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The Journal of Nutrition Vol. 127 No. 3 March 1997, pp. 509S-513S
Copyright ©1997 by the American Society for Nutritional Sciences

Nonhypercholesterolemic Effects of a Palm Oil Diet in Chinese Adults1,2,3

Jian Zhang, Wang Ping, Wang Chunrong, Chen Xiao Shou, and Ge Keyou4

Institute of Nutrition and Food Hygiene, Chinese Academy of Preventive Medicine, Beijing 100050, China

ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
FOOTNOTES
LITERATURE CITED


ABSTRACT

The effects on serum lipids of palm oil (PA) used in Chinese diets were compared with those of soybean oil (SO), peanut oil (PE) and lard (LA) in normocholesterolemic subjects and with that of PE in hypercholesterolemic subjects. Normocholesterolemic subjects [120 men, 18-25 y, total cholesterol (TC) 2.8-5.0 mmol/L] were assigned to four groups to consume test diets for six consecutive weeks after a run-in period of 3 wk. About 30% of dietary energy was derived from fat, 75-80% of which came from test oils. In comparison with the entry level, the average serum TC and LDL cholesterol (LDL-C) were 6.7 and 13.1% lower, respectively, in the PA group and 22.8 and 30.7% higher, respectively, (P < 0.05) in the LA group. At the end of the test, serum TC, LDL-C and the ratio of TC/HDL cholesterol (HDL-C) in the PA group were significantly lower than those of the LA group. Hypercholesterolemic subjects (31 men, 20 women, 32-68 y, TC 5.5-7.0 mmol/L) were divided into two groups. For 6 wk, one group (15 men, 10 women) consumed the PA diet; another group (16 men, 9 women) consumed the PE diet. After a 3-wk interval, the two groups interchanged diets for another 6 wk. The test diets again contained about 30% energy from fat, 60-65% of which came from test oils. Compared with entry values, the PA diet caused significant reductions in serum TC, LDL-C and TC/HDL-C during the first 6 wk and also a significant reduction in TC/HDL-C during the second 6 wk. The PE diet had no significant influence on serum lipids in either experimental period.

Key words: palm oil, serum cholesterol, humans.


INTRODUCTION

Cardiovascular disease5 (CVD) is the leading cause of death in developed countries, and the rate of mortality from CVD is increasing rapidly in China (Beaglehole et al. 1988, Goldbourt et al. 1985, Kannel et al. 1977, Mannien et al. 1988.) Elevated concentrations of plasma total cholesterol (TC) and LDL cholesterol (LDL-C) have proved to be among the risk factors in the development of CVD (Stamler et al. 1986). Dietary fat plays an important role in influencing blood lipid concentrations, thrombotic tendency and thus the onset of CVD (Hetzel et al. 1989, Keys et al. 1986). It is generally believed that diets high in saturated fatty acids increase serum TC and LDL-C and thus increase the risk of cardiovascular disease.

Palm oil represents the second largest volume of vegetable oil produced in the world. It is highly saturated and contains nearly 50% palmitic acid. Thus, Keys et al. (1965) considered palm oil a hypercholesterolemic oil. But this extrapolation of the Keys-Anderson equation about palm oil was not based on actual experimental studies. In fact, some studies in animals and humans have indicated that palm oil is quite different from other hypercholesterolemic fats such as lard or coconut oil (Hornstra and Sundram 1991, Ng et al. 1991, Sundram et al. 1990). Thus, well-controlled studies are required to investigate the effects of palm oil and its relation to cardiovascular disease.

Although the consumption of palm oil in China has increased rapidly in recent years (Fan and Chen 1994), information about the relation of palm oil to health is limited. Few studies relating palm oil intake to human health have appeared in China. A few papers have shown that palm oil could maintain the normal growth of rats and cause a significant reduction of serum cholesterol in rabbits compared with lard (Chen and Fan 1992). Therefore, it is very important to observe the effect of palm oil on serum lipids and the risk of cardiovascular disease.

This investigation includes two experiments, one in normal cholesterolemic subjects and one in mildly hypercholesterolemic subjects. Its purpose is to present more knowledge about the effects of palm oil on serum lipids, using Chinese diets as a basis.

See Table 2 for abbreviations.


