Blood Panels

What it measures: Total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides from a blood draw (fasting traditionally preferred, though non-fasting is now considered acceptable by many guidelines).

Why it matters: LDL particles deposit cholesterol in arterial walls and initiate atherosclerosis; triglycerides mark remnant-lipoprotein and metabolic burden; HDL-C imperfectly reflects reverse cholesterol transport.

Evidence: Decades of RCT evidence (statins, ezetimibe, PCSK9 inhibitors) confirm that LDL-C lowering reduces MI, stroke, and cardiovascular death, with a clear dose-response relationship shown across trials by the Cholesterol Treatment Trialists' Collaboration. This is the best-evidenced test on this entire page.

What it measures: The concentration of apolipoprotein B — one molecule sits on every atherogenic lipoprotein particle (LDL, VLDL, IDL, Lp(a)) — so ApoB is a direct count of circulating atherogenic particle number, rather than a measure of the cholesterol mass carried within them.

Why it matters: Particle number, not cholesterol content, best predicts how much atherogenic material can penetrate the arterial wall. A person can have "normal" LDL-C but a high number of small, cholesterol-depleted LDL particles — common with insulin resistance, obesity, and high triglycerides — and be under-estimated by LDL-C alone.

Evidence: Sniderman AD, Thanassoulis G, Glavinovic T, et al. "Apolipoprotein B Particles and Cardiovascular Disease: A Narrative Review." JAMA Cardiology 2019;4(12):1287–1295 — concludes ApoB outperforms LDL-C and non-HDL-C for cardiovascular risk discrimination, with Mendelian randomisation data supporting a causal, particle-number-driven mechanism. The 2019 ESC/EAS dyslipidaemia guideline names ApoB as a preferred/optional risk marker, especially with high triglycerides, diabetes, obesity, or very low LDL-C.

Sniderman AD, et al. JAMA Cardiol. 2019. PubMed: PMID 31642874 · Full cost breakdown & why it beats LDL-C →

What it measures: An LDL-like particle carrying an additional apolipoprotein(a) component. Level is roughly 70–90% genetically determined and essentially fixed for life after early adulthood — diet and exercise have little effect on it.

Why it matters: Promotes atherosclerosis in an LDL-like manner, inhibits fibrinolysis (pro-thrombotic), and independently drives calcific aortic valve disease.

Evidence: Kamstrup PR, Tybjærg-Hansen A, Steffensen R, Nordestgaard BG. "Genetically Elevated Lipoprotein(a) and Increased Risk of Myocardial Infarction." JAMA 2009;301(22):2331–2339 — genetically elevated Lp(a) tied to a graded increase in MI risk, supporting a causal role. However, as of 2026 no Lp(a)-lowering drug has completed a cardiovascular outcomes trial proving that lowering Lp(a) itself reduces events (pelacarsen and olpasiran trials are ongoing) — so testing today informs risk stratification and more aggressive management of other modifiable risk factors, not yet a targeted prescription.

Kamstrup PR, et al. JAMA. 2009. PubMed: PMID 19509380

What it measures: Glycated haemoglobin, reflecting average blood glucose over roughly the preceding 2–3 months.

Why it matters: Chronic hyperglycaemia glycates proteins throughout the body and drives microvascular (retinal, renal, neural) and macrovascular damage.

Evidence: The global diagnostic and monitoring standard for diabetes. The DCCT and UKPDS trials established that glycaemic control reduces microvascular complications, and WHO/ADA diagnostic thresholds are built on this evidence base.

What it measures: Fasting insulin and glucose combined into the HOMA-IR index (fasting insulin × fasting glucose ÷ 22.5), an estimate of insulin resistance.

Why it matters: Insulin resistance can precede dysglycaemia by years and independently associates with cardiometabolic risk.

Evidence: Matthews DR, Hosker JP, Rudenski AS, et al. "Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man." Diabetologia 1985;28(7):412–419 — the original HOMA validation against the euglycaemic clamp. HOMA-IR correlates with future type 2 diabetes and cardiometabolic risk in cohort studies, but fasting insulin assays are not standardised across laboratories or platforms, reference ranges vary widely, and no major guideline recommends routine HOMA-IR screening in asymptomatic adults, nor is there trial evidence that acting on an isolated elevated HOMA-IR (beyond what glucose/HbA1c already prompt) changes outcomes.

Matthews DR, et al. Diabetologia. 1985. PubMed: PMID 3899825

What it measures: A marker of low-grade systemic inflammation.

Why it matters: Inflammation contributes to atherosclerotic plaque formation and rupture. Genetic (Mendelian randomisation) evidence suggests CRP itself may largely be a bystander marker rather than a direct causal driver, with upstream inflammatory pathways (e.g. IL-6) more likely causal — but as a risk marker it still adds information.

