ApoB/ApoA1 ratio

Cholesterol does not dissolve in blood and therefore travels in particles with a protein on the outside. Every LDL particle, every particle that carries triglycerides and every Lp(a) particle carries exactly one ApoB, and those are the particles that can lodge in the vessel wall. Every HDL particle carries ApoA1, and those are the particles that bring cholesterol back out of the vessel wall. By dividing ApoB by ApoA1 you count numbers against each other instead of weights: how many particles carry cholesterol into the wall, against how many take it back out. That is what sets this ratio apart from the ratios that work with cholesterol values. LDL cholesterol weighs how much cholesterol is in the particles, but a particle with little cholesterol in it lodges in the vessel wall just as well as a full one. Anyone with many small, dense particles, the pattern of belly fat and insulin resistance, therefore has a higher ApoB than their LDL cholesterol suggests, and the ratio shows that. Your report does not print the ratio; you calculate it with the calculator on this page, from ApoB and ApoA1 in g/L, both from the same draw. The result has no unit and no agreed normal value: the large study that made the ratio known expresses risk as a sliding scale across the whole range, not as a boundary. Lower is better, and your own course is the reference point.

The ratio puts two sides of the same story in one number: how many particles can carry cholesterol into the vessel wall, against how many particles take it back out. In a Swedish study that followed well over a hundred and fifty thousand people for years, this ratio predicted the risk of a fatal heart attack more strongly than LDL cholesterol. That is why you meet it in research and on reports from outside the Netherlands. The second reason is that the ratio shows the gain of lifestyle on two sides. Less saturated fat, more fibre and losing weight lower the number of ApoB particles; exercise, losing weight and stopping smoking lift the number of HDL particles and with it ApoA1. Anyone who tackles their lipid profile with diet and exercise therefore often sees the ratio move earlier than LDL cholesterol alone. The honest limitation is that the Dutch risk estimate does not work with it. It works with LDL and non-HDL, and does not recommend measuring apolipoproteins routinely; ApoB is measured mainly when the triglycerides are high or LDL cholesterol seems to underestimate the number of particles. There is also no agreed boundary. So read the ratio as a sharper summary of your lipid profile, and let the decision on a statin fall on LDL and non-HDL.

A low ratio is favourable, and the only question is by which route. Plant-based, fibre-rich eating, a healthy weight and plenty of exercise lower the number of ApoB particles and lift ApoA1, and that is the healthy route. A statin lowers the number of ApoB particles specifically, without ApoA1 moving. A high HDL makes the denominator larger without anything changing about the depositing particles; so always check whether ApoB or LDL itself sits below the limit that fits your risk. A high ratio means proportionally many depositing and few collecting particles are circulating. Usually it is the first and rarely the last: a lot of saturated fat in the diet, from fatty meat, full-fat dairy, butter, coconut fat and biscuits, which lifts the number of ApoB particles; excess weight, little movement and insulin resistance, the pattern that lifts ApoB and lowers ApoA1, so the division moves the wrong way on two sides at once; an underactive thyroid, which slows the breakdown of LDL particles; and rarely familial hypercholesterolaemia, with many ApoB particles from childhood. The ratio belongs beside ApoB and ApoA1 themselves, because a rise through more ApoB means something different from the same rise through less ApoA1, beside non-HDL and LDL, which the risk estimate works on, and beside HDL and the triglycerides, which show which side of the lipid profile moved.