0.5 mg/L, a value that is not in the AHA/CDC statement.[2]
None of that makes a raised value harmless. A 2025 statement from the American College of Cardiology calls the evidence linking inflammation with atherosclerosis compelling and clinically actionable.[46] In apparently healthy people, it notes, a raised hs-CRP marks a higher-risk group.[46] In that group, statins (the standard cholesterol-lowering drugs) cut the risk of a first major heart event, even when LDL cholesterol is normal.[46] Whether a statin makes sense for you is a decision for your doctor, based on your overall risk.
Above 10 mg/L, hs-CRP first points to an infection or another inflammation, which can also be a chronic one. Until that is ruled out, the value cannot be read as a heart-risk marker.[2] So repeat the test about two weeks later, once you are well, and if it stays above 10, have your doctor look for the cause.[2]
Infection is not the only thing that moves the number. Recent injury or surgery and active inflammatory disease push hs-CRP up, while obesity and smoking raise the baseline.[2] Ferritin, your iron-store marker, also rises with inflammation, so read the two side by side. When both are high at once, inflammation may explain the high ferritin rather than full iron stores.[12]
High homocysteine: Is lowering it with folate and B vitamins worth it?
B vitamins are an effective way to bring a high homocysteine down: folate, B12 and B6 typically cut it by about a quarter. In large trials, though, that drop did not reduce heart attacks or deaths.[7][11][34] Stroke is the one possible exception, mainly where folate levels were low to begin with.[33][34] So homocysteine is best read as a risk marker and a clue to your vitamin and kidney status, not as a proven drug target.
That vitamin and kidney link is built into the marker. Homocysteine is an amino acid in your blood that rises when folate, vitamin B12 or B6 run low, and also when kidney function drops.[6] Labs usually flag values above about 15 micromol per liter. An expert review on homocysteine testing puts the upper limit at about 12 in people with good vitamin status.[6] In adults who do not eat food fortified with folic acid, it puts the limit at 15 to 20 or more.[6] Below 10 is often cited as a practical optimum, but that is a practitioner target rather than a guideline cutoff.[6] The exact value also depends on the lab method and the population.[6]
Three large trials tested whether pushing the value down helps, in people at high heart risk, after a heart attack and after a stroke or mini-stroke.[7][8][9] Homocysteine fell in each, yet the combined count of heart attacks, strokes and deaths from vascular disease did not fall clearly.[7][8][9] A later pooled analysis of eight trials widened the picture without changing it.[11] Heart attacks, cancer and death from any cause showed no clear effect either.[11]
Stroke is where the picture shifts a little. A Cochrane review of the trials found a small reduction in stroke,[34] and the high-risk trial, HOPE-2, had already seen fewer strokes.[7] In a large trial in China, people with high blood pressure who got folic acid on top of their blood-pressure drug had about a fifth fewer first strokes.[33] Its authors read this as a benefit in people with high blood pressure and low folate levels.[33] So it may not carry over to well-nourished people.
The trials also produced some unplanned harm signals. In the trial after a heart attack, the group that got all three vitamins trended toward more events.[8] Its authors advised against routine use in that setting.[8] HOPE-2 saw more hospital admissions for unstable angina, chest pain that comes on at rest or quickly gets worse, though only as a secondary finding.[7] B-PROOF, a fracture trial in older people with high homocysteine, gave 400 micrograms of folic acid and 500 micrograms of B12 a day.[10] Cancer was not what it set out to measure, but more people on the vitamins were diagnosed with cancer.[10] A later cancer-registry follow-up of the same trial pointed the same way, mainly for colorectal cancer.[35] The pooled analysis of eight trials, however, found no overall cancer effect, so the data are mixed.[11]
Some trials also used drug-level doses: HOPE-2 gave 2.5 mg of folic acid, 50 mg of vitamin B6 and 1 mg of B12 a day.[7] The folic acid and B6 doses are well above the EU upper limits for long-term intake in adults. Those limits are 1 mg of folic acid.[37] and 12 mg of vitamin B6 a day[36] Long-term high-dose B6 can damage nerves,[36] and high-dose folic acid can hide a vitamin B12 deficiency while the nerve damage from it progresses.[37] So do not self-treat a high homocysteine with high-dose B vitamins. A high value is instead a reason to have B12, folate and kidney function checked with your doctor.[6] Those results, not a vague 'methylation' problem, show which vitamin you actually lack, and that is where a targeted supplement makes sense.
