Do you buy cholesterol myths?

You hear two opposite things about cholesterol: that it's a poison clogging your arteries, and that the whole thing was made up to sell drugs.

Before you look inside the body, make a guess. For nine claims, say whether they're true. The score isn't the point: what's more interesting is which of the two sides gets you more.

Your own estimateNine claims are not a test or a measurement. They show which side your guesses lean to. What you enter isn't stored or sent anywhere unless you save your result yourself.

Your guessClaim 1 of 9

“Cholesterol is poison, the less the better.”

The other side's myth is easy to spot. Ours sounds like common sense.

The orange dots in the animation are LDL particles that carry cholesterol through the blood. Watch how many of them settle in the artery as the figure ages, and use the switches to see what food, a drug or your genes do to it. The coloured markers are common claims about cholesterol, from scare stories and rumours spread by treatment opponents to advertising tricks. Click them.

IllustrationThe animation shows the principle on a model person, not your own levels. It measures nothing and doesn't replace a doctor.

LDL3.4mmol/L

plaque6of 100

The body makes most of its cholesterol itself (the liver, the gut and other organs) and sends it through the blood in LDL particles. Some of them get caught in the artery wall, and over decades they build up into plaque. HDL carries part of the cholesterol back to the liver.

LDL, carries cholesterol from the liver to the bodyHDL, returns cholesterol to the livercholesterol from foodplaque in the artery wall

How it works

Guess: a myth you accept counts towards the side that spreads it. A true claim you reject counts towards the side that denies it. “Partly true” claims don't count towards the score. The split into two sides and the “why it sounds believable” lines are interpretation, not measurement. Your answers aren't stored anywhere.

The moving model is an illustration, not a measurement: starting LDL 3.4 mmol/L (about 130 mg/dL), eggs × 1.03, saturated fat × 1.10, statin × 0.55, inherited disorder × 2. The multipliers match averages from studies: about 200 mg of dietary cholesterol a day (roughly one egg) raises LDL by 0.1 mmol/L (4 mg/dL), getting 10% of energy from saturated fat instead of carbohydrates by 0.36 mmol/L (14 mg/dL), a statin lowers LDL by 30 to 50% or more depending on the dose, and people with the inherited disorder have on average twice the LDL. Each year plaque grows in proportion to how far LDL is above 1.8 mmol/L (about 70 mg/dL). This threshold is chosen for the model; it is not a safe or recommended level. In trials with very low LDL, plaque shrank slightly, which the model doesn't show. The ageing speed, number of dots and plaque shape are chosen for clarity.

This article explains the mechanism and is not a substitute for a doctor: a doctor decides on treatment based on overall risk (in Europe e.g. SCORE2), not on a single lab number alone. The exceptions are very high LDL levels or an inherited disorder, which on their own mean high risk.