Lipid profile: cholesterol, LDL, HDL and triglycerides

• A lipid profile measures the cholesterol and triglycerides carried by the particles in plasma: total cholesterol, LDL cholesterol (LDL-C), HDL cholesterol (HDL-C), non-HDL-C (calculated) and triglycerides, with lipoprotein(a) measured once in a lifetime.
• The panel does not have to be fasting for screening when triglycerides are not raised; a fasting panel is repeated if a non-fasting sample shows triglycerides of 4.5 mmol/L (400 mg/dL) or more. ^{[1] [2]}
• LDL-C is the primary treatment target. It is not directly measured in most laboratories but calculated with the Martin-Hopkins or Sampson equation; the older Friedewald equation is less accurate and should not be used when triglycerides are high. ^{[1] [4]}
• Low HDL-C is a risk marker, not a treatment target: raising HDL-C has not improved outcomes. ^{[1] [2]}
• Targets differ by guideline (ESC/EAS versus ACC/AHA versus NICE) and by cardiovascular risk; local guidance should be used. ^{[2] [5]}

By the end of this page you should be able to:

1. State what each reported component of a lipid profile represents.
2. Interpret measured versus calculated LDL-C and explain when calculation is unreliable.
3. Read a reference range table in SI and conventional units and explain why ranges vary.
4. Recognise secondary (diet, disease, drug) causes of a high or low value.
5. Name common patterns and what each suggests.
6. Interpret three illustrative laboratory sheets and reach a one-sentence clinical conclusion.
7. Describe when to suspect familial hypercholesterolaemia and how the Dutch Lipid Clinic Network score works.
8. Apply the ESC/EAS, ACC/AHA and NICE approaches to LDL-C targets by risk. ^[7]

A lipid profile is one of the most requested sets of blood tests and is the laboratory part of cardiovascular risk assessment. ^[1] It estimates the burden of cholesterol carried by lipoproteins, not the amount of fat in a recent meal: most plasma cholesterol sits in atherogenic, apolipoprotein B-containing particles (LDL, VLDL and its remnants, IDL and lipoprotein(a)), whereas HDL carries cholesterol from tissues back to the liver. ^[2]

This page deals with the panel itself (what it measures, how to read it, common pitfalls). For risk estimation, lifestyle advice and drug treatment see the dyslipidaemia topic. The two topics overlap, but the present page stays on the laboratory side.

The policy of "free to read, no sign-in" means an adult lipid profile is a routine request in primary care. LDL-C in particular behaves like a causal risk factor: lowering it lowers ASCVD event rates in proportion to the reduction achieved. ^[2]

A standard panel reports four main values, plus calculated ones. ^[1]

Total cholesterol is the mass of cholesterol in all circulating lipoproteins: LDL, VLDL and remnants, HDL and lipoprotein(a). ^[2] It is useful as a screening summand, but it does not separate atherogenic from non-atherogenic cholesterol, so a high total can be driven by high HDL and a high-risk profile can be missed if only TC is read.

LDL-C is the cholesterol mass inside LDL particles. It remains the primary end point of most lipid-lowering trials and the primary treatment target. ^[1] LDL particles are the principal driver of atherosclerosis; each one carries a single apolipoprotein B molecule, and the lower the particle number, the lower the vessel-wall exposure. ^[4]

Measured versus calculated. In most laboratories LDL-C is not measured directly. Three calculation approaches are in routine use:

• Friedewald equation (1972): LDL-C = total cholesterol - HDL-C - triglycerides/5 (mg/dL); or - triglycerides/2.2 (mmol/L). It assumes a fixed VLDL:triglyceride ratio, which breaks down at high triglycerides. ^[4]
• Martin-Hopkins (Martin) equation: LDL-C = total cholesterol - HDL-C - triglycerides/adjustable factor, where the factor is looked up in a 180-cell table of triglyceride and non-HDL values. It is preferred for low and intermediate LDL-C and for non-fasting samples. ^{[4] [1]}
• Sampson equation: a quadratic expression with triglycerides and non-HDL terms, valid up to triglycerides of 9.0 mmol/L (800 mg/dL) and closer to the reference ultracentrifuge method. ^[4]

