Cholesterol Calculator

When a lipid panel does not directly measure LDL, it must be estimated. The Friedewald equation (1972) is the historical default: LDL = Total Cholesterol − HDL − (Triglycerides / 5) in mg/dL, or − Triglycerides/2.2 in mmol/L. It assumes a fixed VLDL-to-triglyceride ratio of 1:5, which holds when triglycerides are below about 400 mg/dL (4.5 mmol/L). Above that threshold the assumption breaks down, the equation underestimates LDL, and a different method is required. The Martin–Hopkins equation (Johns Hopkins, 2013) uses an adjustable factor instead of a fixed /5 — the divisor varies by triglyceride and non-HDL level, looked up in a 180-cell table. It improves accuracy especially at TG 200–400 mg/dL and at low LDL (under 70 mg/dL), where Friedewald systematically over- or under-estimates. The Sampson equation (NIH, 2020) is a multivariate formula validated against ultracentrifugation and is increasingly used by US labs as a default. For the vast majority of patients with TG below 200 mg/dL, all three give similar results — within 5 mg/dL. This calculator uses Friedewald; if your triglycerides are above 400 mg/dL, treat the LDL output as approximate and use the directly measured value or non-HDL as the primary metric.

The NCEP Adult Treatment Panel III (ATP III, 2001, updated 2004) is the long-running US framework: Total cholesterol below 200 mg/dL desirable, 200–239 borderline, 240+ high. LDL: under 100 optimal, 100–129 near optimal, 130–159 borderline high, 160–189 high, 190+ very high. HDL: under 40 mg/dL is a risk factor, 40–59 average, 60+ protective. Triglycerides: under 150 normal, 150–199 borderline, 200–499 high, 500+ very high. The 2018 ACC/AHA cholesterol guideline shifted emphasis from rigid LDL targets to a risk-based approach using the Pooled Cohort Equations to estimate 10-year ASCVD risk, with thresholds that prompt statin therapy. UK NHS, Heart UK and the 2014 NICE CG181 guideline use very similar absolute thresholds in mmol/L: total under 5, LDL under 3, HDL above 1.0 (men) / 1.2 (women), triglycerides under 1.7. Heart & Stroke Canada and Heart Foundation Australia publish thresholds aligned with the ACC/AHA approach. The categories shown by this calculator follow ATP III mg/dL conventions; equivalent mmol/L values are noted throughout this article so you can interpret a UK, EU, Australian or NZ lab report.

Non-HDL cholesterol = Total Cholesterol − HDL. It captures every atherogenic particle in a single number: LDL plus VLDL, IDL, chylomicron remnants and Lp(a). Unlike Friedewald LDL, it is calculated from directly measured values (total and HDL) and does not depend on a triglyceride assumption — so it remains accurate at any triglyceride level. The 2014 NICE CG181 guideline (UK) made non-HDL the primary lipid target. The 2018 ACC/AHA cholesterol guideline lists non-HDL as a coequal target with LDL. Heart UK recommends non-HDL for patients with mixed dyslipidemia or diabetes. Targets typically run 30 mg/dL (0.8 mmol/L) above the LDL target — so an LDL goal of <100 corresponds to non-HDL <130; an LDL goal of <70 corresponds to non-HDL <100. If you have type 2 diabetes, metabolic syndrome, or triglycerides above 200 mg/dL, ask your clinician to use non-HDL as the primary metric.

The total cholesterol to HDL ratio expresses cardiovascular risk in a single number: under 3.5 is desirable, 3.5–5.0 is acceptable, above 5.0 signals elevated risk. The LDL/HDL ratio is more focused — under 2.5 desirable, under 3.5 acceptable, above 5 high risk. Both are informational alongside the absolute values, not replacements. A favourable ratio with high LDL still means you have a lot of atherogenic particles circulating, just balanced by a lot of HDL. UK NHS lab reports often print the total/HDL ratio next to the absolute values; Heart Foundation Australia uses it in the Cardiovascular Disease Risk Calculator. Two notes of caution: (1) the ratio is sensitive to HDL changes that may not reflect cardiovascular risk well — for example, alcohol raises HDL but is not protective; (2) very high HDL (>100 mg/dL) artificially flatters the ratio without conferring extra protection. Use the ratio with the absolute LDL and non-HDL values, not as a single answer.

