# Lipid profile (TC) The fats carried in the blood. LDL and non-HDL carry the particles that lodge in artery walls; triglycerides track diet, alcohol and insulin. Type: lab · Unit: mmol/L · Domain: Cardio-Respiratory Health · Accuracy: Laboratory · Importance: Core Also called: cholesterol test, cholesterol panel, lipids, blood fats, triglycerides, good cholesterol, bad cholesterol, fasting lipids, HDL-C, LDL-C, TG, non-HDL-C ## In one sentence The fats carried in your blood, measured as the cholesterol inside each kind of carrier particle (total, HDL and LDL) and as triglycerides, the form in which fat travels to be stored or burned. ## Why it matters Cholesterol does not float free; it rides inside lipoprotein particles, and the particles that can lodge in an artery wall are the ones that carry a protein called apolipoprotein B, of which LDL is by far the most numerous. The European Atherosclerosis Society's consensus panel reviewed more than 200 prospective cohort studies, Mendelian randomization studies and randomized trials, together covering more than 2 million participants, 20 million person-years and 150,000 cardiovascular events, and found a consistent, dose-dependent log-linear association between the amount of LDL cholesterol the arteries were exposed to and atherosclerotic cardiovascular disease, growing with the duration of exposure; the panel's conclusion was that LDL causes it (Ference 2017). In 302,430 people from 68 prospective studies, the hazard for coronary heart disease rose 50 percent per standard deviation of non-HDL cholesterol (about 1.1 mmol/L), while triglycerides carried no independent association once HDL and non-HDL cholesterol were accounted for (Emerging Risk Factors Collaboration 2009). HDL cholesterol is the part people call good, and the evidence has become more careful about it: in people with HDL-raising gene variants, the higher HDL was not accompanied by fewer myocardial infarctions, while the LDL-lowering variants behaved exactly as the trials had shown (Voight 2012), and in 116,508 Copenhagen adults all-cause mortality was U-shaped against HDL, lowest at about 1.9 mmol/L in men and 2.4 in women and higher again at the extremes (Madsen 2017). HDL cholesterol is read here as a marker of metabolic state, not as a quantity to push up. ## What moves it LDL cholesterol: saturated fat in the diet, body weight, an underactive thyroid, the genes of familial hypercholesterolemia, and, in some people, a very-low-carbohydrate diet, which can raise it a great deal (the clinician report notes an active keto plan for this reason). Triglycerides: the last meal (a mean rise of up to 0.3 mmol/L one to six hours after an ordinary meal; Nordestgaard 2016), alcohol, refined carbohydrate and sugar, body weight and insulin resistance, pregnancy; they fall with exercise and weight loss. HDL cholesterol: higher with regular exercise, lower with smoking, excess weight and insulin resistance. An acute illness lowers cholesterol for some weeks afterward, which is one reason the panel asks for no draw within two weeks of being unwell. ## How to measure it well A joint European consensus concluded that fasting is not routinely required for a lipid profile, because HDL cholesterol, apolipoprotein B and lipoprotein(a) are unaffected by a meal and the other analytes shift by 0.2 to 0.3 mmol/L at most (Nordestgaard 2016). VT's panel still asks for a fasting morning draw, because the same draw carries glucose and insulin, which do need it, and because the triglyceride reference range most laboratories print assumes fasting. No alcohol for 48 hours. Most laboratories calculate LDL cholesterol rather than measure it, by the Friedewald equation (Friedewald 1972), which is unreliable when triglycerides are high; the report usually says which. Use the same laboratory each time. ## How Vitality Tracker uses it Each analyte is stored as the laboratory reported it, with the laboratory's own reference range and flag, which VT shows and never overrides. From one draw VT derives non-HDL cholesterol, the total-to-HDL and triglyceride-to-HDL ratios and remnant cholesterol (see [*Non-HDL, the ratios and remnant cholesterol*](https://vitalitytracker.app/knowledge/non-hdl-and-lipid-ratios)), and, when apolipoprotein B is present, the ApoB-to-LDL discordance. Beneath each result the range VT treats as optimal is shown in smaller type, marked *working* until the clinical advisor has reviewed it, and when your doctor treats you to a target, the target you report is shown instead. Typical New Zealand laboratory reference, then VT's working optimal (v0.1): triglycerides < 1.7 mmol/L fasting · < 1.0; HDL cholesterol > 1.0 men, > 1.3 women · ≥ 1.3; LDL cholesterol < 3.4 · < 2.0; non-HDL cholesterol derived · < 2.6. The working values rest on the consensus finding that exposure to LDL is log-linear with no threshold below which it stops mattering (Ference 2017) and on the Madsen finding that more HDL is not always better; they are reference points, not VT's targets for you. Re-test ten to twelve weeks after a diet or treatment change, otherwise yearly; a lipid result is not part of the Vitality Score. ## How far to trust the number Laboratory: the assays are standardized and the analytical error is a few percent. The larger variation is yours: triglycerides swing from day to day with meals and alcohol far more than cholesterol does, so a single triglyceride result is a weaker number than a single LDL result, and a calculated LDL inherits the triglyceride's noise. ## Method Friedewald: LDL-C = TC − HDL-C − TG / 2.2 (all in mmol/L), not used when TG > 4.5 mmol/L. Non-HDL-C = TC − HDL-C. Remnant cholesterol = TC − HDL-C − LDL-C. Conversions from mg/dL: cholesterol × 0.02586, triglycerides × 0.01129 = mmol/L. ## Sources 1. Ference BA, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J 2017;38:2459–72. [doi:10.1093/eurheartj/ehx144](https://doi.org/10.1093/eurheartj/ehx144) 2. Emerging Risk Factors Collaboration. Major lipids, apolipoproteins, and risk of vascular disease. JAMA 2009;302:1993–2000. [doi:10.1001/jama.2009.1619](https://doi.org/10.1001/jama.2009.1619) 3. Voight BF, et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet 2012;380:572–80. [doi:10.1016/S0140-6736(12)60312-2]() 4. Madsen CM, Varbo A, Nordestgaard BG. Extreme high high-density lipoprotein cholesterol is paradoxically associated with high mortality in men and women: two prospective cohort studies. Eur Heart J 2017;38:2478–86. [doi:10.1093/eurheartj/ehx163](https://doi.org/10.1093/eurheartj/ehx163) 5. Nordestgaard BG, et al. Fasting is not routinely required for determination of a lipid profile: a joint consensus statement from the EAS and EFLM. Eur Heart J 2016;37:1944–58. [doi:10.1093/eurheartj/ehw152](https://doi.org/10.1093/eurheartj/ehw152) 6. 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;18:499–502. PMID 4337382 7. Vitality Tracker, Recommended baseline lab panel v0.1; Clinician report content specification, optimal set v0.1 (working). ## Related - [Apolipoprotein B](https://vitalitytracker.app/knowledge/apolipoprotein-b) - [Lipoprotein(a)](https://vitalitytracker.app/knowledge/lipoprotein-a) - [Non-HDL, the ratios and remnant cholesterol](https://vitalitytracker.app/knowledge/non-hdl-and-lipid-ratios) - [ApoB-to-LDL discordance](https://vitalitytracker.app/knowledge/apob-ldl-discordance) - [HOMA-IR](https://vitalitytracker.app/knowledge/homa-ir) - [Getting your blood tests done in New Zealand](https://vitalitytracker.app/knowledge/blood-tests-in-new-zealand) Reviewed October 2026 · v1 Source: https://vitalitytracker.app/knowledge/lipid-profile