|Year : 2017 | Volume
| Issue : 2 | Page : 614-618
Comparison between fasting and nonfasting lipid profile in patients receiving treatment with statin therapy
Walaa F Abdel-Aziza1, Ghada M Soltana1, Ahmed M Ahmed Amer2
1 Cardiology Department, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Cardiology Department, Om El-Masryeen Hospital, Giza, Egypt
|Date of Submission||10-May-2016|
|Date of Acceptance||03-Jul-2016|
|Date of Web Publication||25-Sep-2017|
Ahmed M Ahmed Amer
43 El Araby El-tantawy St, Algomhoria, Almahallah Al-kubra, Gharbia, 31951
Source of Support: None, Conflict of Interest: None
The aim of this study was to assess the effect of ordinary meal on the lipid profile of patients receiving statin therapy.
The lipid profile is an essential investigation for the patient who comes to cardiology outpatient clinic. Numerous guidelines recommend sampling in the fasting state for cardiovascular risk assessment. Fasting for 12–14 h is not only cumbersome and unpleasant for patients, but may result in limited compliance to disease monitoring and treatment.
Patients and methods
This study was performed on 100 patients with dyslipidemia receiving statin therapy whose doses had not changed for 2 or more months (group I), and 100 patients with dyslipidemia not receiving statin therapy (group II). Lipid profile was determined for fasting and postprandial statuses.
The lipid profile parameters in both groups in fasting and postprandial statuses were compared. In group I, the mean fasting serum triglyceride level was 176.21 mg/dl and mean postprandial serum triglyceride level was 213.49 mg/dl (P = 0.0001); the mean fasting low-density lipoprotein (LDL) level was 161.19 mg/dl and mean postprandial LDL was 159.25 mg/dl (P = 0.184). In group II, the mean fasting serum triglyceride level was 231.06 mg/dl and mean postprandial triglyceride level was 284.60 mg/dl (P = 0.005); the mean fasting LDL was 185.18 mg/dl and mean postprandial LDL was 181.32 mg/dl (P = 0.871).
Finally, from this study we found that there is no significant clinical difference between fasting and nonfasting levels of total cholesterol, high-density lipoprotein, and LDL. Thus, we can use the nonfasting tests to follow-up the dyslipidemic patients.
Keywords: cholesterol, high-density lipoprotein, low-density lipoprotein nonfasting cholesterol, nonfasting lipid profile, nonfasting high-density lipoprotein, nonfasting low-density lipoprotein, nonfasting triglyceride, triglyceride
|How to cite this article:|
Abdel-Aziza WF, Soltana GM, Ahmed Amer AM. Comparison between fasting and nonfasting lipid profile in patients receiving treatment with statin therapy. Menoufia Med J 2017;30:614-8
|How to cite this URL:|
Abdel-Aziza WF, Soltana GM, Ahmed Amer AM. Comparison between fasting and nonfasting lipid profile in patients receiving treatment with statin therapy. Menoufia Med J [serial online] 2017 [cited 2019 Aug 24];30:614-8. Available from: http://www.mmj.eg.net/text.asp?2017/30/2/614/215443
| Introduction|| |
Serum lipid profile is an essential investigation for the patient who comes to cardiology outpatient clinic. Numerous guidelines recommend sampling in the fasting state for cardiovascular risk assessment as the levels of triglycerides vary greatly in the nonfasting state. Furthermore, the low-density lipoprotein (LDL) levels, calculated using the Friedewald equation: LDL-cholesterol = total cholesterol−[HDL-cholesterol+(triglycerides/5)] may be underestimated if fasting triglyceride levels are not used .
Many of the risk factors such as age, male, sex, and race cannot be changed (nonmodifiable cardiovascular risk factors), whereas tobacco smoking, diabetes mellitus, high blood cholesterol, high blood pressure, obesity, and physical activity are examples for modifiable cardiovascular risk factors .
Screening for lipid disorders presents unique challenges. Most patients will not have fasted before a routine physician office visit. Therefore, most fasting lipid panels must be either planned before visits or checked at subsequent office visits or additional visits to outpatient phlebotomy centers ,.
Fasting for 12–14 h (and definitely more than 8 h) is not only cumbersome and unpleasant for patients, but may result in limited compliance to disease monitoring and treatment. This may expose at-risk patients to increased risk for adverse cardiovascular outcomes .
Researchers have suggested that, for the majority of people who consume an average-size meal, the overall lipid profiles will have minimal postprandial change . In addition, some research studies in adult patients have suggested that abnormal postprandial triglyceride levels might actually be more highly associated with cardiovascular disease compared with abnormal fasting levels ,.
