Asia Pacific J Clin Nutr (1997) 6(1): 22-25

Palm oil diet may benefit mildly hypercholesterolaemic Chinese adults

 

Zhang Jian, Wang Chunrong, Dai Jianhua, Chen Xiaoshu, Ge Keyou

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

---

The effects on serum lipids and platelet function of diets prepared with palm oil (PA) and peanut oil (PE) were studied in two groups of mild hypercholesterolaemic volunteers (serum TC between 5.5 - 7.0 mmol/L, aged 32-68). There were 15 men and 11 women in PE group and 16 men and 9 women in PA group. Dietary fat provided about 30% of total calories, and the test oil accounted for 60-65% of total dietary fat. During the 3 weeks of pretest period, diets were prepared with peanut oil, the local habitual cooking oil for all subjects. During the next 6 weeks the subjects in PA group consumed a diet prepared with palm oil while subjects in PE group continued to consume a diet prepared with peanut oil. Compared to the entry-level values, the concentrations of serum TC (total cholesterol), LDL-C (low density lipoprotein cholesterol), TC/HDL-C (high density lipoprotein cholesterol) ratio and plasma TXB₂/6-keto-PGF_1a ratio were significantly decreased in PA group (-6.5%, -9.0%, -11.5%, and -22.4%) while not appreciably altered in PE group by the end of the test. No significant change was observed on the whole blood platelet aggregation in both groups. In connection with the results from our previous study in normocholesterolaemic Chinese volunteers, palm oil, used as cooking oil in Chinese diet, will not lead to any adverse effect on blood lipids and thus will not increase CVD risks.

---

Introduction

Cardiovascular disease (CVD) is one of the major causes of death in developed countries and the death caused by CVD is increasing rapidly in China^1-4. It is generally believed that high concentrations of serum total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) are positively related to the risk of CVD and that saturated fatty acids (SFAs) have the potential to increase the blood lipids and promote thrombosis.

Palm oil is the second largest volume of vegetable oil produced in the world. As it is highly saturated and contains about 50% palmitic acid, palm oil was discredited like saturated animal fats, such as butter, lard and tallow. The allegation that palm oil raises total serum cholesterol, thereby increasing the risk of coronary heart disease, however, was not based on actual experimental studies. Recently, studies in animals and in humans indicate that palm oil is quite different from other hypercholesterolaemic fats such as lard or coconut oil^5-7. Therefore, the scientific community needs to conduct controlled studies on the effects of palm oil and its relation to cardiovascular disease and maintain a responsible perspective when reporting its findings or making recommendations concerning consumption of this oil.

The consumption of palm oil in China has increased rapidly in recent years⁸, but the information about the relation of palm oil to health is very limited. A few papers show that palm oil maintains the normal growth of rats and causes a significant reduction of serum cholesterol in rabbits compared to lard⁹. The reports on palm oil in human studies are difficult to find in China. Therefore, it is necessary to undertake properly controlled studies on the effects of palm oil on blood lipids and on the risk of CVD. The previous study showed palm oil had no harmful effect on normal cholesterolaemic subjects in habitual Chinese diet¹⁰. This study observes the effects of palm oil on mildly hypercholesterolaemic volunteers.

Subjects and Methods

Subjects

After excluding known diabetes, hypertension and liver, renal and thyroid disorders, 31 males and 20 females, aged from 32-68 years of age, were selected as subjects. Their serum cholesterol concentration ranged from 5.5-7.0 mmol/L. All subjects worked either on a state owned farm or in a local plant producing micro electric motors. The body weight of the subjects ranged from 54.5 - 79.5 kg in males and from 42.0 - 66.5 kg in females. None of the subjects were taking medication known to affect lipid metabolism.

Diet

Experimental diet was composed of rice, flour, lean pork, chicken, bean curd, and some local green vegetables. The menu was developed around subjects’ preferences and daily meals were prepared in habitual manner by a local cook under the direction of professionals to meet the experimental requirements. RBD palm oil was purchased from the Brother Oil Company, Singapore, while peanut oil was purchased from local edible oil company. According to the food inventory charges, average nutrient intakes were calculated based on the Chinese food composition table. The fatty acids profile and the main nutrients of the test diets were shown in Tables 1 and 2.

Table 1. Fatty acids profile of two test diets.

