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13, 2017
ABSTRACT
Fasting for >8 h, as previously required for lipid profiles, normally only occurs a few hours before breakfast. By contrast,
the nonfasting state predominates most of a 24-h cycle and better captures atherogenic lipoprotein levels. Plasma
contains atherogenic lipoproteins of hepatic origin in the fasting state and additionally those of intestinal origin in the
nonfasting state. Maximal mean changes for random, nonfasting versus fasting levels are þ26 mg/dl for
triglycerides, 8 mg/dl for total cholesterol, 8 mg/dl for low-density lipoprotein cholesterol, þ8 mg/dl for remnant
cholesterol, and 8 mg/dl for non–high-density lipoprotein cholesterol; lipoprotein(a), apolipoprotein B, and
high-density lipoprotein cholesterol are largely unaffected. For patients, laboratories, and clinicians alike, nonfasting lipid
profiles represent a simplification without negative implications for prognostic, diagnostic, and therapeutic options for
cardiovascular disease prevention. Several societies’ guidelines and statements in Denmark, the United Kingdom,
Europe, Canada, Brazil, and the United States endorse nonfasting lipid profiles. (J Am Coll Cardiol 2017;70:1637–46)
© 2017 by the American College of Cardiology Foundation.
Manuscript received June 23, 2017; revised manuscript received August 3, 2017, accepted August 4, 2017.
1638 Nordestgaard JACC VOL. 70, NO. 13, 2017
ABBREVIATIONS LIPIDS, LIPOPROTEINS, AND are apolar toward the lipoprotein core, but are polar
AND ACRONYMS APOLIPOPROTEINS MEASURED IN toward the water phase. These molecules are phos-
LIPID PROFILES pholipids, free cholesterol, and apolipoproteins
apoB = apolipoprotein B
(Table 1). Apolipoproteins act as cofactors for en-
CI = confidence interval
Lipids such as cholesterol and triglycerides, zymes in lipid metabolism and as ligands when lipo-
HDL = high-density lipoprotein
measured as total plasma values in lipid proteins are recognized at cell surfaces. Most
IDL = intermediate-density profiles, are important for most cells. important are apolipopteins B (apoB) and E, which
lipoprotein
Cholesterol is an essential component of cell facilitate removal of low-density lipoprotein (LDL)
LDL = low-density lipoprotein
membranes, and also acts as precursor for and chylomicron remnant/intermediate-density
Lp(a) = lipoprotein(a)
bile acids and steroid hormones. Tri- lipoprotein (IDL) from plasma, respectively.
VLDL = very low-density glycerides are important as energy sources Lipoproteins increase in size and decrease in den-
lipoprotein
and, after storage, act as an energy reserve as sity from high-density lipoprotein (HDL) to LDL to
well as for insulation against cold weather. Unlike lipoprotein(a) (Lp[a]) to IDL to very low-density li-
triglycerides, carbohydrates, and proteins, choles- poprotein (VLDL) to chylomicrons (Table 1). Chylo-
terol cannot be degraded by human cells. Cholesterol micron remnants have size and density like IDL and
that is newly synthesized or taken up via the intestine VLDL.
will therefore remain in the body unless it is con- Cholesterol and triglycerides in the diet are
verted to steroid hormones, lost through skin cell absorbed in the small intestine and incorporated into
detachment, or secreted via bile. chylomicrons (Figure 2). Chylomicrons are transferred
Because lipids will not mix with water, plasma has to the bloodstream via lymph, where it comes in
a lipid transport system consisting of water-soluble contact with the triglyceride-degrading enzyme lipo-
lipoproteins. The cores of lipoproteins consist of protein lipase, mainly in fat and muscle tissue. The
apolar lipid triglycerides and cholesterol esters resulting chylomicron remnants are taken up rapidly
(Table 1) (13). Cholesterol esters are free cholesterol by liver cells.
molecules esterified with a fatty acid coming from Cholesterol in the liver is either secreted via bile as
phospholipids; when cholesterol is measured in bile acids or cholesterol, or will, together with tri-
plasma or lipoproteins, it is a measurement of free glycerides, be packed into VLDL particles that are
and esterified cholesterol combined. To keep tri- secreted into the bloodstream (Figure 2). Triglycerides
glycerides and cholesterol esters in a water solution, in VLDL will be degraded in fat and muscle tissue by
the surface of lipoproteins consists of molecules that the enzyme lipoprotein lipase, and the cholesterol-
rich IDL particle is formed. Some IDL particles are
cleared by liver cells, whereas others are converted to
F I G U R E 1 Nonfasting and Fasting Periods During a 24-h Cycle With Intake of LDL particles through the action of the triglyceride-
Typical Meals degrading enzyme hepatic lipase. LDL particles are
taken up via the LDL receptor in the liver and other
Less than 8 hrs tissues.
since last meal
Lipoprotein(a) particles are LDL particles with an
extra apolipoprotein, apo(a) (Table 1); apo(a) has ho-
mology with plasminogen, and therefore may inter-
Non-fasting fere with fibrinolysis and indirectly promote arterial
Noon
thrombosis (14). HDL particles were previously
thought to be important in atherosclerosis and car-
6 am 6 pm diovascular disease, but the evidence to support this
is becoming weaker and weaker (15,16).
