Limited time offer! 10% off your first blood test order!
20-marker metabolic and cardiovascular panel for men — advanced lipids, glycaemic markers, inflammation, and organ function.
or 4 interest-free payments of £34.75 with Klarna
A 20-marker metabolic and cardiovascular health panel for men — covering advanced lipids including ApoB and Lp(a), glycaemic markers.
Cardiovascular disease is the leading cause of death in men in the UK, and most of its major risk factors are detectable in blood years before symptoms appear. The Men’s Metabolic and Cardiovascular Health Panel is designed to give a thorough assessment of cardiovascular and metabolic risk through 20 carefully selected markers.
Advanced lipids: total cholesterol, LDL, HDL, triglycerides, non-HDL, ApoB, and Lp(a). ApoB provides a direct count of atherogenic particles — more predictive than LDL alone. Lp(a) identifies the 1 in 5 men who carry a genetically elevated cardiovascular risk undetectable on standard panels.
Glycaemic and metabolic: fasting insulin, HbA1c, and glucose — to identify insulin resistance and pre-diabetes before overt type 2 diabetes develops.
Organ function: liver function (ALT, AST, GGT) and kidney function (creatinine, eGFR, urea) — major organs affected by cardiovascular risk factors and medication.
Inflammation: high-sensitivity CRP and homocysteine — independent cardiovascular risk markers not included in standard NHS panels.
Uric acid: associated with gout, hypertension, and metabolic syndrome.
Morning fasted venous draw 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.
Standard lipid panel for cardiovascular risk stratification and monitoring.
Direct particle count of all atherogenic lipoproteins; more predictive of cardiac events than LDL alone.
Genetically elevated in 20% of men; substantially increases heart attack and stroke risk independently of LDL.
Earliest indicator of insulin resistance; elevated years before HbA1c becomes abnormal.
Three-month glycaemic average; identifies pre-diabetes and diabetes risk.
Acute blood glucose in the fasted state; contextualises the insulin level.
Purine metabolism end product elevated in gout and metabolic syndrome; associated with hypertension and cardiovascular risk.
Key liver enzymes assessing hepatocyte health, alcohol effect, and fatty liver risk.
Renal filtration markers essential for cardiovascular risk completeness and statin safety monitoring.
Ultra-sensitive vascular inflammation marker; elevated hsCRP predicts cardiovascular events independently of cholesterol.
B12 and folate-sensitive amino acid; elevated homocysteine is an independent thrombotic and cardiovascular risk factor.
This panel is designed for adults who want a comprehensive, evidence-based picture of their metabolic health — not a GP referral panel.
Men aged 35 and over wanting thorough cardiovascular risk assessment
Those with a family history of premature heart disease or stroke
Men with hypertension, overweight, or metabolic syndrome risk factors
Those on statins wanting to monitor ApoB, liver function, and inflammatory markers
This panel provides comprehensive cardiovascular and metabolic risk data but does not include hormonal markers (testosterone, thyroid, cortisol) that also affect cardiovascular risk in men. Lp(a) is genetically determined and does not change significantly with lifestyle or standard statin therapy — it identifies risk rather than a modifiable target. Elevated hsCRP is non-specific; sources of inflammation other than vascular disease (infection, autoimmune disease) must be excluded in clinical context. fasting insulin is a screening tool and not a formal insulin resistance diagnostic test. eGFR in this panel uses the CKD-EPI formula and is not for acute kidney injury assessment.
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 supportLDL cholesterol measures the cholesterol content carried within LDL particles, but cholesterol content and particle number do not always align — particularly in men with metabolic syndrome, diabetes, or obesity, who often have many small, dense LDL particles with relatively normal total cholesterol. ApoB counts the actual number of atherogenic particles (one ApoB per particle), which is more directly related to the number of particles that can penetrate the arterial wall and form plaques. High-quality evidence from multiple large studies shows ApoB is more predictive of cardiovascular events than LDL, particularly in those with mixed dyslipidaemia.
The European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) guidelines recommend considering Lp(a) above 50 mg/dL (approximately 107 nmol/L) as indicating elevated cardiovascular risk. Approximately 20% of the general population carry Lp(a) at or above this threshold. The risk is not linear — very high Lp(a) (above 180 mg/dL) carries a risk equivalent to the risk associated with heterozygous familial hypercholesterolaemia. Knowing your Lp(a) level informs more aggressive management of other modifiable risk factors, since Lp(a) itself is largely not modifiable by available therapies.
For elevated ApoB, the most effective interventions are: statins (which lower LDL and ApoB by around 40 to 60%), ezetimibe (adds further LDL and ApoB lowering), PCSK9 inhibitors (injectable monthly or bimonthly, lowering LDL and ApoB by 50 to 60%), and lifestyle changes including reduced saturated fat, increased soluble fibre, regular aerobic exercise, and smoking cessation. For elevated Lp(a), standard lifestyle changes have minimal effect. Statins slightly raise Lp(a) in some individuals. PCSK9 inhibitors lower Lp(a) by around 25%. Novel RNA therapies (inclisiran, pelacarsen) targeting Lp(a) specifically are in late-stage trials. The key response to high Lp(a) is aggressive management of every other modifiable risk factor.
Standard CRP is used clinically to detect and monitor acute infection and inflammation, with a detection range typically above 5 to 10 mg/L. High-sensitivity CRP (hsCRP) uses a much more sensitive assay that can detect very low levels (below 1 mg/L) of chronic low-grade vascular inflammation. At these levels, hsCRP is not measuring infection — it is measuring the smouldering arterial inflammation associated with early atherosclerosis and cardiovascular risk. The JUPITER trial demonstrated that individuals with normal LDL but elevated hsCRP (above 2 mg/L) benefited from statin therapy, establishing hsCRP as an independent cardiovascular risk marker worth measuring.
Elevated serum uric acid (hyperuricaemia) is associated with gout — the acute joint inflammation caused by uric acid crystal deposition — but also with hypertension, insulin resistance, kidney disease, and cardiovascular disease. Uric acid is produced from the breakdown of purines (found in red meat, organ meats, shellfish, and alcohol — particularly beer). It is both a marker of metabolic stress and a potential contributor to endothelial dysfunction and hypertension. Reducing alcohol, decreasing fructose intake, and maintaining a healthy weight can lower uric acid, reducing both gout risk and the associated cardiovascular and metabolic burden.
Yes, this panel includes all the key monitoring markers for statin users. LDL, non-HDL, and ApoB show whether the statin is achieving its lipid targets. ALT and AST provide liver safety monitoring (statins very rarely cause hepatotoxicity, but periodic monitoring is standard practice). Creatinine and eGFR provide kidney function context. hsCRP reflects residual inflammatory risk — if high despite adequate LDL lowering, it may prompt consideration of additional anti-inflammatory cardiovascular strategies. HbA1c is relevant because statins are associated with a small increase in type 2 diabetes risk, which is important to monitor over time.