Fatty acid	Palm oil diet %	Peanut oil diet %
14:0	0.8	0.4
16:0	32.7	16.0
16:1	2.0	0.6
18:0	3.7	5.7
18:1	38.8	39.3
18:2	19.6	31.4
18:3	1.7	1.5
20:0	0.2	1.1
20:1	0.1	1.2
22:0	--	1.8

Table 2. Average daily nutrients intake of hyper-cholesterolaemic subjects on palm oil and peanut oil diets.

Test oil	Energy (MJ)	Fat (g)	Protein (g)	Carbohydrate (g)	Fibre (g)	Cholesterol (mg)
PE	10.3	82	70	362	13	166
PA	10.6	85	76	366	14	163

Biochemical Analyses

Serum TC and TG (triglyceride) levels were determined by using enzymatic kits (Chinese Zhong Sheng High-Tech Bioengineering Company, ZS 89001) on Beckman 700s system auto analyser. HDL-C was assayed using enzymatic kits after a precipitation with phosphotungstic acid and magnesium chloride. LDL-C was calculated using the formula of Friedwald. Plasma TXB² and PGF_1a were determined by using ¹²⁵I radio-immunoassay kits purchased from radio-immunoassay laboratory, General Hospital of the People’s Liberation Army of China. Platelet aggregation in whole blood was determined with a chronolog model 500vs aggregometer after introduction of collagen (obtained from Sigma chemical company) using the impedance method¹¹. Collected in a 3.8% solution of sodium citrate (9 parts blood to 1 part citrate), each blood sample was assayed within an hour and the final concentration of collagen was 1 mg/mL blood.

Statistical analyses

The data were analysed with the SPSS/PC+ statistics program (V4.0, SPSS, Chicago, IL). The differences between the two test groups were assessed with t test (two-tailed). In all cases, statistical significance is P < 0.05 and data are presented in the text and tables as means ±SD.

Results

The effects of the two test cooking oils on plasma lipids are shown in Table 3. The average entry concentration of serum TC has not been completely matched in grouping due to some practical problems, but there exists no significant difference between two groups. It would be more reasonable to compare the difference between the entry and the end values of each group rather than the end values of PA and PE groups. As peanut oil is the habitual cooking oil for the subjects, all biochemical indices were not significantly influenced by PE diet. But compared with entry values, PA diet caused a significant reduction in serum TC (-6.5%, P<0.05), LDL-C (-9.0%, P<0.05) and TC/HDL-C ratio (-11.5%, P<0.05).

Table 3. Effects of test oil on serum lipids in hyper-cholesterolaemic Chinese.

Group		Blood Lipids (mmol/L)
		TG	TC	HDL-C	LDL-C	TC/ HDL-C
PE	0wk	1.40±0.52	5.88±0.41	1.23±0.27	4.34±0.45	4.78±1.10
	6wk	1.28±0.54	5.87±0.28	1.22±0.27	4.38±0.39	4.88±1.06
PA	0wk	1.54±0.50	6.11±0.44	1.22±0.17	4.55±0.44	5.05±0.81
	6wk	1.41±0.64	5.71±0.43*	1.28±0.19	4.14±0.36*	4.47±0.59*

Values are means±SD. n=26 in PE group, n=25 in PA group.
*Denotes a significant difference from entry value (P<0.05).

The average plasma concentration of TXB₂ was slightly increased while PGF_1a was slightly decreased in the PA diet group. Thus the plasma TXB₂ /PGF_1a ratio was significantly reduced (Table 4). The whole blood platelet aggregation was determined but no significant changes were observed in either group (Table 5).

Table 4. Effect of test oil on plasma level of TXB₂ and 6-keto-PGF_1a (M ± SD)

Group		TXB2 (pg/ml)	6-keto-PGF1a (pg/ml)	TXB2/ 6-keto-PGF1a
PE	0 wk	83.3±44.7	42.9±14.5	1.85±1.07
	6 wk	87.8±38.0	50.6±18.3	1.74±0.76
PA	0 wk	80.9±18.9	45.9±11.1	1.83±0.49
	6 wk	71.3±26.1	51.2±16.4	1.42±0.45*

Values are means ± SD. N = 18 per group. *Denotes significant difference from entry value (P<0.05).

Table 5. Effect of test oil on whole blood platelet aggregation.

