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Short Communication
Volume 46 - No.4:January 2002 index
 

Indian J Physiol Pharmacol 2002;46 (4);

The Effect of Ingestion of Egg on Serum Lipid Profile in Healthy Young Free-Living Subjects
GAYATRI CHAKRABARTY, R. L. BIJLANI*, S. C. MAHAPATRA, NALIN MEHTA, R. LAKSHMY**, SUMAN VASHISHT** AND S. C. MANCHANDA**
Departments of Physiology and **Cardiology,
All India Institute of Medical Sciences,
New Delhi – 110 029
*Corresponding Author (e-mail: rambij@medinst.ernet.in)
(Received on April 22, 2002)

 

Abstract: Egg is a major source of dietary cholesterol. Previous studies on the effect of egg on serum lipid profile have given conflicting results. Further, the serum lipid response to egg shows marked individual variation. Since the variation is at least partly genetically determined, and the response depends partly on the overall diet, studies on different ethnic groups are important. There is hardly any study on the subject available on Indians. In the present investigation, eighteen healthy young volunteers (7 male, 11 female) on a lacto-vegetarian diet were given one boiled egg per day for 8 wk in a randomized controlled cross-over study. Compared to the values obtained after 8 wk of egg-free period, the mean serum total cholesterol, LDL cholesterol, HDL cholesterol, total cholesterol/HDL ratio, VLDL cholesterol and triglycerides were not significantly different after 8 wk of egg consumption. However, the serum total cholesterol after 4 wk of egg consumption was significantly higher than the control values. Further, seven subjects out of 18 had an appreciable elevation of serum total cholesterol or LDL cholesterol, or both, after 8 wk of egg consumption. The study suggests that in young healthy Indian subjects on a vegetarian diet, consuming one egg per day raises serum cholesterol levels at 4 wk but in the majority baseline values are restored by 8 wk. However, some hyper-responders continue to have elevated serum cholesterol even at 8 wk but in the majority baseline values are restored by 8 wk. Knowing the response of an individual may be important before making egg consumption a regular habit.

 

Key words: egg,dietary,cholesterol, cholesterol                    lipoproteins,                   atherosclerosis




Introduction
Methods
Results
Discussion
Reference



INTRODUCTION

An important feature of egg which is of interest to nutritionists and medical scientists is its high cholesterol content. High dietary intake of cholesterol has a reasonably predictable effect on serum cholesterol. Attempts have been made to express the relationship in quantitative terms in the form of equations (1-3). However, the body needs cholesterol for metabolic functions, and the requirements of the body are met by supplementing dietary cholesterol with endogenous cholesterol synthesis. In view of this, the National Cholesterol Education Program of the U.S.A. allows up to 300 mg dietary cholesterol per day in the Step I diet (4). Further, the endogenous synthesis of cholesterol is regulated to maintain cholesterol homeostasis (5). That is possibly one reason why the effects of feeding cholesterol as such, or in the form of egg, have not been consistent. Although many studies have shown a positive relationship between dietary and serum cholesterol (5-8), some studies have shown no cholesterolaemic response to dietary cholesterol (9-11). Several epidemiological studies have also found no relationship between egg consumption and serum cholesterol or coronary heart disease (12-13). In a meta-analysis of 17 studies, Weggemans et al found that 100 mg of additional dietary cholesterol raises both serum cholesterol and HDL cholesterol such that there is an increase in the ratio of total to HDL cholesterol ratio by 0.02. Hence they concluded that the advice to limit the consumption of eggs is still valid (14). However, it is difficult to describe the effect to dietary cholesterol in general terms on the basis of averages because of a marked individual variation in response (15) which is at least partly genetically determined (16). In view of this, observations made on one ethnic group cannot be extrapolated to other groups, who may be genetically different. We have come across no experimental study on the effect of consumption of eggs on the Indian population. Studies on Indians are important not only because we may be genetically different from the Western populations, on whom most of the previous studies have been done, but also because of other relevant reasons. Indians have a relatively high incidence of coronary artery disease (CAD), and the disease in Indians is premature and extensive (17). The risk factors for CAD are also somewhat different for Indians because of their predilection for insulin résistance syndrome (18). Finally, the Indian diet is typically a vegetarian, high carbohydrate, low fat diet. In such a diet, the only major potential source of cholesterol is the egg. The cholesterol content of one egg (about 250 mg) is within the permissible limit of 300 mg (4). Therefore the effect of egg consumption needs to be examined against the background of the genetic and dietary profile of Indians.
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METHODS

Subjects

The study was conducted on 18 healthy adult volunteers (7 male, 11 female). The subjects were normolipidaemic, and none of the subjects smoked or used alcohol. 