HbA1c: When is it prediabetes, and which value is really optimal?
HbA1c is your long-term blood sugar, averaged over the past two to three months.[5] It measures the share of your hemoglobin (the oxygen carrier in red blood cells) that has sugar stuck to it. Where HOMA-IR flags insulin resistance early, HbA1c shows whether blood sugar has already caught up. The ADA 2026 cutoffs, in the two units lab reports use.[5]:
- Normal: below 5.7% (below 39 mmol/mol)
- Prediabetes: 5.7 to 6.4% (39 to 47 mmol/mol)
- Diabetes: at or above 6.5% (at or above 48 mmol/mol), confirmed on a second test
Those two units are where many people lose the thread, because German lab reports give HbA1c either as a percentage or in mmol/mol. The two scales are not linked by a simple factor, so a few landmarks help. In round numbers, 5.7% is about 39 mmol/mol, 6.0% about 42 and 6.5% about 48[16][32]
Other bodies draw the diabetes line in the same place. The WHO uses the same threshold of 6.5% (48 mmol/mol), adding that a lower value does not rule out diabetes diagnosed by glucose.[14] The German DDG/DGKL recommendation uses the same anchors, with fasting glucose at or above 126 mg/dL (7.0 mmol/L).[15] An HbA1c of 6.5% or higher is in the diabetes range, so it needs a second test and a doctor's visit, not the next self-pay panel.[5]
Below those diagnostic lines, practitioners often name 5.4 to 5.6% as optimal. The ADA line at 5.7% marks where prediabetes begins. It is a diagnostic boundary rather than a tested target, so it sets no optimal value for healthy people.[5] The best outcome data come from the large US ARIC cohort, where the risk of diabetes and heart disease rose step by step from 5.5% upward.[29] Below 5.0%, diabetes risk was lowest and heart risk was no higher. For death from any cause, though, the curve was J-shaped and rose again at the lowest values, so those were not the safest.[29]
The number itself can also mislead, because HbA1c depends on how long your red blood cells live. Iron deficiency, with or without anemia, falsely raises HbA1c without any rise in blood sugar.[13] Other anemias may lower it, though the data are limited.[13] So can anything that shortens red-cell life, such as hemolysis (the breakdown of red cells) or recent blood loss. Hemoglobin variants, inherited forms of the protein, can push it either way depending on the lab method. So read a borderline HbA1c next to ferritin and a blood count. If HbA1c and your glucose values do not fit together, a doctor should decide based on blood glucose.[5][13]
Omega-3 Index: What is a good level, and what if yours is low?