Group	n	Blood platelet aggregation (oms)
		0 wk	6 wk
PE	7	13.4±2.1	14.5±3.4
PA	9	11.4±3.5	13.1±3.0

Discussion

A substantial body of data implies that dietary saturated fat tends to increase serum cholesterol concentrations and promote thrombosis^12-13. Analysis of some saturated fats, such as palm oil, lard, butter and coconut oil reveals that each has distinct profiles and exert different metabolic effects. Recently, studies from humans and experimental animals show that palm oil, despite a high concentration of SFA (mainly palmitic acid), does not increase serum cholesterol concentrations or thrombotic tendencies^14,15.

The Chinese diet contains more vegetables but less animal foods than the western diet. The average per capita intake of cholesterol is less than 300mg/d in most urban area and less than 200mg/d in rural areas. Our former study showed that palm oil used in Chinese diet did not increase serum cholesterol concentration in normocholesterolaemic subjects¹⁰. Some studies show that palmitic acid appears to increase plasma cholesterol in hypercholesterolaemic subjects¹⁶. The results in the present study show that in comparison with PE diet, PA diet induced a reduction of serum TC, LDL-C and TC/HDL-C ratio. This is consistent with results from other laboratories that palmitic acid appears to be non-hypercholesterolaemic when dietary cholesterol intake is low^15,17.

Since the 1950s, numerous studies in humans and in animals have investigated the effects of dietary fat saturation on cholesterolaemia. Keys and Hegsted, respectively, transformed these early results into mathematical regression equations that have been used to predict the average change in serum cholesterol that might be expected for a given change in the percentage of energy consumed from a specific class of fatty acids^16,18. But Lowenstein showed that African pastoral tribes had a low serum cholesterol concentration and a low incidence of coronary heart disease (CHD) mortality despite having high milk-fat intake¹⁹. Pronczuk reported that although tallow and lard contained appreciable amounts of SFAs, they were not much more hypercholesterolaemic then corn oil²⁰. This prompted investigators to question the generally held belief that the 12-16C fatty acids were equivalent in terms of their cholesterol-raising ability. A study and regression analysis showed that myristic acid (l4:0) is four times more potent than palmitic acid in raising serum cholesterol²¹. Hayes et al reported that the exchange of dietary 16:0 for 12:0+14:0 caused a decrease in the plasma cholesterol when dietary total saturated, monounsaturated (MUFAs), and polyunsaturated fatty acids (PUFAs) were held constant²². The same result was obtained in normocholesterolaemic humans, even with 300mg of cholesterol in the diet²³. These results clearly suggest that palmitic acid, the major and most controversial saturated fatty acid in palm oil, was not cholesterolaemic but neutral and the widely held belief that all saturated fatty acids were the same was invalid.

Oleic acid is another major fatty acid (about 40%) in palm oil and was formerly considered neutral. Epidemiologic studies on Mediterranean populations who consume substantial amounts of olive oil (high content of oleic acid) showed that the mortality for CHD in these populations was low²⁴. A significant inverse relationship between red blood cell phosphatidylcholine (RBC-PC) oleate and CVD mortality, particularly CHD was also found in China²⁵. Some animal and human studies also suggest²⁶ that oleic acid has cholesterol-lowering potential as does linoleic acid and has the benefit of lowering LDL-C without decreasing HDL-C levels^27-29. An American group reported that the combination of 16:0+18:1 had some beneficial impact on enhancing HDL-C and LDL-C receptor mRNA abundance in hamsters³⁰. But more work needs to be done to confirm these findings.

Analyses of accumulating data show 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 300mg or less¹⁷. In the present study, the content 14:0 is less than 1.0% in PA diet and the level of 18:2 actually exceeded the threshold levels required to counter the cholesterol-raising effects of 12 and 14-carbon SFAs (Table 1).

It is generally believed that SFAs promote thrombosis¹³ and that PUFAs of n-6 family present in vegetable oils have proaggregatory thrombotic effects while the n-3 PUFAs of seafoods increase bleeding time^31,32. Cook demonstrated that a balance of saturated and unsaturated fatty acids is important to enzymes responsible for synthesis of crucial membrane components and substrates for eicosanoid formation (20:4n-6, 20:5n-3 and 22:6n-3)³³. Garg et al showed that partial replacement of dietary 18:2n-6 by tallow, which contains about 51% stearic acid (18:0) and 29% palmitic acid (16:0), can accelerate the conversion of 18:3n-3 to 20:5n-3 and maximise the inhibition of the conversion of 18:2n-6 to 20:4n-6³⁴. This may partly explain the fact that although palm oil contains nearly 50% palmitic acid, it does not increase arterial thrombotic tendencies and even tends to decrease platelet aggregation compared to the effect of safflower oil (SA) which contains about 70% linoleic acid 18:2n-6³⁵. On the other hand, some studies show that oleic acid (l8:1n-9) has potential to decrease thrombotic tendencies^29,36.