The 2018 multi-society cholesterol guideline recommends Martin-Hopkins (or a direct measurement) in place of Friedewald. ^[4] Friedewald should not be used when triglycerides are above 4.5 mmol/L (400 mg/dL), and the TG/5 approximation begins to drift at about 2.8 mmol/L (250 mg/dL). ^[4] Calculated LDL-C shares the same limitation with direct assays in low ranges and high triglyceride states; direct homogenous LDL-C can therefore be ordered, but it is no more accurate in most everyday samples and costs more. ^{[1] [4]}

HDL-C is the cholesterol content of HDL particles. Low values (under 1.0 mmol/L, 40 mg/dL in men; under 1.3 mmol/L, 50 mg/dL in women) mark increased ASCVD risk. ^[1] HDL-C is a risk marker, not a target: interventional trials that raised HDL-C did not reduce events, and very high HDL-C can paradoxically associate with higher mortality. ^{[1] [2]} Ratios such as total cholesterol to HDL are obsolete. ^[2]

Non-HDL-C = total cholesterol - HDL-C. It captures cholesterol in every atherogenic particle (LDL, VLDL, remnants, IDL, Lp(a)) and is unaffected by fasting. ^{[1] [2]} It is 0.7-0.8 mmol/L (about 30 mg/dL) higher than LDL-C in most people; a larger gap implies remnant accumulation, as in obesity, diabetes or hypertriglyceridaemia. ^[1] In statin-treated patients non-HDL-C and apolipoprotein B predict residual risk better than LDL-C. ^[1] It is a secondary target under ESC/EAS and the 2026 ACC/AHA dyslipidemia guideline. ^{[1] [2]}

Triglycerides circulate on VLDL, chylomicrons and their remnants. A non-fasting level reflects the post-prandial rise (peak 3-4 hours, baseline by about 8 hours in healthy people). ^[1] Triglycerides themselves are not the main culprit; their associated remnant particles are atherogenic and high triglycerides commonly go together with low HDL-C in metabolic syndrome and diabetes. ^[2] Above 5.0-5.7 mmol/L and especially above 11.3 mmol/L (1,000 mg/dL) the acute priority is prevention of pancreatitis. ^{[2] [7]}

Triglycerides and HDL-C are used to screen for secondary dyslipidaemia, not as primary treatment targets.

Lp(a) is an LDL-like particle with an apolipoprotein(a) covalently bound to apolipoprotein B. ^[1] Its level is roughly 90% genetically determined, stable across the lifespan and follows autosomal dominant inheritance. ^[1] It raises ASCVD and aortic stenosis risk independently of LDL-C. Levels are reported in nmol/L (molar) or mg/dL (mass); the two cannot be converted reliably because particle size varies, so a molar assay is preferred. ^{[1] [2]}

Because Lp(a) is genetically fixed, every adult should be tested once in a lifetime, with cascade screening of first-degree relatives if elevated. ^[1]

Fresh samples are not always (or ever) required. Panels can be taken in the non-fasting state for screening; the exception categories, from the German Federal Joint Committee guidance cited in the Parhofer review, are:

• non-fasting triglycerides above 5 mmol/L (440 mg/dL) ^[2]
• known hypertriglyceridaemia ^[2]
• triglyceride-associated pancreatitis ^[2]
• before starting drugs that raise triglycerides ^[2]
• when other tests taken require fasting ^[2]

After a change in treatment, weight, diet or an acute event (myocardial infarction, major surgery), lipids reach a new equilibrium only after 4-6 weeks, so re-measure after that interval before changing treatment again. ^[2]

A panel alone cannot tell whether a value is steady-state, so comment on recent illness in the clinical notes.