The Omega-3 Index is the share of EPA and DHA, the two marine omega-3 fatty acids, in your red-blood-cell membranes, given as a percentage. It reflects about 120 days of intake, a stable average rather than the day-to-day swings in your blood plasma.[17] You also do not need to fast for it.[17]
The index goes back to a 2004 paper by Harris and von Schacky, who proposed it as a risk factor for death from coronary heart disease. It works on a sliding scale: the higher the index, the lower the risk.[17] At 8% or more, protection was greatest, which makes 8% the desirable target, while 4% or below counts as high risk.[17] The often-quoted 'intermediate' band of 4 to 8% is simply the stretch of the same curve in between. So the index reads better as a slope than as three boxes. A later review by the same two authors linked lower values with more sudden cardiac death, where the heart stops without warning.[18]
Any upper end of an 'optimal range' above 8% is a later convention: von Schacky proposes a target range of 8 to 11%.[30] He works for Omegametrix, a lab that sells the test.[30]
Raising the index with capsules is a separate question, and the trials of omega-3 supplements range from a clear drop in heart events to no effect. REDUCE-IT tested 4 g a day of purified EPA (icosapent ethyl) in patients on statins whose triglycerides, a type of blood fat, were high.[19] Major heart and circulation events fell by about a quarter.[19] At that dose, icosapent ethyl is a prescription medicine in the EU, not a supplement.[40] The placebo in REDUCE-IT was mineral oil, though, and LDL and hs-CRP rose in that group.[19] So part of the difference may come from the placebo rather than the drug.[19]
Two other big trials did not repeat that result. One used 4 g a day of an EPA-plus-DHA mix, found no heart benefit and was stopped early because a benefit had become very unlikely.[20] VITAL gave 1 g a day to a general population not selected for low intake and did not lower its main heart or cancer outcomes.[26] Heart attacks alone were lower, but only as a secondary result.[26]
Those trials also carry safety signals. In REDUCE-IT, more people were admitted to hospital with atrial fibrillation, an irregular heart rhythm: 3.1% compared with 2.1%.[19] Serious bleeding was also slightly more common.[19] Across large trials, omega-3 capsules were linked to a higher risk of atrial fibrillation, more so above 1 g a day.[39] If you have an irregular heartbeat or take blood thinners, talk to your doctor before taking omega-3 capsules.
None of these capsule trials selected people for a low index, and in that unselected setting they were mostly neutral.[20][26] That leaves the most interesting question open: whether raising a truly low index prevents heart events. Von Schacky argues that poor absorption of the capsules and the trials' design held the neutral results back.[30] That leaves the index as a clean measure of your status. For a low value, diet is the reasonable first lever: oily sea fish such as salmon, mackerel or herring. Because the index tracks about 120 days, a retest about three to four months after a change shows the fuller effect.[17]
Ferritin and iron deficiency: Why 'within range' can still mean a deficiency
Ferritin reflects your iron stores, but it is also an acute-phase reactant, a protein that rises with any inflammation.[12] So an infection can push it up regardless of your real iron status.[12] That is why it is read alongside hs-CRP, and why WHO gives two sets of cutoffs for iron deficiency.[12] They are in micrograms per liter, which for ferritin is the same number as ng/mL:
- Apparently healthy people aged 5 and older (including non-pregnant women and adults): ferritin below 15 micrograms per liter
- Apparently healthy children under 5: below 12
- With an infection or inflammation at the same time: below 70 (5 and older) and below 30 (children under 5)
With infection or inflammation, WHO's ferritin cutoff sits far higher
Ferritin below which WHO counts iron deficiency, in micrograms per liter
WHO's cutoff of 15 is very specific: a value below it makes iron deficiency very likely.[12] A strict cutoff like that rarely raises a false alarm, but it can miss people. In practice, many doctors use a higher cutoff of below 30 micrograms per liter in adults. A small study of anemic patients, checked against bone marrow or their response to iron, shows the difference. A cutoff of 30 caught about nine in ten iron-deficient patients and was rarely wrong, while a cutoff of 12 missed three in four.[42] So a ferritin that clears the strict line can still hide a deficiency.
That gap makes ferritin the clearest case of 'normal is not optimal', because iron deficiency can cause fatigue even without anemia.[12] Practitioners often link fatigue and hair loss to 'low-normal' values of about 15 to 50 micrograms per liter, in the lower part of the normal range. Those thresholds come from practitioner experience, not from a guideline, so treat them as a clue rather than a settled cutoff.
Restless legs, an urge to move the legs at rest, are a separate case with a threshold of their own. For diagnosed restless legs, the US sleep medicine society AASM passes on a consensus threshold that has not been tested in trials.[27] It suggests iron treatment, prescribed by a doctor, at a ferritin of 75 ng/mL or lower.[27] The same applies when transferrin saturation, a measure of how full the blood's iron carrier is, sits below 20%.[27] Between 75 and 100, it suggests only iron given into a vein.[27] This applies to restless legs only, not as a general ferritin target.
