Comprehensive Cardiovascular and Metabolic Risk Panel

NHS primary care cholesterol screening typically provides a standard lipid profile (total cholesterol, LDL, HDL, triglycerides). This panel extends significantly beyond that: ApoB and Lp(a) add the particle-count and genetic risk dimensions that standard LDL misses. hsCRP adds vascular inflammation context. Homocysteine adds thrombotic risk assessment. Fasting insulin identifies developing insulin resistance before HbA1c becomes abnormal. ALT and eGFR contextualise statin safety. Uric acid adds metabolic syndrome screening. The result is a picture that goes substantially deeper than a standard NHS lipid check — and it includes physician interpretation tailored to your complete result pattern.

HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) is calculated using the formula: fasting insulin (mIU/L) x fasting glucose (mmol/L) divided by 22.5. Your Trupoint Health physician report will calculate and report your HOMA-IR score alongside an interpretation. A score below 1.0 indicates good insulin sensitivity. Values of 1.0 to 2.0 are borderline. Above 2.0 suggests developing insulin resistance. Above 2.9 is consistent with significant insulin resistance in most adult populations. This index gives a single number that captures the interaction between insulin secretion and glucose disposal that individual values cannot.

Non-alcoholic fatty liver disease (NAFLD) is extremely prevalent in people with metabolic syndrome and insulin resistance — and it is a significant independent cardiovascular risk factor, since the inflammatory and metabolic dysfunction of NAFLD directly amplifies atherosclerosis. ALT is the most sensitive routine blood marker for hepatocyte stress and early fatty liver. It is also essential for statin safety monitoring — statins are processed by the liver and should not be used in people with significantly elevated ALT (though statin-related hepatotoxicity is rare). Including ALT provides both metabolic context and medication safety information.

Gout occurs when uric acid crystalises in joints, typically when serum uric acid exceeds approximately 360 to 420 micromol/L (6 to 7 mg/dL) — the saturation threshold. However, many people with elevated uric acid never develop gout, and gout attacks can occasionally occur at lower levels. In addition to gout risk, elevated uric acid is associated with hypertension, insulin resistance, kidney disease, and cardiovascular disease — making it a useful metabolic marker even in people without joint symptoms. Dietary contributors include red meat, organ meats, shellfish, fructose, and alcohol (particularly beer). Losing weight and reducing these dietary triggers can meaningfully lower uric acid.

Yes, it is well-suited for this purpose. LDL, non-HDL, and ApoB show whether the statin is achieving its lipid targets. ALT confirms liver safety. hsCRP reflects residual inflammatory risk — which can remain elevated even when LDL is well-controlled on statins (residual inflammatory risk), and which can prompt consideration of additional anti-inflammatory cardiovascular strategies. HbA1c is relevant because statins carry a small but real risk of increasing diabetes risk, which should be monitored. The HOMA-IR score also contextualises metabolic health as statins are titrated. Annual monitoring using this panel gives a comprehensive picture of statin efficacy and safety.