Fasting In hyperlipidemia, there is a surplus of atherogenic
Midnight
lipoproteins circulating in the blood, and a fraction of
these will penetrate into the arterial intima via simple
size- and concentration-dependent filtration (Figure 3)
More than 8 hrs (17). Chylomicrons and large VLDL with diameters
since last meal
larger than 75 nm are not able to enter the intima (18),
unlike all other lipoproteins (16,17). LDL, lip-
Fasting for more than 8 h for most individuals only represents a few hours in the early oprotein(a) (Lp(a)), IDL, chylomicron remnants, and
morning. VLDL all enter the intima and are trapped, as they
cannot penetrate the elastic laminas in the media.
JACC VOL. 70, NO. 13, 2017 Nordestgaard 1639
SEPTEMBER 26, 2017:1637–46 Lipid Profile, Fasting Versus Nonfasting
Core Surface
Diameter Molecular Density Main
(nm) Weight 106 (Da) (g/ml) Triglycerides Cholesterol Ester Cholesterol Phospholipid Apolipoproteins Apolipoproteins
HDL ¼ high-density lipoprotein; IDL ¼ intermediate-density lipoprotein; LDL ¼ low-density lipoprotein; VLDL ¼ very low-density lipoprotein.
All of these apoB-containing lipoproteins can, to some value and may confuse, rather than enlighten, the
degree, transfer back from the intima to the lumen of clinician.
the artery against the blood pressure gradient, but the A minimal lipid profile consists of plasma total
larger triglyceride-rich lipoproteins IDL, chylomicron cholesterol and triglycerides (Table 2). A standard lipid
remnants and VLDL have particular difficulty leaving profile also includes measurements of LDL cholesterol
the intima due to their larger sizes (16,19,20). and HDL cholesterol. Total cholesterol, HDL choles-
In isolated hypercholesterolemia, when tri- terol, and triglycerides are measured directly, whereas
glycerides are below 176 mg/dl (2 mmol/l), LDL LDL cholesterol can either be measured directly
cholesterol is the main atherogenic component in or calculated by the Friedewald equation if
plasma (Figure 4, left). In combined hyperlipidemia, triglycerides are <400 mg/dl (<4.5 mmol/l): total
when triglycerides are 176 to 880 mg/dl (2 to cholesterol HDL cholesterol triglycerides/2.2 (all
10 mmol/l), cholesterol in LDL, IDL, chylomicron in mmol/l; or triglycerides/5 with values in mg/dl)
remnants, and VLDL combined constitute the (21), with direct measurement of LDL cholesterol at
atherogenic plasma component (Figure 4, middle). triglyceride concentrations $400 mg/dl (4.5 mmol/l).
However, when triglycerides are severely elevated Traditionally, the Friedewald equation has been
above 880 mg/dl (10 mmol/l), chylomicrons and large
VLDL are not atherogenic, whereas LDL, IDL, chylo-
micron remnants, and small VLDL are atherogenic F I G U R E 2 Atherogenic Lipoproteins Present in the Blood During Periods of
Plasma
Cholesterol
mg/dL mmol/L
463 12
309 8
VLDL (+IDL) Chylomicrons
VLDL + IDL
+ large VLDL
+ chylomicron
remnants
Atherogenic
LDL cholesterol Atherogenic
155 4 cholesterol VLDL + IDL
LDL + chylomicron
remnants
Atherogenic
LDL cholesterol
HDL
HDL HDL
0 0
(Top) The visual appearance of the 3 types of hyperlipidemia: isolated hypercholesterolemia; combined hyperlipidemia; and severe hyper-
triglyceridemia. (Bottom) Distribution of atherogenic cholesterol in different lipoproteins, all shown in orange. For severe hypertriglyceridemia,
some cholesterol is found in chylomicrons and large VLDL that likely are not atherogenic (shown in gold), as these lipoproteins are too large to enter
into the intima (see Figure 3). Neutral cholesterol in HDL is shown in green. Abbreviations as in Figures 2 and 3.
*LDL cholesterol can either be measured directly or calculated by the Friedewald equation if triglycerides are <400 mg/dl (4.5 mmol/l): total cholesterol HDL cholesterol triglycerides/2.2 (all in mmol/l;
or triglycerides/5 with values in mg/dl) (21), with direct measurement of LDL cholesterol at triglyceride concentrations $400 mg/dl (4.5 mmol/l). †Remnant cholesterol (¼ triglyceride-rich lipoprotein
cholesterol) is calculated as total cholesterol LDL cholesterol HDL cholesterol, using random, nonfasting or fasting lipid profiles; if LDL cholesterol is also calculated, then remnant cholesterol is
equivalent to triglycerides/2.2 in mmol/l and to triglycerides/5 in mg/dl. ‡Non-HDL cholesterol is calculated as total cholesterol HDL cholesterol and is equivalent to LDL and remnant cholesterol
combined.