SUBJECTS AND METHODS

Experiment I

Subjects. Healthy male subjects were screened using biochemical assays, physical examinations, and questionnaires for family medical history and individual dietary habits. Finally, 120 normocholesterolemic subjects (between 18 and 25 y of age) were selected, based on the following inclusion criteria: 1) serum TC concentration ranging from 2.8 to 5.0 mmol/L; 2) free from diabetic, cardiac, hepatic, renal or bleeding disorders; 3) not using any cholesterol-altering medications; 4) nonsmoking; and 5) body mass index between 18.5 and 25 kg/m2.

Experiment design. Palm oil (PA), soybean oil (SO), lard (LA) and peanut oil (PE) were used as test oils. The 120 subjects were randomly assigned to one of the four groups consuming the test diets for six consecutive weeks after a run-in period of 3 wk. Fasting blood samples were taken at the beginning and the end of the test period and assayed for serum triglycerides (TG), TC and HDL cholesterol (HDL-C) determination.

Diets. Experimental diets included cereals, lean pork and chicken, bean curd and green vegetables. The menu was developed around the subjects' preferences, and daily meals were prepared in the nornmal manner by a local cook under the direction of professionals to meet the experimental requirements. Refined, bleached, deodorized (RBD) palm oil was purchased from the Brother Oil Company, Singapore, Malaysia; soybean oil, peanut oil and lard were purchased from a local supplier of edible oils. Average intake of the main nutrients was calculated using Chinese food composition tables. The fatty acid profile and main nutrients of the test diets are shown in Tables 1 and 2.

Table 1. Fatty acid profile of four test diets in Experiment I

[View Table]

Table 2. Average daily nutrient intake of normocholesterolemic subjects consuming the four test diets1

[View Table]

Biochemical analyses. Serum TC and TG levels were determined by the use of enzymatic kits (Chinese Zhong Sheng High-Tech Bioengineering, AS 89001) in a Beckman 700s system auto analyzer. HDL-C was assayed with enzymatic kits that used phosphotungstic acid and magnesium chloride as the precipitant. LDL-C was calculated using the formula of Friedewald (1972).

Statistical analyses. The data were analyzed with the SPSS/PC+ statistics program (version 4.0, SPSS, Chicago, IL). Comparisons between means of four groups were assessed for significance using Fisher's protected least significance difference test. In all cases, statistical significance was set at P < 0.05, and data in the text, tables and figures are presented as means ± SD.

Experiment II

Subjects. To select hypercholesterolemic subjects, a fasting serum cholesterol concentration of 5.5 mmol/L was set as the cut-off point. After excluding known diabetes, as well as liver, renal, thyroid or hypertensive diseases, 51 subjects (31 men, 20 women, aged 32-68 y) were recruited for this study. Their serum TC concentrations ranged from 5.5 to 7.0 mmol/L. The subjects were working in either a state-owned farm or in a local plant producing microelectric motors. Subjects' body weight ranged from 54.5 to79.5 kg (men) and 42.0 to 66.5 kg (women). None of the subjects were taking medication known to affect lipid metabolism.

Diet. Foodstuffs, diet preparation, compliance monitoring and the calculation of nutrient intake were similar to those of Experiment I. The test diet supplied about 30% of energy as fat 60-65% of which was contributed by the test oils. The fatty acid profile and main nutrients of the diet are shown in Tables 3 and 4.

Table 3. Fatty acids profile of two test diets in Experiment II

[View Table]

Table 4. Average daily nutrient intake of hypercholesterolemic subjects consuming palm oil and peanut oil diets (Experiment II)

[View Table]

Experiment design. PA and PE were used as test oils for hypercholesterolemic subjects. One test group was composed of 15 men and 11 women, and the other group was composed of 16 men and 9 women. The crossover experimental design (two experiment periods of 6 wk, preceded by a base-line diet for 3 wk) was used to control within-subject variability of biochemical measurements. Fasting blood samples were take at the beginning and end of each test period for determination of serum TC, HDL-C and TG.

Biochemical analyses. Methods for determining serum lipids were the same as those used in Experiment I. 

Statistical analyses. The data were analyzed with the SPSS/PC+ statistics program, version 4.0 (SPSS). Comparisons between means of two hypercholesterolemic groups were assessed for significance with a t test (two-tailed). In all cases, statistical significance was set at P < 0.05, and data in the text, tables and figures are presented as means ± SD.