Ranges vary by laboratory, age, sex, ethnicity, fasting status and analytical method; the laboratory's own reference range always wins. The values below are decision values used by the cited guidelines, in SI units with conventional units in brackets. No single number on this list is a diagnosis.

The HDL-C "low" band is sex-specific and the laboratory often reports its own interval by method and age. Lp(a) runs 5-10% higher in women than in men on average. ^[2]

A lipid value is not a diagnosis; it is a pointer to a mechanism. Secondary causes should be excluded before a primary (genetic) lipoprotein disorder is assumed.

Laboratory screening for secondary causes (when causes are "unexplained"): TSH and free T4 for hypothyroidism; fasting glucose and HbA1c; liver function tests; creatinine and (urine) albumin. ^[3]

These are named combinations a clerk could notice on a result sheet; they are patterns, not diagnoses, and must be matched to the patient.

• Isolated high LDL-C, normal triglycerides and HDL-C: primary (genetic) hypercholesterolaemia or a secondary cause such as hypothyroidism or cholestasis. If LDL-C is 4.9 mmol/L (190 mg/dL) or more, evaluate for familial hypercholesterolaemia. ^{[1] [3]}
• High triglycerides with low HDL-C and near-normal LDL-C: "atherogenic dyslipidaemia", common in metabolic syndrome, type 2 diabetes and central obesity. Non-HDL-C and ApoB capture the risk here better than LDL-C. ^{[1] [2]}
• High LDL-C and high triglycerides with low HDL-C: mixed (combined) dyslipidaemia, often familial combined or severe secondary disease. Cascade and family history are important. ^[3]
• Triglycerides at or above 5.7 mmol/L (500 mg/dL), extreme at 11.3 mmol/L (1000 mg/dL): chylomicronaemia; priority is prevention of acute pancreatitis, not ASCVD. ^{[1] [2]}
• Normal or high LDL-C with elevated lipoprotein(a): an independent, genetic risk factor; intensify LDL-C lowering and screen first-degree relatives. ^{[1] [2]}
• Discordant LDL-C and ApoB: a normal LDL-C with a high non-HDL-C or ApoB means more atherogenic particles than the cholesterol suggests; consider metabolic or diabetic dyslipidaemia. ^[1]
• A panel that is "too normal" after an acute illness: repeat in 4-6 weeks before deciding. ^[2]

When LDL-C is 4.9 mmol/L (190 mg/dL) or higher (or total cholesterol 7.5 mmol/L or higher), especially with a family history of premature cardiovascular disease, the phenotypic Dutch Lipid Clinic Network score is applied before a diagnosis of familial hypercholesterolaemia is made. ^{[1] [6]} The working trigger used in UK practice is total cholesterol of at least 7.5 mmol/L or LDL-C of at least 5.0 mmol/L, always after secondary causes have been excluded. ^[6]

Scoring points to remember:

• Tendon xanthomata: 6 points. ^[6]
• Arcus cornealis before 45 years: 4 points. ^[6]
• Premature coronary artery disease in the patient: 2 points. ^[6]
• Premature coronary or vascular disease, or LDL-C above the 95th percentile, in a first-degree relative: 1 point. ^[6]
• LDL-C 8.5 mmol/L or more = 8 points; 6.5-8.4 = 5; 5.0-6.4 = 3; 4.0-4.9 = 1. A mutation in LDLR, APOB or PCSK9 gives 8. ^[6]
• Total: above 8 definite; 6-8 probable; 3-5 possible; under 3 unlikely. ^[6]

Adults meeting criteria should have cascade screening (about half of first-degree relatives are affected) and specialist referral; women stop statins at least 3 months before conception. ^[6]

These are the numbers a laboratory interpretation uses to decide whether a value is "at target"; the underlying risk score differs between systems.