All of these may be reasons why the replacement of habitual peanut oil with palm oil in diet causes a significant reduction in TXB₂/PGF_1a ratio. Contrary to our expectancy, the whole blood platelet aggregation rate was not significantly affected by palm oil. This is probably because of wide range of fluctuation between individuals and the limited number of subjects.

In conclusion, in comparison to peanut oil, PA has a hypocholesterolaemic and antithrombotic effect on mild hypercholesterolaemic Chinese adults. In connection with the results from our former study in normocholesterolaemic Chinese volunteers, we feel confident to say that the large amounts of PA entering into Chinese diet will not lead to any adverse effect on blood lipids, thus will not increase CVD risks.

Acknowledgment. This study was funded partially by Palm Oil Research Institute of Malaysia (PORIM). The author would like to express gratitude to the staff at the Disease Control Station of Shunyi County, Beijing, who gave valuable assistance this study.

---

Palm oil diet may benefit mildly hypercholesterolaemic Chinese adults
Zhang Jian, Wang Chunrong, Dai Jianhua, Chen Xiaoshu, Ge Keyou
Asia Pacific Journal of Clinical Nutrition (1997) Volume 6, Number 1: 22-25

---

References

1. Beaglehole R, Bonita R, Stewart A. Cardiovascular disease mortality trends in the Western Pacific, 1968-1984. NZ Med J 1988; 101:441-3.
2. Goldbourt V, Holtzman E, Neufeld HN. Total and high density lipoprotein cholesterol in the serum and risk of mortality: evidence of threshold effect. Br Med L 1985; 290: 1239- 43.
3. Kannel WB, Castelli W, Gordon T. Serum cholesterol, lipoprotein and risk of coronary heart disease: the Framingham Study. Ann Intern Med 1977; 74: 1-12.
4. Mannien V, Elo O, Frick H. Lipid alteration and decline in the incidence of coronary heart disease in the Helsinki Heart Study. JAMA 1988; 260: 641-51.
5. Hornstra G, Sundram K. The influence of dietary palm oil on cardiovascular risk factors: a human study. Abstracts, PORIM International Palm Oil Conference. 9-14 Sept 1991. Kuala Lumpur, Malaysia: PORIM, 1991: 154-55.
6. Sundram K, Khor KT, Ong ASH. Effect of dietary palm oil and its fractions on rat plasma and high density lipoprotein lipids. Lipids 1990; 25(4): 187-93.
7. Tony KW Ng, Hassan K, Lim JB, Lye MS, Ishak R. Nonhypercholes-terolemic effects of a palm-oil diet in Malaysian volunteers. Am J Clin Nut. 1991; 53: 1015s-20s.
8. Fan WX and Chen XS. Food uses of palm oil in China. Food and Nutrition Bulletin 1994; 15(2): 147-8.
9. Chen XS, Fan WX. Studies of utilization and health effect of palm oil in China. Nutrition Research 1992; 12(Suppl.1): 23-29
10. Wang Ping, et al. Effects of palm oil on blood lipids and thrombosis in Chinese young healthy volunteers (abstract). China Oils and Fats 1995; 20(1): 39.
11. Glazier J: Measurement of platelet aggregation in whole blood. ACPR (26-30) April 1987.
12. Grundy SM, Denke MA. Dietary influences on serum lipids and lipoproteins. J Lipid Res 1990; 31: 1149-72.
13. Jakubowzki JA, Ardlie NG. Modification of human platelet function by a diet enriched in saturated or polyunsaturated fat. Atherosclerosis 1978; 31: 335-44.
14. Cottrell RC. Introduction: nutritional aspects of palm oil. Am J Clin Nutr 1991; 53(Suppl): 989S-1009S.
15. Tony KW Ng. A critical review of the cholesterolaemic effects of palm oil. Food and Nutrition Bulletin 1994; 15(2): 112-118.
16. Keys A, Anderson JT, Grande F. Prediction of serum cholesterol responses of man to changes in fats in the diet. Lancet 1957;2:959-66.
17. Khosla P and Hayes KC. Cholesterolaemic effects of the saturated fatty acids of palm oil. Food and Nutr Bulletin 1994; 15(2): 119-125.