Whatever makes a value look low, do not start iron tablets because of a ferritin value alone. A doctor should confirm the deficiency and look for the cause, such as blood loss or a gut disorder like celiac disease.[12]
More is not better at the other end either. In otherwise healthy people, a ferritin above 150 in women who still menstruate may point to a risk of iron overload.[12] For men and for women who no longer menstruate, the line is 200, and in people who are ill it is 500.[12] A high ferritin alone does not prove overload and needs a doctor's work-up to find the cause.[12] Together with a high transferrin saturation, it can point to hemochromatosis, an inherited iron overload that can be treated when it is found early.[44]
Vitamin D: Deficiency, optimum, and what the big VITAL trial actually showed
25-OH-D is the storage form of vitamin D in your blood, and two threshold systems for it are in use that disagree. The US Institute of Medicine (IOM) considered 20 ng/mL (50 nmol/L) already enough for bone health, while the Endocrine Society's 2011 thresholds set the bar higher.[22]:
- Deficiency: below 20 ng/mL (below 50 nmol/L)
- Insufficiency: 20 to below 30 ng/mL (50 to below 75 nmol/L)
- Sufficient: at or above 30 ng/mL (at or above 75 nmol/L)
The German line used by the RKI follows the lower IOM logic and treats 50 nmol/L as the common threshold[24]:
- Deficient: below 30 nmol/L (below 12 ng/mL)
- Suboptimal: 30 to below 50 nmol/L (12 to below 20 ng/mL)
- Adequate for bone health: at or above 50 nmol/L (at or above 20 ng/mL)
By that German line, more than half of German adults fell short in the RKI's DEGS1 survey from 2008 to 2011[24] That held both in the original measurements and after the lab values were standardized internationally.[24][43] Supplement use may have changed this since.[24] Many longevity practitioners aim higher still, at 30 to 50 ng/mL (75 to 125 nmol/L). That is above what counts as adequate for bone health, and it is not a longevity value tested against health outcomes.[22]
Whether more vitamin D helps people who already have enough was tested in the VITAL trial. It gave 25,871 US adults, most of whom were not deficient, 2,000 IU of vitamin D3 a day for about five years.[21] Compared with placebo, it lowered neither cancer nor major cardiovascular events.[21]
The Endocrine Society's 2024 guideline is just as cautious. It found no clear evidence for any optimal 25-OH-D level to prevent disease, so it no longer names a target level.[23] Because it also found no trial evidence that routine testing helps, it advises against routine testing in people without a specific reason.[23] That holds even for the groups in which it suggests taking vitamin D without testing first: ages 1 to 18, 75 and older, pregnancy, and adults with high-risk prediabetes.[23] For healthy adults under 75, it advises against doses above the normal recommended intake.[23] None of this applies to people with an established reason for vitamin D treatment or testing.[23]
A genuine deficiency is worth correcting with your doctor, and with more than half of German adults below the line in DEGS1 it is a common gap.[24] Beyond that, more is not better. The upper limit for long-term intake in adults is 100 micrograms (4,000 IU) of vitamin D a day, in the EU and the US alike.[25][38] A 25-OH-D above 150 ng/mL (above 375 nmol/L) is the hallmark of vitamin D intoxication, with too much calcium in the blood.[25] The IOM also flagged possible harm from long-term levels above 50 ng/mL, based on studies that show a link rather than proof.[25] If you want to supplement beyond the usual intake, dose and monitoring belong in a conversation with your doctor.
