Fasting vs non-fasting lipid samples

Measurement of lipid profiles in the fasting versus non fasting state is a controversial issue. This is especially true in people with diabetes, who often have high serum triglyceride levels, since triglycerides are the lipid fraction most affected by food intake.

Previous guidelines for assessing cardiovascular risk in patients recommend that lipid profiles are measured with the patient in a fasting state for at least 8 hours,[1][2] to decrease within individual variability in results. In addition, the majority of prospective studies that have been used to create modern cardiovascular risk prediction strategies and also clinical trials of statin treatment, have incorporated fasting lipid profiles. Furthermore the Friedewald equation that is used to calculate LDL cholesterol concentrations assumes a constant ratio between triglycerides and cholesterol in VLDL particles, which may be altered in the post prandial state. There is also evidence, however, that in some situations non fasting markers are better predictors of cardiac events.[3]

A recent cross sectional study of data from 209,180 people in Alberta, Canada linked self reported fasting duration with lipid fraction levels.[4] There were minimal differences in mean levels of total cholesterol and HDL cholesterol among non fasting individuals, compared with those who had fasted for at least 9 hours. The mean calculated LDL cholesterol levels showed greater variation (up to 10% among groups of patients with different fasting intervals) and mean triglyceride levels varied by up to 20%. The authors concluded that fasting times showed little association with lipid subclass concentrations and suggested that fasting for routine lipid measurements is largely unnecessary.

The situation may be different in people with diabetes. One of the problems in diabetic dyslipidaemia is excessive post prandial lipaemia, along with increased serum triglycerides and low concentrations of HDL cholesterol. Each of these factors may contribute to the increased risk of atherosclerosis and cardiovascular disease in people with diabetes. A previous study examined the influence of normal food intake on the concentration of lipids, lipoproteins and apolipoproteins in 58,434 patients from the Copenhagen General Population Study, of whom 2270 suffered from diabetes mellitus.[5] It was found that in patients with and without diabetes, plasma triglycerides increased by a maximum of only 0.2 mmol/L after normal food intake compared with fasting concentrations. Reductions in LDL cholesterol after normal food intake were attributed to haemodilution caused by fluid intake. Apolipoprotein B concentrations did not change after food intake and non HDL cholesterol was also stable. The authors emphasised one limitation of their study was that the number of individuals with diabetes was small. A more recent study investigated the agreement between fasting and post prandial LDL cholesterol concentrations in 74 patients with type 2 diabetes.[6] Lipid levels were measured for 6 hours after consumption of a fat rich breakfast. LDL cholesterol results (both measured and calculated) were significantly lower in the post prandial state, compared with the fasting state. Using calculated post prandial LDL cholesterol results, 38% of patients with diabetes and two thirds of statin users were misclassified into lower Adult Treatment Panel III risk categories. This raised the possibility that the use of non fasting LDL cholesterol levels may be falsely reassuring in patients with diabetes.

It appears the evidence is growing that non fasting lipid profiles can be used for cardiovascular risk assessment in the general population. Fasting samples are preferable in people with diabetes and indeed in all individuals with serum triglyceride levels greater than 4.5 mmol/L (in whom the Friedewald equation for calculating LDL should not be used). Further prospective studies are required to compare the association of fasting and non fasting lipid profiles from the same individuals with subsequent cardiovascular outcomes.


  1. ^ National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002; 106(25): 3143-3421.

  2. ^ De Backer G, Ambrosioni E, Borch Johnsen K, et al. Third Joint Task Force of European and Other Societies on Cardiovascular Disease Prevention in Clinical Practice. European guidelines on cardiovascular disease prevention in Clinical Practice. Eur Heart J. 2003; 24(17): 1601-1610.

  3. ^ Nordestgard BG, Benn M, Schnohr P, Tybjaerg Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007; 298(3): 299-308.

  4. ^ Sidhu D, Naugler C. Fasting time and lipid levels in a community based population: a cross sectional study. Arch Intern Med. 2012; 172(22): 1707-1710.

  5. ^ Langsted A, Nordestgaard BG. Nonfasting lipids, lipoproteins, and apolipoproteins in individuals with and without diabetes: 58 434 individuals from the Copenhagen General Population Study. Clin Chem. 2011; 57(3): 482 489.

  6. ^ Lund SS, Petersen M, Frandsen M, et al. Agreement between fasting and postprandial LDL cholesterol measured with 3 methods in patients with type 2 diabetes mellitus. Clin Chem. 2011; 57(2): 298-308.


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