RESULTS

Experiment I

Compared with the entry level, the average serum TC and LDL-C were 6.7 and 13.1% lower, respectively, in the PA group, whereas they were 22.8 and 30.7% higher, respectively, in the LA group (Fig. 1). At the end of the test, the average serum TC/LDL-C and TC/HDL-C ratios in the PA group were significantly lower than those in the LA group (P < 0.05) and similar to levels in the SO group (Table 5). Although peanut oil is rich in polyunsaturated fatty acid, it decreased HDL-C levels and increased the TC/HDL-C ratio. At the end of the test, the HDL-C level in the PE group was significantly lower than that in the PA group (P < 0.05), and thus the ratio of TC/HDL-C was significantly higher than that in the PA group (P < 0.05).
Fig. 1. Changes in total cholesterol (TC); low density lipoprotein cholesterol (LDL-C); high density lipoprotein cholesterol (HDL-C) and the ratio of TC to HDL-C in sera of normochlesterolemic subjects fed palm oil (PA), soybean oil (SO), peanut oil (PE) or lard (LA) for 6 wk.
[View Larger Version of this Image (21K GIF file)]

Table 5. Effects of test oil diet on serum lipids in normocholesterolemic subjects1,2

[View Table]

Experiment II

The results of serum lipids in the first period of Experiment II are presented in Figure 2 and Table 6. Because peanut oil is the habitual cooking oil of the hypercholesterolemic subjects, the PE diet had no significant influence on serum cholesterol. Compared with entry values, however, the PA diet cause a significant reduction in TC (-6.5%, P < 0.05), LDL-C (-9.6%, P < 0.05) and TC/HDL-C ratio (-11.5%, P < 0.05). After the 3-wk washout period, the serum cholesterol values returned to their original level. In the second period of Experiment II, the two experiment groups exchanged test oils. Consumption of the palm oil diet led to a slight nonsignificant decrease in TC and LDL-C (-3.6 and -6.1%, respectively) and a 5.7% increase in HDL-C level. The ratio of TC/HDL-C, however, was significantly decreased (11.2%, P < 0.05). The PE diet, as in the first period, had no significant influence on serum cholesterol levels (Fig. 3, Table 7).
Fig. 2. Changes in serum lipid fractions (see Fig. 1 legend for abbreviations) in hypercholesterolemic subjects (15 men, 11 women) fed peanut oil (PE) and (16 men, 9 women) fed palm oil (PA) for 6 wk.
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Table 6. Effects of test diet oil on serum lipids in hypercholesterolemic Chinese in period I, Experiment II1

[View Table]


Fig. 3. Changes in serum lipid fractions (see Fig. 1 legend for abbreviations) in hypercholesterolemic subjects (15 men, 11 women) switched from peanut oil (PE) to palm oil (PA) or 16 men, 9 women switched from palm oil (PA) to peanut oil (PE). Each 6-wk dietary period followed a 3-wk washout period.
[View Larger Version of this Image (17K GIF file)]

Table 7. Effects of test diet oil on serum lipids in hypercholesterolemic Chinese in period II, Experiment II1

[View Table]


DISCUSSION

Although it has been established that saturated fatty acids (SFA) from animal and vegetable sources in human diets tend to cause an elevation of serum cholesterol concentrations, recent studies in both humans and experimental animals suggest that palm oil, despite a high concentration of SFA (mainly palmitic acid), is an exception to this general proposition. Based on the characteristics of the Chinese diet, this study is the first to investigate the influence of palm oil on serum lipids in both normo- and hypercholesterolemic subjects. Compared with a Western diet, the test diet contained more rice and bean curd but fewer animal products. The average cholesterol intake was <300 mg/d for normocholesterolemic subjects except those who consumed the diet prepared with lard and about 200 mg/d for the hypercholesterolemic subjects. The results showed that palm oil had no adverse effect on serum lipids and ccould significantly decrease serum TC, LDL-C, and TC/HDL-C when compared with lard and peanut oil. This is consistent with reports from other laboratories that palmitic acid appears to be nonhypercholesterolemic when dietary cholesterol intake is low (Khosla and Hayes 1994, Ng 1994). Some studies showed that palmitic acid appears to increase plasma cholesterol in hypercholesterolemic subjects (Keys et al. 1986, Mattson and Grundy 1985, Ng 1994). In the present study, compared with peanut oil (the habitual edible oil of the hypercholesterolemic subjects), the results showed that replacement of PE by PA can cause a reduction of serum TC, LDL-C and TC/HDL-C.