In our study, we will discuss the difference between the lipid parameters [total cholesterol, triglycerides, high-density lipoprotein (HDL), and LDL] in both fasting and postprandial statuses.
| Patients and Methods|| |
This prospective study was conducted on 200 patients from a cardiology department outpatient clinic of Faculty of Medicine (Menoufia University) from August 2014 to February 2016. The patients were divided into two groups.
Group I comprised 100 patients with dyslipidemia receiving statin therapy whose doses had not changed for 2 or more months.
Group II included 100 patients with dyslipidemia not receiving statin therapy.
All individuals included in the study were subjected to the following:
- Full history taking was carried out with special reference to the risk factors for heart diseases and sudden cardiac death
- Personal history as regards name, age, sex, residence, special habits of medical importance, such as smoking, diabetes mellitus, systemic arterial hypertension, previous ischemic events, and also family history was taken
- Clinical examination was performed for all patients, including general examination, vital signs (blood pressure and pulse) and obesity, which was measured in the clinic using BMI equation (kg/m 2), and local cardiac examination
- In addition, laboratory investigation was carried out. A venous blood sample was taken in the morning after 12 h overnight fasting and another sample was taken after breakfast meal by 2 h to make a comparison for lipid parameters levels in both statuses.
Serum cholesterol, triglycerides, HDL, and LDL were measured using Synchron CX4 clinical system Beckman Coulter Inc., Brea, CA (standard clinical laboratory methods).
Mean (±SD), frequencies (number of cases), and relative frequencies (percentages) were used when appropriate. For comparing categorical data, the paired samples t-test was performed. All tests were two-tailed; a P value less than 0.05 was considered significant and 95% confidence interval was calculated for each plot. Statistical calculations were performed using SPSS (Statistical Package for the Social Sciences; SPSS Inc., Chicago, Illinois, USA) version 17 for Microsoft Windows .
| Results|| |
We compared the lipid profile parameters in dyslipidemic patients receiving statin therapy (group I) and dyslipidemic patients not receiving statin therapy (group II) in both fasting and postprandial statuses.
In group I, the mean level of serum cholesterol (242.018 vs. 237.92 mg/dl; P = 0.202), LDL (161.19 vs. 159.25 mg/dl; P = 0.184), and HDL (45.96 vs. 45.84 mg/dl; P = 0.153) was not significantly different in both fasting and nonfasting states, but the mean serum concentration of triglycerides (176.21 vs. 213.49 mg/dl; P = 0.002) was significantly higher in nonfasting than in fasting state [Table 1] and [Figure 1].
|Table 1: Comparison between laboratory findings of the lipid parameters in fasting and postprandial status in patients in group I|
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|Figure 1: Lipid parameters in fasting and postprandial statuses in dyslipidemic patients with statin treatment (group I).|
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In group II, we found that the mean level of serum cholesterol (272.88 vs. 269.08 mg/dl; P = 0.523), LDL (185.18 vs. 181.32 mg/dl; P = 0.871), and HDL (41.73 vs. 41.92 mg/dl; P = 0.238) was not significantly different in both fasting and nonfasting states, but the mean serum concentration of triglycerides (231.06 vs. 284.60 mg/dl; P = 0.005) was significantly higher in the nonfasting than in the fasting state [Table 2] and [Figure 2].
|Table 2: Comparison between laboratory findings of the lipid parameters in fasting and postprandial status in patients in group II|
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|Figure 2: Lipid parameters in fasting and postprandial statuses in dyslipidemic patients not receiving statin therapy (group II).|
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| Discussion|| |
Hyperlipidemia is a risk factor for cardiovascular disease, and fasting lipoprotein measurements, according to ATP III recommendation guidelines, is currently considered the standard of care when assessing a patient's lipid profile. In a clinical setting, this creates an inconvenience for patients and providers alike. However, recent studies have raised doubt as to the need to measure fasting lipids, thus changing clinical practice ,.
The studies in this review directly compared fasting versus nonfasting lipid concentrations as a risk factor for cardiovascular prediction . Some studies focused specifically on triglyceride concentration ,, whereas Mora et al.  and Langsted et al.  included all fractions of a clinically available lipid panel.
On comparison of lipid profile parameters in our study in dyslipidemic patients in both fasting and postprandial statuses, the mean level of serum cholesterol (242.018 vs. 237.92 mg/dl), LDL (161.19 vs. 159.25 mg/dl), and HDL (45.96 vs. 45.84 mg/dl) was not significantly different in both statuses, but the mean serum concentration of triglycerides (176.21 vs. 213.49 mg/dl) was significantly higher in the nonfasting than in the fasting state.