The Friedewald equation assumes that VLDL contributes triglycerides/5 worth of cholesterol. That assumption holds for typical patients but fails in three situations. First, when triglycerides exceed 400 mg/dL (4.5 mmol/L), the VLDL particles become triglyceride-rich and cholesterol-poor — Friedewald then underestimates LDL. Second, in chylomicronemia (TG > 1000 mg/dL, often genetic or pancreatitis-related), Friedewald is meaningless. Third, at very low LDL (<70 mg/dL) achieved by high-intensity statin therapy or PCSK9 inhibitors, Friedewald systematically underestimates LDL by 5–10 mg/dL — clinically relevant when adjusting therapy. In all three cases, prefer (a) directly measured LDL, (b) Martin–Hopkins or Sampson estimates, or (c) non-HDL cholesterol as the primary metric. Your lab can run direct LDL on request; many UK and Canadian labs default to direct LDL when triglycerides exceed 200 mg/dL.

Apolipoprotein B (ApoB) is the structural protein on every atherogenic particle — LDL, VLDL, IDL and Lp(a). Each particle carries exactly one ApoB, so an ApoB count tells you the number of atherogenic particles regardless of how much cholesterol each carries. Two patients with identical LDL of 130 can have ApoB values 30% apart depending on particle size and number; the patient with more particles has higher cardiovascular risk. The 2021 Canadian Cardiovascular Society dyslipidemia guideline endorses ApoB as a primary target alongside non-HDL. The 2019 ESC/EAS guideline (used in the UK and EU) uses ApoB targets directly: <80 mg/dL for moderate risk, <65 for high risk, <55 for very-high risk. Lipoprotein(a), or Lp(a), is a genetically determined particle that promotes both atherosclerosis and clotting. Levels are 80–90% genetic and largely unchanged by diet, exercise or statins. Heart UK, the European Atherosclerosis Society and 2018 ACC/AHA all recommend a one-time Lp(a) measurement in adults — particularly with personal or family history of premature heart disease. Lp(a) above 50 mg/dL (~125 nmol/L) raises ASCVD risk meaningfully even when LDL is well controlled. Most labs in the UK, Canada and Australia offer ApoB and Lp(a) on request.

Diet, exercise and weight loss can lower LDL by 20–30% in motivated patients — comparable to a low-intensity statin. The Mediterranean diet (olive oil, nuts, fish, vegetables, whole grains, low red meat) lowers LDL by 5–15% in randomized trials. Soluble fiber (oats, beans, psyllium husk, barley) at 5–10 g/day drops LDL by another 5–10%. Plant sterols and stanols (2 g/day in fortified spreads or supplements) reduce LDL ~10% by competing for intestinal absorption. The Portfolio Diet — combining Mediterranean, soluble fiber, plant sterols, soy protein and almonds — lowered LDL by ~30% in trials, equivalent to a statin. Aerobic exercise (150 minutes/week moderate or 75 minutes vigorous, per ACC/AHA, NHS, Heart Foundation Australia and Health Canada) raises HDL 3–6 mg/dL and lowers triglycerides 10–20%. Weight loss of 10 lb (4.5 kg) lowers LDL ~5 mg/dL on average. Smoking cessation raises HDL within weeks and reduces oxidative LDL modification — among the highest-impact non-drug interventions. None of these replace medication for high-risk patients with very high LDL or established cardiovascular disease, but they are first-line for borderline-high LDL and an important adjunct at every stage.

Medication is added to lifestyle when 10-year ASCVD risk is high, when LDL stays significantly above target despite diet and exercise, or when there is established cardiovascular disease, diabetes with risk factors, or familial hypercholesterolemia. Statins (atorvastatin, rosuvastatin, simvastatin) are first-line and lower LDL by 30–50% at moderate doses, 50%+ at high intensity. They also reduce LDL particle number, stabilize plaque and have anti-inflammatory effects. Side effects (muscle aches, modest diabetes risk increase) are well characterized; intolerance is less common in placebo-controlled trials than in clinical practice (the 'nocebo' effect). Ezetimibe (Zetia / Ezetrol) blocks intestinal cholesterol absorption and adds another 15–25% LDL reduction; commonly added to statin or used alone for statin-intolerant patients. PCSK9 inhibitors (evolocumab, alirocumab, inclisiran) are injectable biologics that drop LDL by 50–60% on top of a statin — used when LDL targets aren't met, in familial hypercholesterolemia, or for very-high-risk patients. Bempedoic acid is an oral option for statin intolerance. Bile acid sequestrants and fibrates have niche roles. Decisions on which medication, what dose, and when belong with your clinician — this calculator and article are educational, not personal medical advice.