• ESC/EAS 2019 with 2021-2025 updates: LDL-C goals under 1.4 mmol/L (55 mg/dL) in very high risk, 1.8 (70) in high risk, 2.6 (100) in moderate risk and 3.0 (115) in low risk; non-HDL secondary targets 2.2, 2.6, 3.4 and 3.8 (85, 100, 130, 145) mmol-compatible with the same risk groups. ^{[2] [5] [7]}
• 2026 ACC/AHA: three LDL-C bands by treatment group: under 2.6 mmol/L (100 mg/dL), 1.8 (70) and 1.4 (55), with corresponding non-HDL targets 3.4 (130), 2.6 (100) and 2.2 (85) and ApoB targets 0.9, 0.7 and 0.55 g/L. ^{[1] [2]}
• NICE (2014 guideline, retained in later updates): statin-based primary prevention when 10-year risk is at least 10% (QRISK), atorvastatin 20 mg for primary prevention and 80 mg for secondary prevention, and a treatment aim of at least a 40% reduction in non-HDL-C at 3 months; no universal treat-to-target LDL-C rule. ^{[5] [7]}

All values are illustrative samples invented for teaching and are not real patient data. Units, thresholds and rules used to interpret them come from the cited guidelines; the values themselves need no citation.

Interpretation:

1. Took non-fasting sample; triglycerides are under 4.5 mmol/L (400 mg/dL), so calculation is acceptable.^{[1] [2]}
2. LDL-C is below the low-risk threshold.^{[2] [4]}
3. HDL-C is not low for sex.^[1]
4. Triglycerides are desirable and non-HDL-C is concordant (gap about 0.5 mmol/L).^[1]
5. No pattern of mixed or atherogenic dyslipidaemia.

Clinical conclusion: this illustrates a low-risk lipid profile; routine screening, lifestyle advice and repeat testing at the usual screening interval are appropriate.

Interpretation:

1. LDL-C is over 4.9 mmol/L (190 mg/dL), so statin therapy is indicated irrespective of risk calculation and should be started after checking that secondary causes are excluded. ^{[1] [5]}
2. Triglycerides are normal, so the LDL-C calculation is reliable. ^[4]
3. Lp(a) of 55 nmol/L sits in the "not elevated" band. ^[2]
4. Family history of premature cardiovascular disease, tendon xanthomas or arcus cornealis before 45 years and a DLCN score would be sought; a score above 8 is definite FH. ^[6]
5. Screening laboratory tests for secondary causes (TSH and free T4, fasting glucose/HbA1c, liver and renal tests, drugs) should be checked before diagnosing primary disease. ^[3]

Clinical conclusion: this illustrates probable or definite familial hypercholesterolaemia (DLCN depends on history and examination); arrange phenotyping, cascade screening of first-degree relatives, and high-intensity statin with a 50% LDL-C reduction target.

Interpretation:

1. Because triglycerides are 3.4 mmol/L, a Martin-Hopkins or Sampson calculation was used rather than Friedewald. ^{[1] [4]}
2. LDL-C alone underestimates risk; non-HDL-C is 5.2 mmol/L with a gap of 1.6 mmol/L, indicating remnant particles and an atherogenic phenotype. ^[1]
3. Low HDL-C plus high triglycerides fits metabolic syndrome/type 2 diabetes risk. ^[2]
4. Secondary causes (obesity, uncontrolled glucose, alcohol, drug therapy) should be identified first. ^[3]
5. Under NICE risk-based care the treatment aim is a reduction in non-HDL-C of at least 40% at 3 months; ESC/EAS would also quote an LDL-C goal by risk group (about 70 mg/dL, 1.8 mmol/L in high risk). ^{[2] [5]}

Clinical conclusion: this illustrates atherogenic (mixed) dyslipidaemia; address adiposity, glucose and alcohol first, then use statin-based therapy with non-HDL-C and, if available, ApoB to monitor.

