High cholesterol
A standard cholesterol panel is not a risk assessment, because ApoB counts the particles that damage arteries and Lp(a) shows inherited risk it cannot see.
LDL cholesterol estimates the cargo. ApoB counts the vehicles, and it is the vehicles that lodge in an artery wall. Two patients with identical LDL can carry materially different risk, and ApoB is what separates them. Lp(a) is largely genetically determined, measured once, and changes the threshold for everything else.
Insulin resistance, which produces the small dense particle pattern a standard panel reads as reassuring. Genetics, including familial hypercholesterolemia and elevated Lp(a). Visceral adiposity and hepatic fat. Hypothyroidism, a treatable and commonly missed cause. Saturated fat intake in susceptible individuals. Alcohol. And low fiber intake.
Insulin sensitivity first, since it drives particle number and size. Viscous fiber intake, which meaningfully lowers ApoB. Zone 2 conditioning and resistance training. Thyroid correction where it is the cause. And lipid-lowering therapy where risk warrants it — declining a statin on principle is not a clinical position, it is a risk decision made without the numbers.
ApoB as the primary marker. Lp(a) once, since it does not meaningfully change. A full lipid panel for context, plus the triglyceride to HDL ratio. Fasting insulin and HOMA-IR. hs-CRP. Complete thyroid function. Liver enzymes. Coronary calcium scoring is discussed where risk stratification is genuinely uncertain.
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