Longevity blood test ranges: all 8 markers in one table
All eight markers fit in one table, with each lab range next to its lower-risk or practitioner target. Where the target column says convention or practitioner target, no outcome trial stands behind the exact number.[4][2] That covers fasting insulin, HOMA-IR below 1.5, hs-CRP below 0.5, HbA1c below 5.4 and the ferritin symptom thresholds. So read that column as orientation, and check the notes below the table for the exceptions:
| Marker | Lab range (conventional and SI) | Lower-risk or practitioner target | Sources |
|---|---|---|---|
| HOMA-IR | upper limit 2.35 in healthy Germans (unitless, assay-dependent) | healthy median ~1.1; below ~1.5 is a practitioner convention | .[1][3][4] |
| Fasting insulin | wide and assay-dependent; use the range on your report | ~2 to 6 micro-U/mL; ~12 to 36 pmol/L (practitioner convention) | [3][4] |
| hs-CRP | below 1 low / 1 to 3 average / above 3 high (mg/L) | below 1 mg/L (AHA/CDC low-risk band); below 0.5 (no guideline) | [2] |
| Homocysteine | upper limit ~12 to 15–20 micromol/L, method-dependent | below 10 micromol/L (practitioner target) | [6][11][34] |
| HbA1c | normal below 5.7% (below 39 mmol/mol); diabetes 6.5 or more (48 or more) | below 5.4 to 5.6% (practitioner target) | [5][14][16][29] |
| Omega-3 Index | 4% or below high risk / 8% or more desirable (sliding scale) | 8 to 11% (von Schacky; upper bound a later convention) | [17][30] |
| Ferritin | deficiency below 15 micrograms/L (healthy, 5 and older) | below 30 for deficiency (many doctors); symptoms linked below ~50 (no guideline) | [12][27][42] |
| Vitamin D (25-OH-D) | deficient below 20 ng/mL (below 50 nmol/L) by ES 2011 | 30 to 50 ng/mL; 75 to 125 nmol/L (practitioner target) | [22][23][24][25][38] |
| ApoB / Lp(a) | in the sister lipid guide | see the ApoB and Lp(a) guide | (sister guide) |
Sources: the studies and guidelines listed in the right-hand column.
Notes on the rows above:
- HOMA-IR: 2.35 is the 97.5th percentile of healthy adults, and there is no universal cutoff for insulin resistance; the practitioner target is not outcome-tested[3][4]
- Fasting insulin: the target has no outcome-trial backing, and the mortality signal is for HOMA-IR.[4]
- hs-CRP: above 10 mg/L points to an infection or other inflammation, so repeat the test once you are well.[2]
- Homocysteine: the upper limit is ~12 with good vitamin status and 15–20 on an unfortified diet, and lowering it has not been shown to protect the heart.[6][11][34]
- HbA1c: prediabetes runs from 5.7 to 6.4 (39 to 47); in ARIC the lowest values were not the safest for mortality.[5][29]
- Omega-3 Index: 4 to 8% is the intermediate stretch of the same sliding scale.[17]
- Ferritin: the deficiency cutoff is below 70 with inflammation; possible overload risk starts above 150 (menstruating women) / 200 (men, non-menstruating women) and needs a work-up; for restless legs only, the AASM consensus suggests iron at 75 or lower.[12][27]
- Vitamin D: ES 2011 calls 30 or more (75 or more) sufficient, IOM/RKI call 20 or more (50 or more) adequate, and ES 2024 names no target; the intake limit is 4,000 IU a day, and toxicity starts above 150 ng/mL.[22][23][24][25][38]
A value just outside a practitioner target is a reason to look closer with your doctor, not a diagnosis in itself. That conversation gets further when you bring the result, the range your lab printed and the reason you got tested in the first place.
Frequently asked questions
Which blood values should I test for longevity?
How much does a longevity blood test cost?
Do I need to fast for a longevity blood test?
Why is my blood value 'normal' but still not optimal?
At what HbA1c do I have prediabetes?
Is it worth lowering high homocysteine with B vitamins?
What is a good Omega-3 Index?
My Omega-3 Index is low. What should I do?
Is an hs-CRP value below 1 mg/L good?
At what ferritin do I have iron deficiency?
Should I test vitamin D, and at what value is it a deficiency?
Does statutory insurance cover a longevity blood test?
How often should I repeat a longevity blood test?
Can supplements falsify my blood test results?
How much vitamin D is too much?
