Apolipoprotein A-1 (ApoA-1) Unit Converter
Apolipoprotein A-1 (ApoA-1) Unit Converter
Convert apolipoprotein A-1 between g/L, mg/dL and mg/L. It is the HDL counterpart of apoB, and it reads the opposite way round: for apoA-1 it is a low result, not a high one, that carries the risk.
Apolipoprotein A-1 (ApoA-1) converter
g/L ⇄ mg/dLApolipoprotein A-1 1.02 g/L in a man
Formula and conversion factors
g/L = mg/dL ÷ 100
mg/L = g/L × 1000
- × 100
- the same factor as for apoB and for every other protein reported in g/L against mg/dL; a gram is 1,000 mg and a litre is 10 dL
- no molar unit
- apoA-1 is reported by mass and no molar unit is in clinical use, so none is offered here
- not one per particle
- an HDL particle carries several apoA-1 molecules — commonly two to five, varying with particle size — so apoA-1 is not the HDL particle count in the way apoB is the atherogenic particle count
- direction of risk
- low is the abnormal end. The reference interval's lower limit is the clinically meaningful boundary and the upper limit varies widely between assays
Worked example
Apolipoprotein A-1 1.02 g/L in a man
1.02 × 100 = 102 mg/dL
1.02 × 1,000 = 1,020 mg/L
Below the male reference interval of 1.10–1.70 g/L (110–170 mg/dL)
The same value in a woman would be further below her interval of 1.20–1.90 g/L, which is why the sex has to be chosen before the result is read
Low is the adverse direction for apoA-1, so this is the finding worth acting on, not a high one
Reference intervals differ between sources — the lower limit does not
| Source | Men (g/L) | Women (g/L) |
|---|---|---|
| Common immunoturbidimetric assay range, used on this page | 1.10 – 1.70 | 1.20 – 1.90 |
| FINRISK 2007 population reference sample | 1.1 – 2.0 | 1.2 – 2.3 |
| Figure below which apoA-1 is generally called low | < 1.10 | < 1.20 |
ApoB and apoA-1 are not mirror images
| Apolipoprotein B | Apolipoprotein A-1 | |
|---|---|---|
| Carried on | LDL, IDL, VLDL, remnants, Lp(a) | HDL |
| Molecules per particle | Exactly one | Several — commonly two to five, varying with particle size |
| Is it a particle count? | Yes | No — it counts protein, not particles |
| Adverse direction | High | Low |
| Modifiable by treatment? | Substantially, by statins and ezetimibe | Modestly; no HDL-raising therapy has yet shown outcome benefit |
The HDL side of the ratio, and why it reads backwards
Apolipoprotein A-1 is the principal structural protein of high-density lipoprotein and the partner measurement to apoB. The conversion is the same as for apoB and every other protein reported in g/L: multiply by 100 for mg/dL, so 1.02 g/L is 102 mg/dL. Reference intervals are sex-specific because women run higher throughout adult life — roughly 1.10 to 1.70 g/L in men against 1.20 to 1.90 g/L in women on a common immunoturbidimetric assay, with the FINRISK population sample reaching 2.0 and 2.3 respectively.
The direction of abnormality is the opposite of apoB’s, and getting it the wrong way round is the commonest error on this test. A high apoB is a problem; a high apoA-1 is not, and is generally either neutral or favourable. It is a low apoA-1 that carries risk, and the causes are mostly the familiar cardiometabolic ones: smoking, poorly controlled diabetes, central obesity, chronic kidney disease, nephrotic syndrome and some beta-blockers. Because only the lower limit is clinically meaningful, the disagreement between sources about where the interval ends matters far less than it looks.
ApoA-1 is not the HDL equivalent of apoB, and the difference is structural rather than semantic. Each atherogenic particle carries exactly one apoB molecule, which is what makes apoB a particle count. An HDL particle carries several apoA-1 molecules — commonly two to five, and the number changes with particle size and remodelling — so the apoA-1 concentration cannot be divided by anything to yield an HDL particle number. It measures the protein, and the relationship between that protein and the number of particles shifts as the particles do.
On its own, apoA-1 adds relatively little to an HDL cholesterol that has already been measured, and it should be read with the same caution that now attaches to HDL-C: the association with risk is robust, the causal interpretation is not, and every attempt to lower cardiovascular events by raising HDL pharmacologically has failed. Its value lies mainly in the denominator of the apoB/apoA-1 ratio, where it contributes the protective term to a single number that outperforms either apolipoprotein alone and does not require the patient to have fasted.
Frequently asked questions
How do I convert apoA-1 from g/L to mg/dL?
Multiply by 100. An apoA-1 of 1.02 g/L is 102 mg/dL, and 1.40 g/L is 140 mg/dL. Divide by 100 to go the other way. There is no molar unit, because apoA-1 is reported as a mass concentration.
What is a normal apolipoprotein A-1 level?
Roughly 1.10 to 1.70 g/L in men and 1.20 to 1.90 g/L in women on a common immunoturbidimetric assay, with wider upper limits in some population samples. Only the lower limit carries clinical meaning, so use the issuing laboratory’s own figure.
Is a high apoA-1 a problem?
Generally not. Unlike apoB, where high is the adverse direction, apoA-1 reads the other way round: a low value is what tracks increased cardiovascular risk. A high apoA-1 is usually neutral or favourable, and is seen with heavy alcohol intake and with oestrogen therapy.
Does apoA-1 count HDL particles the way apoB counts LDL particles?
No. Each atherogenic particle carries exactly one apoB molecule, so apoB is a particle count. An HDL particle carries several apoA-1 molecules — commonly two to five, depending on particle size — so apoA-1 measures protein, not particle number.
What lowers apolipoprotein A-1?
Smoking, poorly controlled diabetes, central obesity and the metabolic syndrome, chronic kidney disease and nephrotic syndrome, severe hypertriglyceridaemia, and some beta-blockers. Rare genetic causes such as Tangier disease and apoA-1 variants produce very low values.
Related calculators
References
- Leiviskä J, Sundvall J, Alfthan G, Jauhiainen M, Salomaa V. Apolipoprotein A-I, apolipoprotein B, and apolipoprotein B/apolipoprotein A-I ratio: reference intervals compared with values in different pathophysiological conditions from the FINRISK 2007 study. Clin Chim Acta. 2011;412(11–12):1146–1150.
- Walldius G, Jungner I, Holme I, Aastveit AH, Kolar W, Steiner E. High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. Lancet. 2001;358(9298):2026–2033.
- Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020;41(1):111–188.