LDL Cholesterol Calculator

Most labs do not measure LDL cholesterol directly – they calculate it. Enter total cholesterol, HDL and triglycerides to calculate LDL-C with the classic Friedewald formula and the newer NIH (Sampson) equation, which stays accurate at higher triglycerides.

 

 

 

Try an example:

NIH (Sampson 2020) equation, valid to triglycerides of 800 mg/dL; Friedewald shown for comparison (valid below 400 mg/dL).

LDL-C (NIH/Sampson equation)

123 mg/dL

  • Friedewald120 mg/dL
  • Non-HDL cholesterol150 mg/dL

For reference: Near optimal (100–129 mg/dL)

Slightly above optimal.

Next step: Your target depends on your overall cardiovascular risk.

Friedewald: LDL = TC − HDL − TG ÷ 5 (mg/dL)

NIH/Sampson: LDL = TC/0.948 − HDL/0.971 − (TG/8.56 + TG × non-HDL/2140 − TG²/16100) − 9.44

On this page
  1. Calculated LDL cholesterol in brief
  2. Why LDL matters
  3. The equations
  4. Worked examples
  5. LDL categories
  6. Ranges by age and sex
  7. When calculated LDL is unreliable
  8. Fasting or non-fasting?
  9. What raises and lowers LDL
  10. Interpreting your result alongside other values
  11. LDL in children and young adults
  12. Tracking LDL over time
  13. When to see a doctor
  14. Frequently asked questions

Calculated LDL cholesterol in brief

LDL cholesterol (LDL-C) – often called "bad" cholesterol – is the main target of cholesterol-lowering treatment. Most laboratories do not measure it directly. Instead, they calculate it from three values in a standard lipid panel: total cholesterol, HDL cholesterol and triglycerides.

The calculator above uses the NIH equation (also known as the Sampson equation), published in 2020 by researchers at the US National Institutes of Health. It is more accurate than the older Friedewald equation when triglycerides are high or LDL is low, and it can be used with triglycerides up to 800 mg/dL (about 9 mmol/L). The Friedewald result is shown alongside for comparison, together with non-HDL cholesterol.

You can enter values in mg/dL or mmol/L. To convert cholesterol between the two, divide mg/dL by 38.67 (or multiply mmol/L by 38.67). Triglycerides use a different factor: divide mg/dL by 88.57.

For most adults, an LDL below 100 mg/dL (2.6 mmol/L) is considered optimal, but the right target for you depends on your overall cardiovascular risk. People with established heart disease, diabetes or very high risk are often advised to aim much lower.

Why LDL matters

LDL particles carry cholesterol through the bloodstream to tissues. When there are too many of them, they enter the walls of arteries, where the cholesterol they carry is retained and triggers inflammation, forming atherosclerotic plaques. Over decades, plaques narrow arteries and can rupture, causing heart attacks and strokes.

The evidence that LDL causes atherosclerotic cardiovascular disease is unusually strong. It comes from genetic studies (people born with variants that lower LDL have much lower lifetime risk), from inherited conditions such as familial hypercholesterolaemia (which cause very high LDL and early heart disease), and from large randomised trials of LDL-lowering medicines. A 2017 consensus statement from the European Atherosclerosis Society concluded that the relationship is causal and that risk reduction depends on both how much and for how long LDL is lowered. In statin trials, each 1 mmol/L (about 39 mg/dL) reduction in LDL reduced major vascular events by roughly a fifth.

This is why guidelines use LDL as the primary treatment target, and why the accuracy of the calculation matters most for people at the low and high ends of the range.

The equations

Friedewald (1972)

LDL-C = total cholesterol − HDL-C − triglycerides ÷ 5 (all in mg/dL)

In mmol/L, the triglyceride term is triglycerides ÷ 2.2. The equation assumes that very-low-density lipoprotein (VLDL) cholesterol is a fixed one-fifth of triglycerides. This works reasonably well when triglycerides are normal, but the ratio of triglycerides to VLDL cholesterol actually varies, so Friedewald underestimates LDL when triglycerides are high or LDL is low. It should not be used when triglycerides are 400 mg/dL (4.5 mmol/L) or higher.