An initial study and regression analysis showed that myristic acid (14:0) is four times as potent as palmitic acid in raising serum cholesterol (Wood 1992), but an earlier study with modified (transesterified) fat led to a differing opinion, namely, that the effects of 12:0, 14:0 and 16:0 are equivalent (McGandy et al. 1970). The discrepancies between the prediction of the Key equation and the results from studies in animals and humans on palm oil suggest that the effect of SFA on serum lipids requires re-examination. Hayes et al. (1991) reported that the exchange of dietary 16:0 for 12:0 + 14:0 caused a decrease in the plasma cholesterol when dietary total saturated, monosaturated and polyunsaturated fatty acids were held constant. In a collaborative study, the same result was obtained in normocholesterolemic humans, even with 300 mg of cholesterol in the diet (Sundram et al. 1991). These results clearly suggest that palmitic acid, the major and most controversial saturated fatty acid in palm oil, was not cholesterolemic but neutral under those conditions and that the widely held belief that all saturated fatty acids are the same is invalid.

Oleic acid is another major fatty acid (about 40%) present in palm oil. Epidemiologic studies of Mediterranean populations who consume substantial amounts of olive oil (high content of oleic acid) have found that the mortality rate for coronary heart disease (CHD) in these populations is low (Christakis et al. 1980). In addition, a significant inverse relationship between red blood cell-phosphatidylcholine (RBC-PC) oleate and CVD mortality, particularly CHD, was also found in China (Fan et al. 1990). Some studies in animals and humans have also shown that oleic acid has the same cholesterol-lowering effect as that of linoleic acid and has the additional benefit of not decreasing the HDL-C level (Mattson and Grundy 1985, Rudel et al. 1990, Wang et al. 1993). One study has even indicated that the effects of palmitic acid on serum lipids in normocholesterolemic subjects is similar to that of oleic acid (Ng et al. 1992). Recently, an American group reported that the combination of 16:0 + 18:1 had some beneficial effect on enhancing HDL-C and LDL-C receptor mRNA abundance in hamsters (Lindsey et al. 1990).

Analyses of accumulating data showed that 85% of the observed variation in serum cholesterol could be explained solely on the basis of 14:0 and 18:2 when dietary cholesterol intake was <= 300 mg (Khosla and Hayes 1994). The level of 14:0 was <1.0% in the palm oil diet, and the level of 18:2 actually exceeded the threshold levels required to counter the cholesterol-raising effects of the 12-carbon SFA. Studies on intramolecular fatty acid distribution in palm oil triglycerides showed that the 16:0 content in palm oil (esterified in the alpha -position) is quite different from that in butterfat or lard (esterified at the beta -position) and that it does not raise blood cholesterol levels (Kritchevsky 1988). The results from our laboratory showed that the cholesterol-raising effect of lard was significantly decreased after being interesterified, which means that palmitic acid was transferred from the beta -position to the alpha -position (Zhang et al. 1992). This may explain why PA did not increase the serum cholesterol level as LA did, even though their fatty acid composition is similar. In conclusion, on the basis of the results of present studies in normo- and hypercholesterolemic subjects, we may conclude that the use of palm oil in food processing and in the Chinese diet should be safe and will not increase the risk of CVD.


FOOTNOTES

1   Presented in a symposium at the VIIth Asian Conference of Nutrition held in Beijing, China, October 7-11, 1995. The symposium and the publication of symposium proceedings were supported in part by an educational grant from the Malaysian Palm Oil Promotion Council. Guest editor for the publication of symposium proceedings as a supplement to The Journal of Nutrition was David Kritchevsky,The Wistar Institute, Philadelphia, PA.
2   Supported by a research grant provided by the Palm Oil Research Institute of Malaysia.
3   The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.
4   To whom correspondence and reprint requests should be addressed.
5   Abbreviations used: CHD, coronary heart disease; CVD, cardiovascular disease; HDL-C, HDL cholesterol; LA, lard; LDL-C, LDL cholesterol; PA, palm oil; PE, peanut oil; RBC, red blood count; SFA, saturated fatty acid; SO, soybean oil; TC, total cholesterol; TG, triglyceride.


LITERATURE CITED


0022-3166/97 $3.00 ©1997 American Society for Nutritional Sciences




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Copyright © 1997 by American Society for Nutrition