Evidence: Ridker PM, Danielson E, Fonseca FAH, et al. (JUPITER trial) "Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein." N Engl J Med 2008;359:2195–2207 — statin therapy in patients with normal LDL-C but hs-CRP ≥2mg/L significantly reduced major cardiovascular events. ACC/AHA guidelines list hs-CRP as an optional "risk-enhancing factor" for intermediate-risk patients, not a universal screen.

Ridker PM, et al. N Engl J Med. 2008. PubMed: PMID 18997196

What it measures: Serum 25-hydroxyvitamin D, the standard measure of vitamin D status.

Why it matters: Regulates calcium/bone metabolism; proposed but less-established roles in immune and cardiovascular function.

Evidence: Manson JE, Cook NR, Lee IM, et al. (VITAL trial) "Vitamin D Supplements and Prevention of Cancer and Cardiovascular Disease." N Engl J Med 2019;380:33–44 — 25,871 adults randomised to vitamin D3 2000IU/day vs placebo showed no significant reduction in cancer or major cardiovascular events over 5 years. Frank deficiency (<20ng/mL) still matters for bone health and should be corrected in at-risk groups, but routine supplementation "for longevity" in an otherwise-replete healthy adult is not supported by the best available trial evidence.

Manson JE, et al. N Engl J Med. 2019. PubMed: PMID 30415629 · USPSTF (2021), PMID 33847711: insufficient evidence to recommend routine screening. Full pricing and evidence breakdown: Vitamin D test cost in Singapore.

What it measures: Iron storage protein; also an acute-phase reactant that rises with inflammation independent of iron status.

Why it matters: Both iron deficiency (fatigue, cognitive effects) and iron overload (hereditary haemochromatosis — organ damage via oxidative stress in liver, heart, and pancreas) are common and often silent early on.

Evidence: Well-established role in diagnosing iron-deficiency anaemia and in screening for hereditary haemochromatosis, particularly with a family history or unexplained abnormal liver enzymes. Interpretation always requires pairing with iron studies/transferrin saturation and an inflammatory marker, because ferritin alone is confounded by concurrent inflammation.

US Preventive Services Task Force. Ann Intern Med. 2006. PubMed: PMID 16880462 · Full cost breakdown & who should test →

What it measures: Serum total testosterone, ideally drawn fasting in the morning and confirmed on a second sample if low.

Why it matters: Affects muscle mass, bone density, libido, mood, and erythropoiesis. Low levels (hypogonadism) are linked to reduced quality of life and, observationally, higher cardiometabolic risk.

Evidence: Lincoff AM, Bhasin S, Flevaris P, et al. (TRAVERSE trial) "Cardiovascular Safety of Testosterone-Replacement Therapy." N Engl J Med 2023;389:107–117 — 5,246 hypogonadal men with symptoms and cardiovascular risk randomised to testosterone gel vs placebo; testosterone was non-inferior to placebo for major adverse cardiac events, resolving a long-standing safety question, though nonfatal arrhythmia (including atrial fibrillation) was more frequent with testosterone. Endocrine Society guidelines recommend testing only in men with symptoms of hypogonadism plus a confirmed low level — not as a routine "optimisation" screen in asymptomatic men.

Lincoff AM, et al. N Engl J Med. 2023. PubMed: PMID 37326322 · Full cost breakdown & who should test →

What it measures: Thyroid-stimulating hormone as the primary screen, with free T4 added if TSH is abnormal.

Why it matters: Thyroid hormone regulates metabolic rate; both hypo- and hyperthyroidism have wide-ranging effects on weight, mood, cardiovascular, and bone health, and subclinical disease (especially in older women) is common.

Evidence: Testing is well-evidenced and clearly indicated once symptoms, goitre, or risk factors (postpartum, autoimmune disease, family history, amiodarone/lithium use) are present. The US Preventive Services Task Force's 2004 recommendation statement found the evidence insufficient to recommend for or against routine screening of asymptomatic, non-pregnant adults (Grade I) — fair evidence TSH detects subclinical disease, poor evidence that treating screen-detected cases improves outcomes; a 2015 USPSTF update reached materially the same conclusion.

US Preventive Services Task Force. Ann Intern Med. 2004. PubMed: PMID 14734336 · Full cost breakdown & who should test →

What it measures: Serum creatinine (used to estimate glomerular filtration rate), urea, sodium, and potassium.

Why it matters: Reduced kidney function is both a marker and a driver of cardiovascular risk, and chronic kidney disease is frequently asymptomatic until advanced.

Evidence: eGFR staging per KDIGO guidelines robustly predicts progression to renal failure, cardiovascular events, and mortality across large international cohorts — one of the best-validated tests in general medicine.

What it measures: Liver enzymes and bilirubin, screening for hepatocellular injury (ALT/AST) and cholestasis (ALP/GGT/bilirubin).