Martin-Hopkins (2013)

The Martin-Hopkins method replaces the fixed factor of 5 with one of 180 factors chosen from a table according to the triglyceride and non-HDL cholesterol levels. It is more accurate than Friedewald, particularly at low LDL levels, and is used by some laboratories, but it requires the lookup table rather than a single formula.

NIH/Sampson (2020)

LDL-C = TC/0.948 − HDL-C/0.971 − (TG/8.56 + TG × non-HDL-C/2140 − TG²/16100) − 9.44 (all in mg/dL)

This equation was developed using more than 8,000 samples in which LDL was measured by the reference method (beta-quantification). Its VLDL term varies with both triglycerides and non-HDL cholesterol, which allows it to remain accurate at triglyceride levels up to 800 mg/dL. In validation studies, it performed as well as or better than Martin-Hopkins and clearly better than Friedewald in people with hypertriglyceridaemia.

Worked examples

All values below were calculated with the equations above (mg/dL):

TotalHDLTriglyceridesNIH (Sampson) LDLFriedewald LDL
20050150123120
17060909492
150401009190
180452509385
22040450104not valid
2404560095not valid

When triglycerides are normal, the two equations agree within a few mg/dL. As triglycerides rise, Friedewald increasingly underestimates LDL compared with the NIH equation. At 250 mg/dL, the gap is 8 mg/dL; at 450 mg/dL, Friedewald no longer applies.

In mmol/L, the first example is: total cholesterol 5.17, HDL 1.29, triglycerides 1.69 mmol/L, giving an NIH LDL of about 3.19 mmol/L.

Calculating in mmol/L step by step

If your results are in mmol/L, the simplest approach is to convert them to mg/dL, apply the equation and convert back:

  1. Multiply total cholesterol and HDL by 38.67, and triglycerides by 88.57.
  2. Apply the NIH equation in mg/dL.
  3. Divide the result by 38.67 to get LDL in mmol/L.

For example, total cholesterol 5.5 mmol/L (213 mg/dL), HDL 1.2 mmol/L (46 mg/dL) and triglycerides 2.0 mmol/L (177 mg/dL) give an NIH LDL of about 134 mg/dL, or 3.48 mmol/L. Friedewald in mmol/L gives 5.5 − 1.2 − 2.0 ÷ 2.2 = 3.39 mmol/L. The calculator handles these conversions automatically.

LDL categories

The calculator uses the widely cited categories from the US National Cholesterol Education Program, which remain a common reference for adults:

LDL-C (mg/dL)LDL-C (mmol/L)Category
Below 100Below 2.6Optimal
100–1292.6–3.3Near optimal
130–1593.4–4.1Borderline high
160–1894.1–4.9High
190 or higher4.9 or higherVery high

Modern guidelines focus less on these categories and more on your overall risk, which takes into account age, sex, blood pressure, smoking, diabetes, kidney function, family history and other factors.

Targets by risk

The 2019 European Society of Cardiology and European Atherosclerosis Society (ESC/EAS) guidelines set LDL goals by risk group:

Risk categoryLDL-C goal
Very high risk (e.g. established cardiovascular disease)Below 55 mg/dL (1.4 mmol/L) and at least 50% reduction from baseline
High riskBelow 70 mg/dL (1.8 mmol/L) and at least 50% reduction
Moderate riskBelow 100 mg/dL (2.6 mmol/L)
Low riskBelow 116 mg/dL (3.0 mmol/L)

US guidelines from the American College of Cardiology and American Heart Association (2018) emphasise percentage reductions with statins and use LDL thresholds of 70 mg/dL for considering additional treatment in people with very high-risk cardiovascular disease. Your clinician will apply the guideline used in your country.

Ranges by age and sex

LDL tends to rise with age in both sexes. Women typically have lower LDL than men before menopause and similar or higher levels afterwards, as oestrogen levels fall.

GroupTypical desirable LDL
Children and adolescents (2–19 years)Below 110 mg/dL (2.8 mmol/L) is acceptable; 130 mg/dL (3.4 mmol/L) or more is high
Adults 20 and overBelow 100 mg/dL (2.6 mmol/L) is optimal
Adults with diabetes aged 40–75Statin treatment is generally recommended regardless of LDL, with lower targets for those at higher risk
Adults with cardiovascular diseaseOften below 70 mg/dL (1.8 mmol/L) or 55 mg/dL (1.4 mmol/L)

In pregnancy, LDL and triglycerides rise naturally, especially in the third trimester, and calculated LDL should be interpreted with that in mind.