In our study, we noticed that the mean difference in serum total cholesterol decreased by 4.1 mg/dl, the mean difference in serum LDL decreased by 2.66 mg/dl, and the mean difference in serum HDL levels reduced by 0.12 mg/dl. However, serum triglycerides increased in postprandial state by 37.28 mg/dl when compared with fasting state in dyslipidemic patients receiving statin therapy. These results are in agreement with those of Langsted et al. , who stated that the maximum changes in lipid parameter levels after normal food and fluid intake from the fasting status were − 0.2 mmol/l (−7.73 mg/dl) for serum total cholesterol, −0.2 mmol/l (−7.73 mg/dl) for serum LDL, and − 0.1 mmol/l (−3.87 mg/dl) for serum HDL and increased by 0.3 mmol/l (26.57 mg/dl) for serum triglycerides. Therefore, they explained that the increased triglycerides and decreased HDL cholesterol was in response to normal food intake even after the correction for albumin levels and thus correction for hemodilution due to fluid intake. Therefore, the changes in these levels are most likely due to food intake rather than fluid intake. Thus, there was no significant clinical difference between fasting and nonfasting levels of total cholesterol, HDL, and LDL.
Although the increases in triglycerides by 0.3 mmol/l (26.57 mg/dl) are likely attributable directly to fat intake, the parallel reduction in HDL-***cholesterol by − 0.1 mmol/l (−3.87 mg/dl) is likely due to bidirectional lipid exchange between triglyceride-rich lipoproteins and HDL particles. Lipid transfer proteins mediate the transfer of triglycerides from triglyceride-rich lipoproteins to HDL, with a back-transfer of cholesteryl ester from HDL to triglyceride-rich lipoproteins .
This is in accordance with the findings of Lund et al.  as well as regards the decrement in LDL***-cholesterol level; they showed that the levels of LDL-cholesterol were lower in the nonfasting than in the fasting status by about 7.35 mg/dl, using the direct method measurement of LDL cholesterol.
In our study, we found a difference between fasting and nonfasting lipid concentrations. The mean level of total cholesterol, as well as LDL-cholesterol (161.19 vs. 159.25 mg/dl) and HDL (45.96 vs. 45.84 mg/dl), was decreased in nonfasting status in comparison with the fasting status (242.018 vs. 237.92 mg/dl). However, there was an increase in the triglyceride level in the nonfasting status compared with the fasting status (176.21 vs. 213.49 mg/dl). These results are in agreement with those of Mora et al. , which were based on the difference between the fasting and the nonfasting lipid concentrations; they found that the mean level of total cholesterol was decreased in nonfasting status in comparison with the fasting status (209 vs. 206 mg/dl). Moreover, LDL-cholesterol (123 vs. 117 mg/dl) and HDL-cholesterol were not changed in both statuses, but triglyceride level did not show an increment in the nonfasting status compared with the fasting status (115 vs. 133 mg/dl). These results are in agreement with our study results.
However, our results were contradictory to the findings of Sidhu and Naugler , which included about 209 180 individuals who showed minimal changes in total cholesterol and HDL-cholesterol in postprandial status than in fasting one, but showed a greater variation in LDL-cholesterol by 10% in general population and by 20% in triglyceride levels. This may be due to the larger sample size than ours. Despite these results, they finally concluded that the fasting time showed little association with lipid subclass levels in a community-based population, which suggests that fasting for routine lipid levels is largely unnecessary.
Nordestgaard et al.  favored the use of nonfasting rather than fasting lipid measurements. Moreover, the fact that lipid profiles change minimally mostly in response to typical food intakes favors the use of nonfasting lipid measurements ,. On the basis of such evidence, hospitals in Copenhagen and elsewhere in Denmark now use nonfasting lipid profiles as the standard and suggest a repeat fasting triglyceride measurement only if nonfasting concentrations exceed 4 mmol/l (352 mg/dl) .
From this study, we also noticed a difference between the mean levels of lipid concentration in all studied groups for both fasting and postprandial statuses, as the mean levels of total cholesterol, LDL, and triglycerides were higher in dyslipidemic patients not under antidyslipidemic medication than the dyslipidemic patients receiving statin therapy. On comparison of the mean difference in lipid parameters for both groups, we found that total cholesterol (fasting status, 30.87 mg/dl; postprandial, 31.16 mg/dl), LDL (fasting status, 23.99 mg/dl; postprandial, 22.07 mg/dl), and triglyceride (fasting status, 54.85 mg/dl; postprandial, 71.11 mg/dl) were greater in patients not under antidyslipidemic therapy, whereas HDL decreased (fasting status, −4.23 mg/dl; postprandial, −3.92 mg/dl).