Sources46
- Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. (1985). Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologiadoi:10.1007/BF00280883
- Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO 3rd, et al. (2003). Markers of inflammation and cardiovascular disease: application to clinical and public health practice (AHA/CDC scientific statement). Circulationdoi:10.1161/01.CIR.0000052939.59093.45
- Matli B, Schulz A, Koeck T, Falter T, Lotz J, Rossmann H, Pfeiffer N, Beutel M, Muenzel T, Strauch K, Wild PS, Lackner KJ. (2021). Distribution of HOMA-IR in a population-based cohort and proposal for reference intervals. Clinical Chemistry and Laboratory Medicinedoi:10.1515/cclm-2021-0643
- Zhang X, Li J, Zheng S, Luo Q, Zhou C, Wang C. (2017). Fasting insulin, insulin resistance, and risk of cardiovascular or all-cause mortality in non-diabetic adults: a meta-analysis. Bioscience Reportsdoi:10.1042/BSR20170947
- American Diabetes Association Professional Practice Committee for Diabetes. (2026). 2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes 2026. Diabetes Caredoi:10.2337/dc26-S002
- Refsum H, Smith AD, Ueland PM, Nexo E, Clarke R, McPartlin J, Johnston C, Engbaek F, Schneede J, McPartlin C, Scott JM. (2004). Facts and recommendations about total homocysteine determinations: an expert opinion. Clinical Chemistrydoi:10.1373/clinchem.2003.021634
- Lonn E, Yusuf S, Arnold MJ, Sheridan P, Pogue J, Micks M, McQueen MJ, Probstfield J, Fodor G, Held C, Genest J Jr (HOPE-2 Investigators). (2006). Homocysteine lowering with folic acid and B vitamins in vascular disease (HOPE-2). New England Journal of Medicinedoi:10.1056/NEJMoa060900
- Bonaa KH, Njolstad I, Ueland PM, Schirmer H, Tverdal A, Steigen T, Wang H, Nordrehaug JE, Arnesen E, Rasmussen K (NORVIT Trial Investigators). (2006). Homocysteine lowering and cardiovascular events after acute myocardial infarction (NORVIT). New England Journal of Medicinedoi:10.1056/NEJMoa055227
- VITATOPS Trial Study Group. (2010). B vitamins in patients with recent transient ischaemic attack or stroke (VITATOPS). Lancet Neurologydoi:10.1016/S1474-4422(10)70187-3
- van Wijngaarden JP, Swart KMA, Enneman AW, Dhonukshe-Rutten RAM, van Dijk SC, Ham AC, Brouwer-Brolsma EM, et al. (2014). Effect of daily vitamin B-12 and folic acid supplementation on fracture incidence in elderly individuals with an elevated plasma homocysteine concentration (B-PROOF). American Journal of Clinical Nutritiondoi:10.3945/ajcn.114.090043
- Clarke R, Halsey J, Lewington S, Lonn E, Armitage J, Manson JE, Bonaa KH, Spence JD, Nygard O, Jamison R, et al. (B-Vitamin Treatment Trialists' Collaboration). (2010). Effects of lowering homocysteine levels with B vitamins on cardiovascular disease, cancer, and cause-specific mortality: meta-analysis of 8 randomized trials involving 37,485 individuals. Archives of Internal Medicinedoi:10.1001/archinternmed.2010.348
- World Health Organization. (2020). WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations. Geneva: World Health Organizationncbi.nlm.nih.gov
- English E, Idris I, Smith G, Dhatariya K, Kilpatrick ES, John WG. (2015). The effect of anaemia and abnormalities of erythrocyte indices on HbA1c analysis: a systematic review. Diabetologiadoi:10.1007/s00125-015-3599-3
- World Health Organization. (2011). Use of Glycated Haemoglobin (HbA1c) in the Diagnosis of Diabetes Mellitus: Abbreviated Report of a WHO Consultation. Geneva: World Health Organizationncbi.nlm.nih.gov