Modern guidelines tie LDL targets to cardiovascular risk, not a single number for everyone. Primary prevention with low risk: no specific LDL target — focus on lifestyle and reassessment every 4–6 years. Primary prevention with moderate risk (10-year ASCVD 5–7.5%): LDL under 130 mg/dL (3.4 mmol/L) is reasonable. Primary prevention with elevated risk (≥7.5–20%): LDL under 100 mg/dL (2.6 mmol/L), with consideration of moderate-intensity statin per 2018 ACC/AHA. High risk (diabetes, ASCVD ≥20%, chronic kidney disease): LDL under 70 mg/dL (1.8 mmol/L), high-intensity statin recommended. Very high risk (established ASCVD, recurrent events): LDL under 55 mg/dL (1.4 mmol/L) per 2019 ESC/EAS, often with PCSK9 inhibitor on top of maximally tolerated statin plus ezetimibe. Familial hypercholesterolemia: LDL under 100 mg/dL (2.6 mmol/L) for primary prevention, under 70 mg/dL with established disease. UK NICE CG181 recommends a 40% non-HDL reduction from baseline as the threshold for medication intensification in primary prevention, regardless of absolute target.

Familial hypercholesterolemia (FH) is the most common serious genetic disorder, affecting roughly 1 in 250 adults — about 1.3 million Americans, 270,000 Britons, 100,000 Canadians and 100,000 Australians. The vast majority are undiagnosed. FH causes LDL above 190 mg/dL (5 mmol/L) from birth, regardless of diet or weight, and dramatically raises early heart attack risk: untreated men with FH have a 50% risk of a coronary event by age 50, women by age 60. Suspect FH if your untreated LDL exceeds 190 mg/dL, you have tendon xanthomas (cholesterol deposits in Achilles or knuckle tendons), corneal arcus before age 45, or first-degree relatives had heart attacks before age 55 (men) / 65 (women). The Dutch Lipid Clinic Network score and Simon Broome criteria are used for clinical diagnosis; genetic testing confirms it. Heart UK runs a national FH cascade-screening programme, where confirmed cases are followed up to test their first-degree relatives. The US FH Foundation, FH Australasia Network and CANRISK in Canada do similar. Treatment is lifelong high-intensity statin, often plus ezetimibe and a PCSK9 inhibitor, started in adolescence for most patients. With early treatment, life expectancy approaches that of the general population.

Recommendations vary slightly by country but converge on the same principle: test in early adulthood, then every 4–6 years if low risk, sooner if elevated. United States — ACC/AHA: lipid panel at age 9–11 and 17–21, then every 4–6 years for adults ≥20 with low risk; annually for those at higher risk or on therapy. United Kingdom — NHS Health Check covers cholesterol every 5 years between ages 40 and 74; Heart UK recommends earlier and more frequent testing for those with a family history. Canada — Canadian Cardiovascular Society: every 5 years from age 40 (men) or 50 (women), or earlier with risk factors; First Nations and Métis adults from age 30. Australia — Heart Foundation Australia: Heart Health Check every 1–2 years from age 45, or 30 for First Nations Australians, including a fasting lipid panel and 5-year CVD risk score. All four countries recommend earlier screening if there is a family history of premature heart disease (under 55 men / 65 women), familial hypercholesterolemia, diabetes, chronic kidney disease, or known cardiovascular disease.

The United States, Canada and most of Asia report cholesterol in milligrams per deciliter (mg/dL). The United Kingdom, EU, Australia, New Zealand and most of the rest of the world use millimoles per liter (mmol/L). The conversion depends on which lipid you're converting. For total cholesterol, LDL and HDL: divide mg/dL by 38.67 to get mmol/L (or multiply mmol/L by 38.67 to get mg/dL). For triglycerides the factor is different — divide mg/dL by 88.57 — because triglyceride molecules have a different molecular weight than cholesterol. Quick reference: total cholesterol 200 mg/dL ≈ 5.2 mmol/L; LDL 100 mg/dL ≈ 2.6 mmol/L; HDL 40 mg/dL ≈ 1.0 mmol/L; HDL 60 mg/dL ≈ 1.5 mmol/L; triglycerides 150 mg/dL ≈ 1.7 mmol/L; triglycerides 400 mg/dL ≈ 4.5 mmol/L. This calculator accepts mg/dL inputs; if your lab reports in mmol/L, multiply by 38.67 (or 88.57 for triglycerides) before entering the values. Conversions noted throughout this article so a UK or AU reader can interpret US-style category labels.