ApoA1 ¼ apolipoprotein A1; ApoB ¼ apolipoprotein B; other abbreviations as in Table 1.
1642 Nordestgaard JACC VOL. 70, NO. 13, 2017
0
that the use of nonfasting lipid profiles is evidence-
Fasting 0-1 1-2 2-3 3-4 4-5 5-6 6-7 7-8 driven, whereas continued use of fasting lipid pro-
Time Since Last Meal, Hours files is largely belief-driven (Central Illustration).
Indeed, a main argument for keeping fasting lipid
The mean maximal increase in triglycerides of 26 mg/dl (0.3 mmol/l) and in remnant profiles is that “We have always done it that way!”
cholesterol of 8 mg/dl (0.2 mmol/l), compared with fasting levels, occurs 3 to 4 h after when today, prospective evidence from more than
the last meal. 300,000 individuals is available suggesting that
nonfasting lipid profiles are as good as, if not better
than, fasting lipid profiles in predicting future car-
diovascular events (5,51–54).
For example, in the Emerging Risk Factors Collab-
F I G U R E 6 Mean Maximal Change in Lipids, Lipoproteins, oration, the hazard ratio for predicting coronary heart
and Apolipoproteins in Random, Nonfasting Compared With
disease per 43 mg/dl (1.1 mmol/l) higher non-HDL
Fasting Lipid Profiles in Individuals in the General Population
cholesterol was 1.72 (95% confidence interval [CI]:
Copenhagen General Population Study 1.51 to 1.95) in 20 studies combined using nonfasting
N = 92,285 lipid profiles and including 103,354 subjects, of whom
mmol/L mg/dL
3,829 had an event, whereas the corresponding value
Triglycerides +0.3 +26
in 48 studies combined using fasting lipid profiles in
Total cholesterol –0.2 –8 199,076 subjects, of whom 8,956 had an event, was
1.41 (95% CI: 1.30 to 1.53) (51). Similarly, 3 large ran-
LDL cholesterol –0.2 –8
domized trials of statin therapy used nonfasting lipid
Remnant cholesterol +0.2 +8 profiles (5).
NonHDL cholesterol –0.2 –8 The pros and the new evidence for using random,
nonfasting lipid profiles reflect that many new
Lipoprotein(a) No change
guidelines and consensus statements endorse non-
Apolipoprotein B No change fasting lipid profiles for most patients (3–9,11,12),
whereas a few older guidelines still recommend
HDL cholesterol No change
fasting lipid profiles for most patients (Central
Apolipoprotein A1 No change Illustration) (29).
IMPLICATIONS FOR THE PATIENT. From the
Decreased Increased
Maximal Change After Normal Food Intake perspective of the patient, a random, nonfasting lipid
profile is practical compared with a fasting lipid pro-
file because it does not interfere with the patient’s
These changes all are clinically insignificant. Adapted with
permission from Nordestgaard et al. (5). Abbreviations as in normal life and allows going to the laboratory for the
Figures 2 and 3. blood draw at any time of the day (Central
Illustration). Nonfasting sampling will also be safe,
JACC VOL. 70, NO. 13, 2017 Nordestgaard 1643
SEPTEMBER 26, 2017:1637–46 Lipid Profile, Fasting Versus Nonfasting
Direct comparison of arguments for and against use of random, nonfasting, and fasting blood sampling. Nonfasting blood sampling can occur anytime during the 24-h
cycle, irrespective of what and when the individual ate before blood sampling. By contrast, a fasting blood sample can only be drawn after a period without food
intake for 8 or more hours, which often means that a natural small fast of a few hours in the early morning will be extended, possibly until noon, before the blood is
drawn.
time, being perfectly fine clinically, and maybe IMPLICATIONS FOR THERAPEUTIC OPTIONS. Because
focus less on exactly how standardly and precisely statin therapy (and other lipid-lowering therapy)
we can measure an analyte (50). In addition, use is decided on the basis of an individual’s global
of nonfasting lipid profiles will improve patient flow cardiovascular risk, including the presence of car-
in laboratories, as it eliminates large numbers of diovascular disease, familial hypercholesterolemia,
people all coming for blood draws early in the and diabetes, and not just on plasma lipid values in
morning. all major guidelines (4,6,7,11,12,29), minor changes in
JACC VOL. 70, NO. 13, 2017 Nordestgaard 1645
SEPTEMBER 26, 2017:1637–46 Lipid Profile, Fasting Versus Nonfasting
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