Experimental design

The study was conducted in the form of a randomized controlled trial with a cross-over design. The study started with a lead-in period of 2 wk, during which the subjects were requested to consume a relatively constant egg-free lacto-vegetarian diet, to make no changes in the cooking medium, to avoid baked foods (because they may contain eggs), and to maintain a relatively constant physical activity.

After the lead-in period of 2 wk, the subjects were randomly divided into two groups, group I (n = 8; 4 female; 4 lactovegetarians, 3 lacto-ovo-vegetarians, 1 non-vegetarian) and Group II (n = 10; 3 male, 7 female; 5 lactovegetarians, 3 lacto-ovo-vegetarian) and Group II (n = 10; 3 male, 7 female; 5 lactovegetarians, 3 lacto-ovo-vegetarians, 2 non-vegetarian). Group I consumed for 8 wk one boiled egg every day but otherwise the diet continued to be as during the lead-in period (experimental treatment). Group II consumed for 8 wk a diet similar to that during the lead-in period (control). At the end of the 8-wk dietary period, the two groups crossed over for a period of 8 wk (Fig. 1).

Fig.1

click for full view

Fasting blood samples were collected at the beginning of the lead-in-period (2 wk), the end of the lead-in period (0 wk), 4 wk, 8 wk, 12 wk and 16 wk.

The protocol of the study was approved by the Ethics Committee of the All India Institute of Medical Sciences, and the volunteers gave their informed written consent for participation in the study.

Diet

When required by the study, the subjects had the boiled egg at any meal of the day, usually at lunch. The eggs provided to the subjects weighted about 50 g each, and their composition was as shown in Table I. The subjects maintained a report card in which they made a daily entry regarding taking, or not taking, the egg, and also recorded any major changes in their diet or physical activity.

TABLE I: Composition of the eggs used in the study.

Constituent

Amount

 

 

Protein (g/100 g egg)

10.4

Carbohydrate (g/100 g egg)

2.76

Fat (g/100 g egg)

11.62

Saturated fatty acids (%)

32.62

Monounsaturated fatty acids (%)

45.70

n-6 Polyunsaturated fatty acids (%)

45.56

 

n-3 Polyunsaturated fatty acids (%)

0.29

Cholesterol (g/100 g egg)

600.00

Energy (kcal/100 g egg)

155.78

Measurements

Serum lipid profile was assessed from the mean of values obtained on two consecutive days. The measurements included total cholesterol, total triglycerides, HDL cholesterol and LDL cholesterol, which were estimated using kits from Randox Laboratories Ltd., Ardmore, U.K. Briefly, cholesterol or triglycerides in the sample were oxidized enzymatically releasing hydrogen peroxide. Hydrogen peroxide, in the presence of peroxidase interacts with 4-cholorophenol and 4-aminoantipyrene to yield quinoneimine, which can be measured calorimetrically from absorbance at 546 nm. HDL cholesterol was measured after precipitating LDL and VLDL by addition of phosphototungstic acid in the presence of magnesium ions. LDL was measured after precipitating it with heparin at pH 5.04. The inter-assay and within-assay variations were respectively 6.98% and 3.64% for cholesterol, 13.85% and 3.02% for triglycerides, 11.77% and 2.74% for HDL. VLDL cholesterol and total cholesterol: HDL cholesterol ratio were calculated from the above measurements.

Statistical analysis

The values of all outcome measures at –2 wk, 0 wk, 4 wk, 8 wk, 12 wk and 16 wk were first tabulated for the two groups separately. There was no period effect on any of the parameters studies. Therefore pooling the results from the two groups was considered valid. Then the 16 wk values of Group I and 8 wk values of Group II were pooled to get the control (no egg) values. This was considered appropriate because these were the values based on antecedent egg-free diet for 8 wk in Group I and for 10 wk in Group II. The 8 wk values of Group I and 16 wk values of Group II were pooled to get the effect of the egg treatment for 8 wk (fig. 1). The ‘no egg’ values were compared with ‘egg values’ by Student’s t-test for paired observations. Similar pooling and comparisons were also done for ‘no egg’ treatment with 4 wk of ‘egg’ treatment to see the time course of changes, if any. A comparison was also made to see the changes, if any, during the lead-in period. Since 0 wk values were compared with 4 wk as well as 8 wk values by Student’s t-test, differences were considered significant if P<0.05/2, i.e. P<0.025, using Bon Ferroni’s correction (19).
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RESULTS

The characteristics of subjects are given in Table II. There was no significant difference between the subjects in the two groups with respect to the characteristics shown in the Table as well as in terms of the serum lipid profile. As observed in the table, the cholesterol intake increased by 300 mg/d during the experimental (egg) period as compared to the control period.

TABLE II : Characteristics of subjects.