- Landgraf R, Heinemann L, Schleicher E, Gerdes C, Petersmann A, Mueller-Wieland D, et al. (Deutsche Diabetes Gesellschaft). (2023). Definition, Klassifikation, Diagnostik und Differenzialdiagnostik des Diabetes mellitus: Update 2022 (DDG/DGKL Praxisempfehlung). Die Diabetologiedoi:10.1007/s11428-022-00997-z
- Hoelzel W, Weykamp C, Jeppsson JO, Miedema K, Barr JR, Goodall I, et al. (IFCC Working Group on HbA1c Standardization). (2004). IFCC reference system for measurement of hemoglobin A1c in human blood and the national standardization schemes in the United States, Japan, and Sweden: a method-comparison study. Clinical Chemistrydoi:10.1373/clinchem.2003.024802
- Harris WS, von Schacky C. (2004). The Omega-3 Index: a new risk factor for death from coronary heart disease? Preventive Medicinedoi:10.1016/j.ypmed.2004.02.030
- von Schacky C, Harris WS. (2007). Cardiovascular risk and the omega-3 index. Journal of Cardiovascular Medicine (Hagerstown)doi:10.2459/01.JCM.0000289273.87803.87
- Bhatt DL, Steg PG, Miller M, Brinton EA, Jacobson TA, Ketchum SB, Doyle RT Jr, Juliano RA, Jiao L, Granowitz C, et al. (2019). Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia (REDUCE-IT). New England Journal of Medicinedoi:10.1056/NEJMoa1812792
- Nicholls SJ, Lincoff AM, Garcia M, Bash D, Ballantyne CM, Barter PJ, Davidson MH, Kastelein JJP, Koenig W, McGuire DK, et al. (2020). Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular Risk (STRENGTH). JAMAdoi:10.1001/jama.2020.22258
- Manson JE, Cook NR, Lee IM, Christen W, Bassuk SS, Mora S, Gibson H, Gordon D, Copeland T, D'Agostino D, et al. (VITAL Research Group). (2019). Vitamin D Supplements and Prevention of Cancer and Cardiovascular Disease (VITAL). New England Journal of Medicinedoi:10.1056/NEJMoa1809944
- Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Murad MH, Weaver CM. (2011). Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology and Metabolismdoi:10.1210/jc.2011-0385
- Demay MB, Pittas AG, Bikle DD, Diab DL, Kiely ME, Lazaretti-Castro M, Lips P, Mitchell DM, Murad MH, Powers S, et al. (2024). Vitamin D for the Prevention of Disease: an Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology and Metabolismdoi:10.1210/clinem/dgae290
- Rabenberg M, Scheidt-Nave C, Busch MA, Rieckmann N, Hintzpeter B, Mensink GBM. (2015). Vitamin D status among adults in Germany: results from the German Health Interview and Examination Survey for Adults (DEGS1). BMC Public Healthdoi:10.1186/s12889-015-2016-7
- Marcinowska-Suchowierska E, Kupisz-Urbanska M, Lukaszkiewicz J, Pludowski P, Jones G. (2018). Vitamin D Toxicity: A Clinical Perspective. Frontiers in Endocrinology (Lausanne)doi:10.3389/fendo.2018.00550
- Manson JE, Cook NR, Lee IM, Christen W, Bassuk SS, Mora S, Gibson H, Albert CM, Gordon D, Copeland T, et al. (VITAL Research Group). (2019). Marine n-3 Fatty Acids and Prevention of Cardiovascular Disease and Cancer (VITAL). New England Journal of Medicinedoi:10.1056/NEJMoa1811403
- Winkelman JW, Berkowski JA, DelRosso LM, Koo BB, Scharf MT, Sharon D, et al. (2025). Treatment of restless legs syndrome and periodic limb movement disorder: an American Academy of Sleep Medicine clinical practice guideline. Journal of Clinical Sleep Medicinedoi:10.5664/jcsm.11390
- IGeL-Monitor, Medizinischer Dienst Bund. (2022). Frueherkennungsuntersuchung auf Vitamin-D-Mangel (IGeL-Bewertung)igel-monitor.de
- Selvin E, Steffes MW, Zhu H, Matsushita K, Wagenknecht L, Pankow J, Coresh J, Brancati FL. (2010). Glycated Hemoglobin, Diabetes, and Cardiovascular Risk in Nondiabetic Adults. New England Journal of Medicinedoi:10.1056/NEJMoa0908359
