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Seven-marker panel combining full lipids with hsCRP and homocysteine to assess both cholesterol burden and vascular inflammatory risk.
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A seven-marker panel combining the full lipid profile with high-sensitivity CRP and homocysteine.
Cardiovascular risk is not just about cholesterol — it is about what cholesterol does to blood vessels in the context of chronic inflammation. The Lipid and Inflammation Panel combines the standard five-part lipid profile with two key vascular inflammation markers: high-sensitivity CRP and homocysteine.
High-sensitivity CRP (hsCRP) is a sensitive marker of low-grade vascular inflammation that predicts cardiovascular events independently of LDL cholesterol. It was the central measure in the landmark JUPITER trial, which led to the regulatory approval of rosuvastatin for primary cardiovascular prevention in people with normal LDL but elevated hsCRP.
Homocysteine is an amino acid that accumulates when B12, folate, or B6 metabolism is impaired. Elevated homocysteine damages the endothelial lining of blood vessels, promotes platelet aggregation, and increases the risk of both arterial and venous thrombosis. Unlike Lp(a), elevated homocysteine is readily treatable with targeted B-vitamin supplementation.
Home fingerstick kit available; fasted collection required. GMC-physician reviewed results within 3 to 5 working days.
Understand what each marker measures, why it matters, and what the science says — not just a list of numbers.
Five-marker lipid panel for cardiovascular risk stratification.
Sensitive vascular inflammation marker; values above 2 mg/L indicate elevated cardiovascular inflammatory burden.
B12 and folate-sensitive amino acid; elevated levels are an independent, treatable cardiovascular and thrombotic risk marker.
This panel is designed for adults who want a comprehensive, evidence-based picture of their metabolic health — not a GP referral panel.
Those who have already had a standard cholesterol test and want to add inflammatory context
People with borderline LDL wanting to understand whether inflammation is adding to their risk
Those with a family history of stroke or blood clots wanting homocysteine assessment
Individuals on B12 or folate supplementation wanting to monitor the cardiovascular effect
hsCRP and homocysteine elevations require clinical interpretation. CRP elevated during or after infection or acute illness reflects acute inflammation, not chronic vascular risk — retest once recovered. Homocysteine is non-specific; elevated levels can result from B12/folate deficiency, kidney disease, hypothyroidism, or genetic MTHFR variants — the clinical significance depends on the cause. Triglycerides must be measured fasted for accurate LDL calculation. This panel does not include ApoB or Lp(a), which provide additional cardiovascular risk data beyond the standard lipid panel.
From order to physician-reviewed report in as little as three working days.
Three options designed to fit your schedule, location, and preference — all producing a laboratory-standard sample.
Adults 18+ in mainland UK. Not suitable if you have had a transfusion in the last 3 months.
Order anytime; kit dispatched within 24 hours Mon–Fri.
Allow 24–48 hours for sample transit on top of lab processing time.
Adults 18+ within 20 miles of a serviced city centre.
Mon–Sun, 06:00–20:00. Next-day booking typical.
Sample reaches the lab within 24 hours of collection.
Adults 16+ with photo ID. Paediatric draws by appointment at selected sites.
Mon–Fri, with Saturday hours at most metropolitan locations.
Samples processed same-day at the receiving clinic.
Every test is processed in a UKAS ISO 15189-accredited laboratory, overseen by GMC-registered physicians, and governed by UK GDPR. No overseas processing, no offshore data.
Follow these guidelines to ensure accurate, reproducible results. Most markers are sensitive to recent food, exercise, and sleep.
Can't find your answer? Our clinical support team is available Monday to Friday, 9am–5pm.
Contact supportYes. Research consistently shows that a significant proportion of people who suffer heart attacks and strokes have LDL cholesterol within the normal range. This occurs because LDL cholesterol content does not perfectly capture atherogenic particle number (ApoB does this better), because vascular inflammation independently drives plaque formation regardless of cholesterol level, and because other risk factors — homocysteine, Lp(a), insulin resistance, hypertension — contribute to cardiovascular events through pathways other than LDL. The JUPITER trial specifically demonstrated that people with normal LDL but elevated hsCRP benefited significantly from statin therapy, establishing inflammation as an independent treatment target.
An hsCRP above 3 mg/L indicates elevated vascular inflammatory burden in the cardiovascular risk context (assuming the elevation is not due to acute infection or other inflammatory conditions). This level is associated with a significantly higher cardiovascular event risk, independent of cholesterol levels. At this level, the JUPITER trial and subsequent guidelines support considering statin therapy even with normal LDL. Lifestyle factors that reduce hsCRP include: aerobic exercise, losing weight (particularly visceral fat), reducing refined carbohydrates and added sugar, quitting smoking, improving sleep quality, and managing chronic stress. Your physician report will contextualise your result and recommend appropriate steps.
Homocysteine accumulates in the blood when the enzyme-driven conversion to methionine (requiring B12 and folate) or to cysteine (requiring B6) is impaired. Elevated homocysteine damages blood vessel linings through several mechanisms: it generates reactive oxygen species that impair endothelial function; it directly damages endothelial cells; it activates platelets and increases clotting tendency; and it promotes smooth muscle cell proliferation that thickens arterial walls. The result is a prothrombotic, pro-atherosclerotic state. Because the underlying mechanism is nutritional in most cases, correcting B12 and folate deficiency can meaningfully reduce homocysteine and thereby reduce vascular risk.
The most effective approach is a combination of folic acid (400 to 800 mcg daily), B12 (at least 500 mcg daily), and B6 (10 to 25 mg daily). This combination addresses all three enzyme pathways through which homocysteine is metabolised. Folic acid has the strongest evidence for homocysteine lowering. In the UK, flour is fortified with folic acid, which has reduced population homocysteine levels — but individuals with poor absorption, vegans, and those with MTHFR variants may still be deficient. Retesting homocysteine after 3 months of supplementation confirms whether levels have normalised. Discuss supplementation with your GP, particularly if you are on methotrexate or other folate-antagonist medications.
No. Do not stop or change any medication before this test without consulting your prescribing doctor. If you are on a statin, your lipid results will reflect your treated levels — which is exactly what your physician and you want to monitor. Knowing your treated LDL, non-HDL, and hsCRP on a statin helps assess whether your current dose is achieving its target. If you want to test your untreated baseline, discuss this with your GP before stopping medication.
For those using this panel as part of routine cardiovascular risk monitoring, annual testing is appropriate once on a stable supplement or lifestyle regimen. If hsCRP is elevated and you are implementing lifestyle changes (exercise, diet, weight loss), retesting at 3 to 6 months gives meaningful feedback on the inflammatory response to your interventions. For homocysteine, if deficiency is identified and you start B-vitamin supplementation, retesting at 3 months confirms whether levels have normalised. Your physician report will recommend a specific retesting interval based on your results.
