What Your Cholesterol Test Didn't Tell You

Elevated LDL cholesterol is treated, in much of standard practice, as a problem with a known solution: a statin. The decision pathway is well-established — calculate cardiovascular risk score, if above threshold prescribe statin, retest LDL at follow-up. It is efficient, guideline-driven, and misses several things that matter enormously for the individual patient sitting in front of you.

This is not an argument against statins. For secondary prevention — patients who have already had a cardiovascular event — the evidence for statins is robust and the benefit is clear. For primary prevention in high-risk patients, the picture is more nuanced. What this post addresses is what standard cholesterol testing and risk scoring does not tell you — and why that matters for how the finding is understood and what, if anything, should be done about it.

The Cause of Elevated Cholesterol Matters

Elevated LDL cholesterol is not a disease. It is a finding. Like elevated blood pressure or elevated fasting glucose, it is a signal that something in the underlying physiology is worth understanding. The most common cause of elevated cholesterol and triglycerides in the modern population is insulin resistance and metabolic syndrome — not dietary cholesterol, not genetic hypercholesterolaemia, and not a statin deficiency.

When insulin resistance is the driver, the lipid pattern has characteristic features: elevated triglycerides, low HDL, normal or modestly elevated LDL-C but with a shift toward small dense LDL particles, and an elevated TG:HDL ratio. Treating this pattern with a statin lowers LDL-C on paper while leaving the underlying metabolic dysfunction untouched. The result: the number improves, the risk does not necessarily.

Hypothyroidism is another common and entirely reversible cause of elevated cholesterol. Every patient with newly identified elevated cholesterol should have thyroid function assessed — specifically TSH, free T3, and free T4, not just TSH. Treating an elevated cholesterol that is secondary to untreated hypothyroidism with a statin treats the effect while missing the cause.

The CoQ10 Problem

Statins inhibit HMG-CoA reductase — the rate-limiting enzyme in the mevalonate pathway that produces cholesterol. The same pathway also produces CoQ10 (ubiquinol/ubiquinone), the essential electron carrier in mitochondrial oxidative phosphorylation. Statin use depletes endogenous CoQ10 synthesis. The clinical consequences: myopathy (muscle pain and weakness), fatigue, and potentially impaired cardiac mitochondrial function in the very organ statins are prescribed to protect.

The evidence for CoQ10 supplementation in statin users is mixed, but the mechanistic depletion is well-established. For any client on a statin, particularly those experiencing muscle symptoms or fatigue, CoQ10 supplementation (100–200mg ubiquinol daily) is a reasonable clinical consideration. A baseline CoQ10 level before statin initiation and monitoring during therapy is almost never performed in standard practice.

Lp(a) — The Risk Factor Nobody Checks

Lipoprotein(a) — Lp(a) — is a genetically determined independent cardiovascular risk factor. Elevated Lp(a) doubles or triples cardiovascular risk regardless of LDL-C level. Statins do not reduce Lp(a) — they may actually increase it slightly. PCSK9 inhibitors reduce Lp(a) modestly. But Lp(a) level is almost never measured in standard NHS cardiovascular risk assessment.

A patient with normal LDL-C on a statin but elevated Lp(a) remains at significantly elevated cardiovascular risk that the standard monitoring misses. Lp(a) should be measured once in every adult — it is genetically stable throughout life and does not require repeat testing unless treatment specifically targeting it is initiated.

The cholesterol number tells you what your LDL is. It does not tell you what kind of LDL particles you have, whether insulin resistance is driving them, whether Lp(a) is adding independent risk, or whether your thyroid needs attention before a statin is considered. These are the questions that determine whether the finding matters and what to do about it.