- von Schacky C. (2014). Omega-3 Index and Cardiovascular Health. Nutrientsdoi:10.3390/nu6020799
- Tabak AG, Jokela M, Akbaraly TN, Brunner EJ, Kivimaki M, Witte DR. (2009). Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study. Lancetdoi:10.1016/S0140-6736(09)60619-X
- National Glycohemoglobin Standardization Program (NGSP). (2026). IFCC Standardization of HbA1c (NGSP/IFCC master equation)ngsp.org
- Huo Y, Li J, Qin X, et al. (CSPPT Investigators). (2015). Efficacy of folic acid therapy in primary prevention of stroke among adults with hypertension in China: the CSPPT randomized clinical trial. JAMAdoi:10.1001/jama.2015.2274
- Martí-Carvajal AJ, Solà I, Lathyris D, Dayer M. (2017). Homocysteine-lowering interventions for preventing cardiovascular events. Cochrane Database of Systematic Reviewsdoi:10.1002/14651858.CD006612.pub5
- Oliai Araghi S, Kiefte-de Jong JC, van Dijk SC, et al. (2019). Folic Acid and Vitamin B12 Supplementation and the Risk of Cancer: Long-term Follow-up of the B Vitamins for the Prevention of Osteoporotic Fractures (B-PROOF) Trial. Cancer Epidemiology, Biomarkers & Preventiondoi:10.1158/1055-9965.EPI-17-1198
- EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA); Turck D, et al. (2023). Scientific opinion on the tolerable upper intake level for vitamin B6. EFSA Journaldoi:10.2903/j.efsa.2023.8006
- EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA); Turck D, et al. (2023). Scientific opinion on the tolerable upper intake level for folate. EFSA Journaldoi:10.2903/j.efsa.2023.8353
- EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA); Turck D, et al. (2023). Scientific opinion on the tolerable upper intake level for vitamin D, including the derivation of a conversion factor for calcidiol monohydrate. EFSA Journaldoi:10.2903/j.efsa.2023.8145
- Gencer B, Djousse L, Al-Ramady OT, Cook NR, Manson JE, Albert CM. (2021). Effect of Long-Term Marine ω-3 Fatty Acids Supplementation on the Risk of Atrial Fibrillation in Randomized Controlled Trials of Cardiovascular Outcomes: A Systematic Review and Meta-Analysis. Circulationdoi:10.1161/CIRCULATIONAHA.121.055654
- European Medicines Agency. (2026). Vazkepa (icosapent ethyl): EPAR, medicine overview (accessed 2026-10-22)ema.europa.eu
- Li D, Ferguson A, Cervinski MA, Lynch KL, Kyle PB. (2020). AACC Guidance Document on Biotin Interference in Laboratory Tests. Journal of Applied Laboratory Medicinedoi:10.1093/jalm/jfz010
- Mast AE, Blinder MA, Gronowski AM, Chumley C, Scott MG. (1998). Clinical utility of the soluble transferrin receptor and comparison with serum ferritin in several populations. Clinical Chemistrydoi:10.1093/clinchem/44.1.45
- Rabenberg M, Scheidt-Nave C, Busch MA, Thamm M, Rieckmann N, Durazo-Arvizu RA, et al. (2018). Implications of standardization of serum 25-hydroxyvitamin D data for the evaluation of vitamin D status in Germany, including a temporal analysis. BMC Public Healthdoi:10.1186/s12889-018-5769-y
- European Association for the Study of the Liver. (2022). EASL Clinical Practice Guidelines on haemochromatosis. Journal of Hepatologydoi:10.1016/j.jhep.2022.03.033
- Bundesministerium der Justiz. (2026). Gebührenordnung für Ärzte (GOÄ), §5 and Anlage (Gebührenverzeichnis) (accessed 2026-10-22)gesetze-im-internet.de
- Mensah GA, Arnold N, Prabhu SD, Ridker PM, Welty FK. (2026). Inflammation and Cardiovascular Disease: 2025 ACC Scientific Statement: A Report of the American College of Cardiology. Journal of the American College of Cardiologydoi:10.1016/j.jacc.2025.08.047
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