 

Group I

Group II

 

 

 

Age (years)

24.0±5.71

23.7±2.26

Weight (kg)

 

 

At –2 wk

57.31±7.95

55.70±6.15

At 16 wk

57.38±7.23

55.55±6.12

Height (m

 

 

BMI (kg/m2)

 

 

At – 2 wk

20.68±1.26

20.73±1.81

At 16 wk

20.73±1.23

20.06±2.13

Haemoglobin (g/100 mL)

11.78±1.23

12.06±2.13

Fasting plasma

 

 

Glucose (mg/100 mL)

96.61±5.61

86.02±9.82

Cholesterol intake (mg/d)

 

 

Control period

50.97±35.42

48.95±26.32

Egg period

350.97±35.42

348.95±26.32

All values are mean ± S. D

TABLE III: Serum lipid profile after control and experimental treatment.

Parameter

After control

(egg-free diet) treatment

After experimental

(egg consumption) treatment

 

 

4 wk

8 wk

Total cholesterol (mg/dL)

175.99±29.27

186.05±29.28

184.77±31.22

LDL cholesterol mg/dL)

94.18±36.63

98.66±24.80

100.18±29.77

HDL cholesterol (mg/dL)

60.63±8.03

60.20±5.87

57.89±9.09

Total cholesterol/HDL cholesterol ratio

2.97±0.71

3.14±0.74

3.28±0.80

VLDL cholesterol (mg/dL)

24.82±8.02

27.78±10.02

28.29±7.48

Triglycerides (mg/dL)

104.99±27.78

113.44±32.32

114.23±30.54

All values are Mean ± S. D

*P<0.025

Egg was the major source of dietary cholesterol during the experimental period, and milk and milk products its only source during the control period. There was no significant change in body weight or body mass indeed (BMI) during the course of the study.

Since there was no period effect on any of the parameters studied, the results from the two groups were pooled. The lipid profile at the end of the control (egg-free) dietary period and that after 4 wk and 8 wk of experimental treatment (egg consumption) has been shown in Table III. Serum total cholesterol after 4 wk of egg consumption was significantly higher than the control value. No other value after 4 wk or 8 wk of egg consumption from the corresponding control value.

Scrutiny of individual responses revealed that four of the subjects had a considerable increase in serum total cholesterol, ranging from + 19.3% to +34.6% and five of the subjects had a rise in serum LDL cholesterol ranging from + 13.0% to + 72.8% after 8 wk of egg consumption. Two subjects were common to these groups. Thus seven subjects out of 18 (38.9%) had an appreciable rise in total cholesterol or LDL cholesterol, or both, after 8 wk of egg consumption.
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DISCUSSION

In the present study, consumption of one boiled egg per day for 8 wk led to a serum lipid profile not significantly different from that resulting from consumption of an egg-free diet for 8 wk. Lack of effect of egg consumption is consistent with several previous studies on populations with various ethnic backgrounds (9-11). However, there are also several studies in which an increase in dietary cholesterol intake through egg consumption or otherwise has led to an increase in serum cholesterol (6-8). This may be partly related to the amount of dietary cholesterol. Some of the studies in which a positive relationship has been observed between dietary cholesterol and serum cholesterol have given 600-1500 mg dietary cholesterol per day (5, 20). An even more important factor responsible for the conflicting results from various studies seems to be the duration of the study. In general, studies based on 4 wk or less of egg consumption have shown an increase in serum cholesterol (5-8, 20) whereas longer studies involving 8 wk or more of egg consumption failed to find any significant rise in serum cholesterol (9-11). Our dietary period was 8 wk but we studied serum lipids also at the mid-point of the dietary period. We also observed a significant rise in total serum cholesterol at 4 wk. Thus it seems that the homeostatic mechanisms which regulate cholesterol biosynthesis in response in changes in dietary cholesterol intake (5) take about 8 wk to be fully effective.

Although the average serum cholesterol level did not show any significant change after 8 wk of egg consumption, we observed considerable individual variation in response. The phenomenon of hypo- and hyper-responders is well known (15), and seems to have a genetic basis (16).

Our study has been done on healthy young volunteers on a vegetarian diet. Similar studies on Indian populations are required also on older hyperlipidaemic subjects whose dietary pattern may be different. Therefore the present study itself cannot be used for making general recommendations. But it suggests that, like other populations, Indians also show marked individual variations in response. Ascertaining the response of an individual to egg consumption is therefore important before making egg a regular item of the diet.

ACKNOWLEDGEMENTS

We could like to thank the Indian Council of Medical Research for financial support (ID No. 2000-00460). We are grateful to the volunteers for their cooperation. Ms. Promila Kapoor and Ms. Suman Thakur provided able technical assistance, and Mr. Satish Sachdeva provided efficient secretarial assistance.
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