These results are in accordance with those of Collins et al. , who showed the blood lipid differences between those administered simvastatin and those administered placebo, with an average difference in LDL-cholesterol during the study of 1·3 mmol/l (50.27 mg/dl) being produced in statin use [whereas the actual use of 40 mg simvastatin daily would reduce LDL-cholesterol by an average of about 1·5 mmol/l (58.01 mg/dl) in this population]. The difference in total cholesterol was 1.7 mmol/l (65.74 mg/dl), and that in triglyceride was 0.4 mmol/l (35.43 mg/dl), whereas HDL-cholesterol was raised by 0.02 mmol/l (0.77 mg/dl).
Finally, from this study we found that there was no significant clinical difference between fasting and nonfasting levels of total cholesterol, HDL, and LDL. Therefore, we can use the nonfasting tests to follow-up dyslipidemic patients.
The limitations of our study were that the samples were obtained from a relatively small portion of patients with hyperlipidemia; therefore, the results demonstrated in this study may not be exactly the same as those in the entire population with hyperlipidemia. This requires a prospective study and follow-up for an adequate period of time. A larger population of hyperlipidemia patients will also be necessary to assess whether such abnormalities of cardiovascular events might be useful from a prognostic point of view. This research needs to be applied several times after meal intake (2, 4, and 6 h).
| Conclusion|| |
We found that there is no significant clinical difference between fasting and nonfasting levels of total cholesterol, HDL, and LDL. Thus, we can use the nonfasting tests to follow-up the dyslipidemic patients.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Baibata D, Ionescu G, Petcov B, Mancas S. Non-high-density lipoproteins cholesterol and cardio-metabolic risk. Maedica Buchar 2015; 10:33–38.
Reda AA, Walaa FA, Rehab IY, Mohammed M, Elsawaf G. Risk factor profile and in-hospital complications in patients admitted with acute coronary syndrome in Menoufia Governorate. Menoufia Med J 2014; 27:342–346. [Full text]
Devaney BL, Gordon AR, Burghardt JA. Dietary intakes of students. Am J Clin Nutr 1995; 61(Suppl): 205S–212S.
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; 106:3143–3421.
Nigam PK. Serum lipid profile: fasting or non-fasting? Indian J Clin Biochem 2011; 26:96–97.
Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, Ridker PM. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA 2007; 298:309–316.
Nordestgaard 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; 298:299–308.
Knapp RG, Miller MC. Clinical epidemiology and biostatistics. National Medical Series (NMS) from Williams and Wilkins. Baltimore 1992; 3:34.
Atar IA, Atar I, Aydınalp A, Ertan C, Bozbaş H, Ozin B, et al.
Is there any relationship between coronary artery disease and postprandial triglyceride levels?. Anadolu Kardiyol Derg 2011; 11:201–206.
Sidhu D, Naugler C. Fasting time and lipid levels in a community-based population: a cross-sectional study. Arch Intern Med 2012; 172:1707–1710.
Eberly LE, Stamler J, Neaton JD. Relation of triglyceride levels, fasting and nonfasting, to fatal and nonfatal coronary heart disease. Arch Intern Med 2003; 163:1077–1083.
Mora S, Rifai N, Buring JE, Ridker PM. Fasting compared with nonfasting lipids and apolipoproteins for predicting incident cardiovascular events. Circulation 2008; 118:993–1001.
Langsted A, Freiberg JJ, Nordestgaard BG. Fasting and nonfasting lipid levels: influence of normal food intake on lipids, lipoproteins, apolipoproteins, and cardiovascular risk prediction. Circulation 2008; 118:2047–2056.
Zilversmit DB. Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins. Clin Chem 1995; 41:153–158.
Lund SS, Petersen M, Frandsen M, Smidt UM, Parving HH, Vaag AA, Jensen T. Agreement between fasting and postprandial LDL-cholesterol measured with 3 methods in patients with type 2 diabetes mellitus. Clin Chem 2011; 57:298–308.
Nordestgaard BG, Langsted A, Freiberg JJ. Nonfasting hyperlipidemia and cardiovascular disease. Curr Drug Targets 2009; 10:328–335.
Nordestgaard BG, Benn M. Fasting and nonfasting LDL cholesterol: to measure or calculate?. Clin Chem 2009; 55:845–847.
Collins R, Armitage J, Parish S, Sleigh P, Peto R. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet 2002; 360:7–22.
[Figure 1], [Figure 2]
[Table 1], [Table 2]