When calculated LDL is unreliable

  • Triglycerides above 800 mg/dL (9 mmol/L): none of the equations is reliable; a direct LDL measurement is needed, and the high triglycerides themselves need attention.
  • Very low LDL (below about 40 mg/dL): errors in the calculation become proportionally larger; this matters mainly for people on intensive therapy such as PCSK9 inhibitors.
  • Type III hyperlipoproteinaemia (dysbetalipoproteinaemia): abnormal remnant particles make all equations inaccurate.
  • Non-fasting samples with very high triglycerides: acceptable in most people, but a fasting repeat may be advised if triglycerides exceed about 400 mg/dL.
  • Lipoprotein(a): the cholesterol in Lp(a) is included in "LDL-C" whether calculated or directly measured, so people with very high Lp(a) may have a misleading LDL value.

Fasting or non-fasting?

For most people, a non-fasting lipid panel is acceptable. A 2016 joint consensus statement from the European Atherosclerosis Society and the European Federation of Clinical Chemistry and Laboratory Medicine concluded that non-fasting samples are appropriate for routine assessment, since triglycerides rise only modestly after a typical meal and LDL changes little. Fasting samples may still be requested when non-fasting triglycerides are above about 400 mg/dL (4.5 mmol/L), when assessing hypertriglyceridaemia, or after pancreatitis.

What raises and lowers LDL

Factors that raise LDL

  • Genetics: familial hypercholesterolaemia (FH) affects about 1 in 250–300 people and causes high LDL from birth. An LDL of 190 mg/dL (4.9 mmol/L) or higher in an adult should prompt consideration of FH.
  • Diet: saturated fat and trans fat raise LDL more than dietary cholesterol does.
  • Weight gain and physical inactivity.
  • Medical conditions: hypothyroidism, nephrotic syndrome, cholestatic liver disease and some medicines (for example, certain diuretics, retinoids, corticosteroids and some immunosuppressants).
  • Menopause.

Factors that lower LDL

  • Dietary changes: replacing saturated fat with unsaturated fat; increasing soluble fibre (oats, barley, beans); plant sterols and stanols.
  • Weight loss, where appropriate.
  • Medicines: statins are first-line and typically lower LDL by 30–50% or more depending on intensity; ezetimibe adds about 20%; PCSK9 inhibitors and inclisiran add around 50% or more; bempedoic acid is an option for people who cannot take statins.

Interpreting your result alongside other values

LDL is only one part of the picture:

  • Non-HDL cholesterol (total minus HDL) includes all atherogenic particles and does not depend on fasting or on triglyceride assumptions. Many guidelines use it as a secondary target.
  • Apolipoprotein B (apoB) counts the atherogenic particles directly and can be useful when triglycerides are high.
  • Lipoprotein(a) is genetically determined; measuring it at least once in adulthood is recommended by European guidelines.
  • HDL cholesterol is associated with lower risk at population level, but raising it with medicines has not reduced events.

LDL in children and young adults

Cholesterol screening in childhood helps identify familial hypercholesterolaemia early, when lifelong treatment offers the greatest benefit. The US National Heart, Lung, and Blood Institute recommends universal lipid screening once between ages 9 and 11 and again between 17 and 21, with earlier testing for children with a family history of early heart disease or very high cholesterol. In the UK and some other countries, screening tends to focus on relatives of people with FH (cascade testing).

In children, an LDL of 130 mg/dL (3.4 mmol/L) or more is considered high, and persistently raised values – particularly above 160 mg/dL (4.1 mmol/L) with a positive family history, or 190 mg/dL (4.9 mmol/L) or more – suggest FH. Treatment begins with diet and lifestyle; statins may be started from around age 8 to 10 in children with FH.

