This is not ordinary high cholesterol. In familial hypercholesterolemia (FH), the liver's LDL receptor is broken from birth, so half the clearance capacity is gone and LDL piles up ¹. Carriers run untreated LDL of 190 to 450 mg/dL from day one ².

What matters is time, not the number alone. Plaque grows with how long LDL has been crossing into your artery walls, so by forty an FH carrier holds the cumulative exposure of a typical seventy-year-old. Each 40 mg/dL of lower lifelong LDL cuts coronary risk about 54% ³. Finding it early resets the clock.

Treated early, the loaded gun unloads. Dutch children with confirmed FH put on statins from ages eight to eighteen reached age thirty-nine with a 1% cardiovascular-event rate, matching their unaffected siblings; their untreated parents had run 26% by the same age ⁴. Found late, the same drugs still work with less margin: ezetimibe adds 15 to 20% more LDL lowering, and a PCSK9 inhibitor another 55 to 60% on top ⁵.

Two things should trigger a check: an untreated LDL your diet can't explain, or a family history of early heart disease.

Treatment escalates in a fixed order: a high-intensity statin first, then ezetimibe, then a PCSK9 inhibitor if the target isn't hit. Children with FH usually start a statin between eight and ten ⁶.

The number to sit with is the cascade yield. FH is dominant, so each first-degree relative of a carrier has a 50% chance of having it too. Systematic testing of a confirmed carrier's family finds it in about one in two relatives, the highest hit rate in clinical genetics ⁷. Each undiagnosed family means three to eight people who could start a statin in their twenties heading toward a forty-something heart attack instead.