1. Fasting assumptions. Do not require fasting for every screen. A routinely booked panel can be read non-fasting; only repeat fasting when triglycerides are 5.0 mmol/L (440 mg/dL) or more non-fasting, in known hypertriglyceridaemia, after pancreatitis, before triglyceride-raising drugs, or when glucose or drug levels are also needed. ^[2]
2. Friedewald misuse. Friedewald triglycerides/5 becomes unreliable around 2.8 mmol/L (250 mg/dL) and should not be used above 4.5 mmol/L (400 mg/dL). Use Martin-Hopkins or Sampson in those samples and interpret low-range LDL-C with care. ^{[1] [4]}
3. Unit and ratio errors. Stick to one unit set per sheet, convert total/LDL with 38.6 and triglycerides with 88.6. Do not use total cholesterol:HDL or LDL:HDL ratios; they are no longer supported by guidelines. ^{[1] [2]}
4. Treating HDL. Raising HDL-C does not reduce events; low HDL is information, not a drug target. ^{[1] [2]}
5. Mass versus molar Lp(a). Ranges in mg/dL or nmol/L cannot be converted reliably because particle size varies; laboratories provide their own conversion. A single lifetime test is usually enough. ^{[1] [2]}
6. Ignoring secondary causes. Hypothyroidism, nephrotic syndrome, cholestasis, obesity, diabetes, alcohol and drugs all move the panel; diagnose primary disease only after they are excluded. ^[3]
7. Reading during acute illness. Cholesterol may be transiently low after infarction or surgery; repeat after 4-6 weeks before concluding. ^[2]
8. Target mismatch. ESC/EAS gives LDL-C goals by risk (under 1.4, 1.8, 2.6, 3.0, 3.4 and 4.9 mmol/L for the appropriate groups), the 2026 ACC/AHA table gives goals by treatment group (under 100, 70 and 55 mg/dL for LDL-C), and NICE uses risk-based statin dose plus a target non-HDL-C reduction of at least 40%. Guidelines genuinely differ; use the version adopted locally. ^{[2] [1] [5]}
9. Unit conversion mistakes for treatment thresholds: LDL-C 70 mg/dL = 1.8 mmol/L; 55 mg/dL = 1.4 mmol/L; 100 mg/dL = 2.6 mmol/L; 190 mg/dL = 4.9 mmol/L. ^[4]

• A lipid profile reports total cholesterol, LDL-C, HDL-C, triglycerides and (calculated) non-HDL-C; risk assessment needs the results in clinical context.
• Screening panels can be non-fasting when triglycerides are under 4.5 mmol/L (400 mg/dL); fasting panels are used for high or known hypertriglyceridaemia and their complications. ^{[1] [2]}
• LDL-C is the primary target. Calculate with Martin-Hopkins or Sampson; Friedewald loses accuracy when triglycerides are raised or LDL-C is very low. ^{[1] [4]}
• Non-HDL-C is a reliable secondary target, fasting-independent, and better than LDL-C in metabolic and statin-treated patients. ^{[1] [2]}
• HDL-C below 1.0 mmol/L (men) or 1.3 mmol/L (women) marks risk but is not treated as a target. ^[1]
• Triglycerides under 1.7 mmol/L are desirable; 5.7 mmol/L or more is severe and 11.3 mmol/L or more greatly increases pancreatitis risk. ^{[1] [2]}
• Lipoprotein(a) is genetic and stable; measure molar nmol/L once per lifetime and screen relatives if elevated. ^{[1] [2]}
• Secondary causes (diet/obesity/diabetes, alcohol, hypothyroidism, renal and liver disease, drugs) must be excluded before primary disease is diagnosed. ^[3]
• Familial hypercholesterolaemia is suspected at LDL-C 4.9 mmol/L (190 mg/dL) or more; the Dutch Lipid Clinic Network Score grades it definite above 8. ^{[1] [6]}
• Guideline LDL-C goals differ: ESC/EAS under 1.4 and 1.8 mmol/L in very high and high risk, ACC/AHA aligns with 55, 70 and 100 mg/dL bands, NICE uses statin dose plus a ≥40% non-HDL reduction. ^{[1] [2] [5]}
• Panels need 4-6 weeks after a change in therapy or an acute event to reach steady state. ^[2]