Tracking LDL over time

Single LDL results vary by about 5–10% from one test to the next because of biological variation and laboratory differences. When tracking treatment:

  • compare results from the same laboratory where possible
  • recheck 4–12 weeks after starting or changing medicine, then every 3–12 months as advised
  • look at the percentage reduction from your baseline, which many guidelines use as a treatment goal
  • keep a record of triglycerides too, since a large change in triglycerides alters calculated LDL

When to see a doctor

Speak with a clinician if:

  • your LDL is 160 mg/dL (4.1 mmol/L) or higher, or 190 mg/dL (4.9 mmol/L) or higher, which may indicate familial hypercholesterolaemia
  • you have a family history of early heart disease (a male relative before 55 or a female relative before 65) or very high cholesterol
  • you have diabetes, kidney disease, high blood pressure or previous heart attack or stroke
  • your triglycerides are above 500 mg/dL (5.6 mmol/L) – very high triglycerides increase the risk of pancreatitis
  • you are on cholesterol treatment and your LDL is not reaching your target

Seek emergency care for chest pain, sudden weakness, difficulty speaking, or other symptoms of heart attack or stroke.

Frequently asked questions

Why does my lab report differ from this calculator?

Your laboratory may use Friedewald, Martin-Hopkins, the NIH equation or a direct measurement. Each gives slightly different values, especially when triglycerides are high or LDL is low.

Is the NIH equation better than Friedewald?

In validation studies, it was more accurate, particularly when triglycerides are high. When triglycerides are normal, the two give very similar results.

Can I calculate LDL if my triglycerides are 900 mg/dL?

No. Above 800 mg/dL, no equation is reliable. A direct LDL or apoB measurement is needed, and the high triglycerides themselves should be assessed.

Is LDL of 130 mg/dL bad?

It is borderline high by population categories. Whether it needs treatment depends on your overall cardiovascular risk.

Does dietary cholesterol raise LDL?

For most people, dietary cholesterol (as in eggs) has a smaller effect than saturated and trans fats, though some people respond more strongly.

How quickly can LDL change?

Statins lower LDL within about 4–6 weeks. Diet changes typically show their effect within a few weeks to three months.

What is a direct LDL test?

A direct LDL test measures LDL cholesterol chemically rather than calculating it. It is used when triglycerides are very high, but methods vary between manufacturers and are not always more accurate than the NIH equation at normal triglyceride levels.

Does exercise lower LDL?

Regular aerobic exercise has a modest effect on LDL, usually a few percent, but it raises HDL slightly, lowers triglycerides and reduces cardiovascular risk independently.

Can LDL be too low?

Very low LDL levels achieved with medicines – even below 30 mg/dL (0.8 mmol/L) – have been studied in large trials, and no major safety problems have been found over several years of follow-up. People with genetically very low LDL also tend to have low cardiovascular risk. Very low LDL without treatment, however, can occasionally point to conditions such as hyperthyroidism, malabsorption or liver disease.

Does LDL need to be checked every year?

Adults without risk factors are often checked every four to six years. People on treatment or with higher risk are checked more often, typically once or twice a year after the initial adjustment period.

Do plant sterols really lower LDL?

Yes. Foods fortified with plant sterols or stanols, taken at about 1.5–3 grams a day, lower LDL by roughly 7–12% in studies. They work by reducing cholesterol absorption from the gut and can be combined with other dietary changes or with statins. Whether they reduce heart attacks has not been tested directly.

Is LDL the same as total cholesterol?

No. Total cholesterol includes LDL, HDL and the cholesterol carried in triglyceride-rich particles. Two people with the same total cholesterol can have very different LDL levels, which is why the full lipid panel matters more than total cholesterol alone.

Sources

  1. Sampson M, et al. A New Equation for Calculation of Low-Density Lipoprotein Cholesterol in Patients With Normolipidemia and/or Hypertriglyceridemia. JAMA Cardiol 2020
  2. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972
  3. Martin SS, et al. Comparison of a novel method vs the Friedewald equation for estimating low-density lipoprotein cholesterol levels. JAMA 2013
  4. Ference BA, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. Eur Heart J 2017
  5. Mach F, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias. Eur Heart J 2020
  6. Nordestgaard BG, et al. Fasting is not routinely required for determination of a lipid profile. Eur Heart J 2016
  7. MedlinePlus – LDL: The "Bad" Cholesterol

Related tools