Why it matters: Detects metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD) — now the most common liver disease in developed countries and linked to cardiometabolic risk — plus alcohol-related and other liver disease.

Evidence: Elevated ALT is an established, if imperfect, screening flag for MASLD, which itself predicts progression to fibrosis/cirrhosis and correlates with cardiovascular risk. Professional guidance supports opportunistic case-finding in at-risk groups (obesity, diabetes, metabolic syndrome) rather than framing this as a universal population screen with its own independent evidence base.

What it measures: Serum B12 and folate levels.

Why it matters: Both are required for DNA synthesis and neurological function; deficiency causes macrocytic anaemia and, if prolonged, irreversible neurological damage.

Evidence: Well-established diagnostic tests for macrocytic anaemia and neuropathy workup. Deficiency is common in the elderly, in vegans/vegetarians, after bariatric surgery, and with long-term metformin or proton-pump inhibitor use. Routine universal screening of asymptomatic, low-risk young adults is not guideline-recommended.

What it measures: Serum urate, the end product of purine metabolism.

Why it matters: Directly causes gout via urate crystal deposition. Observationally associated with hypertension, metabolic syndrome, and cardiovascular disease.

Evidence: Mendelian randomisation studies have largely failed to confirm a causal role for uric acid in cardiovascular outcomes, suggesting the observational association reflects confounding (obesity, alcohol, kidney function, diet) rather than a direct causal pathway. Clearly useful for diagnosing and monitoring gout; not validated as a standalone cardiovascular or longevity risk marker, and no guideline recommends treating asymptomatic hyperuricaemia to reduce cardiovascular risk.

What it measures: EPA+DHA content of red blood cell membranes as a percentage of total fatty acids — reflects omega-3 status over roughly the preceding 3–4 months, unlike a single dietary recall.

Why it matters: Omega-3 fatty acids incorporate into cell membranes, affecting membrane fluidity, electrical stability (arrhythmia risk), and inflammatory eicosanoid production.

Evidence: Harris WS, von Schacky C. "The Omega-3 Index: a new risk factor for death from coronary heart disease?" Preventive Medicine 2004;39:212–220 — proposed the index and found an index ≤4% carried substantially higher coronary heart disease death risk than ≥8%. Subsequent cohort data are broadly supportive, but outcome-trial evidence for supplementing specifically to raise the index is mixed: VITAL (general population, low-dose marine omega-3) was neutral for major cardiovascular events, while REDUCE-IT (high-dose purified EPA in higher-risk patients) showed benefit. The index is a reasonable status marker; "test and target a number" has not itself been proven in a trial to change outcomes for an average-risk person.

Harris WS, von Schacky C. Prev Med. 2004. PubMed: PMID 15208005

What it measures: A sulfur amino acid intermediate in methionine metabolism, elevated by B12/folate/B6 deficiency and some genetic polymorphisms (e.g. MTHFR).

Why it matters: Proposed to promote endothelial dysfunction and thrombosis; strongly and consistently associated with cardiovascular events in observational cohorts.

Evidence: Lonn E, Yusuf S, Arnold MJ, et al. (HOPE-2 trial) "Homocysteine Lowering with Folic Acid and B Vitamins in Vascular Disease." N Engl J Med 2006;354:1567–1577 — folic acid + B6 + B12 lowered homocysteine by ~25% in 5,522 high-risk patients but did not reduce major cardiovascular events overall (a stroke reduction was seen, but not MI or cardiovascular death). This is a textbook example of a biomarker with strong observational association but no proven causal benefit from intervention; later Mendelian randomisation data are similarly unsupportive of a direct causal cardiovascular role. Still clinically useful within a B12/folate deficiency workup.

Lonn E, et al. N Engl J Med. 2006. PubMed: PMID 16531613

What it measures: A liver/biliary enzyme, often included in standard liver panels, sensitive to alcohol intake and hepatic oxidative stress.

Why it matters: Rises with alcohol use, cholestasis, and hepatic oxidative stress; some cohort studies associate elevated GGT, even within the "normal" range, with cardiometabolic risk and all-cause mortality, plausibly as a marker of oxidative stress or unmeasured alcohol intake.

Evidence: A well-validated component of cholestatic liver injury workup and an alcohol-use marker. The independent "longevity marker" association beyond its role in standard liver assessment is observational, non-specific, and not incorporated into any major risk calculator or guideline as a standalone target.

What it measures: Red cells, white cells, platelets, and their subtypes/indices.

Why it matters: Screens for anaemia, infection/inflammation, and haematologic malignancy signals (e.g. abnormal white cell counts), several of which are common and often silent.

Evidence: One of the most validated, universally guideline-endorsed basic tests in medicine — cheap, safe, and high-yield for case-finding across a wide range of conditions.