18. Hegsted DM, McGandy RB, Myers ML, Stare FJ. Quantitative effects of dietary fat on serum cholesterol in man. Am J Clin Nutr 1965; 17: 281-95.
19. Lowenstein FW. Epidemiologic investigation in relation to diet in groups who show little atherosclerosis and are almost free of coronary ischemic heart disease. Am J Clin Nutr 1964; 15: 175-86.
20. Pronczuk A, Patton GM, Stephan ZF, Hayes KC. Species variation in the atherogenic profile of monkeys: relationship between dietary fats, lipoproteins and platelet aggregation. Lipids 1991; 26: 213-22.
21. Wood R. Biological effects of palm oil in humans. In: Chow CK, ed. Fatty acids in food and their health implications. New York: Marcel Dekker 1992: 647-61.
22. Hayes KC, Pronczuk A, Lindsey S, Diersen-Schade D. Dietary saturated fatty acids (l2:0, 14:0, 16:0) differ in their impact on plasma cholesterol and lipoproteins in nonhuman primates. Am J Clin Nutr. 1991; 53: 491-98.
23. Sundram K, Hassan AH, Siru OH, Hayes KC. Dietary palmitate lowers cholesterol relative to laurate and myristate in humans. Am J Clin Nutr 1994; 59: 841-846.
24. Christakis G, Fordrce MK, Kurtz CS. The biological and medical aspects of olive oil. 3rd International Congress on the Biological Value of Olive oil. Madrid: International Olive Oil Council, 1980: 85-120.
25. Fan WX, R Parker, Parpia B, Qu YSH, Cassano P, Crawford M, Leyton J, Jean T, Li JY, Chen JS, Campbell TC. Erythrocyte fatty acids, plasma lipids, and cardiovascular disease in rural China. Am J Clin Nutr. 1990; 52: 1027-36.
26. Hayes KC. Saturated fats and blood lipids: new slant on an old story. Can J Cardiol 1995; 11 suppl G:39G-46G.
27. Mattson FH & Grundy SM. Comparison of effects of dietary saturated, monounsaturated and polyunsaturated fatty acids on plasma lipids and lipoproteins in man. J Lipid Res 1985; 26: 194-202.
28. Rudel LL, Haines JL, Sawyer JK. Effects on plasma lipoproteins of monounsaturated, saturated, and polyunsaturated fatty acids in the diet of African green monkeys. J Lipid Res. 1990; 31: 1873-82.
29. Wang P, Wang CR, Zhang J, Fan WX. Effect of teaseed oil on blood lipids and platelet function in animals. ACTA NUTRIMENTA SINICA 1993; 15(4): 377-383.
30. Lindsey S, Benattar J, Pronczuk A, Hayes KC. Dietary palmitic acid (16:0) enhances high density lipoprotein cholesterol and low density lipoprotein receptor mRNA abundance in hamsters. Proc Soc Exp Biol Med 1990; 195:261-69.
31. Croft KK, Beilin LJ, Vandongen R, and Mathews E. Dietary modification of fatty acid and prostaglandin synthesis in the rat. Biochim. Biophys Acta 1984; 795: 196-207.
32. Marshall LA, and Johnston PV. Modulation of Tissue Prostaglandin Synthesizing Capacity by Increased Ratios of Dietary alpha-Linolenic Acid to Linoleic Acid. Lipids 1982; 17: 905-913.
33. Cook HW, Spence MW. Interaction of (n-3) and (n-6) fatty acids in desaturation and chain elongation of essential fatty acids in cultured glioma cells. Lipids 1987; 22(9):613-619.
34. Garg ML, Wierzbicki AA, Thomson ABR, Clandinin MT. Dietary saturated fat level alters the competition between linolenic and linoleic acid. Lipids 1989; 24: 334-9.
35. Hornstra G, Hennissen AAHM, Tan DTS, Kalaufuse R. Unexpected effect of dietary palm oil on atherothrombosis (rat) and atherosclerosis (rabbit). In: Galli L, Fedelli E, eds. Fat production and consumption: technology and nutritional implications. (NATO-ASR series A. Life Sciences.) New York: Plenum Publishing Co, 1987: 69-82.
36. Barradas MA et al. Oleic acid supplementation alters platelet function and membrane phospholipid arachidonic acid content. Biochem Soc Trans 1989, 17: 505.

Copyright © 1993 [Asia Pacific Journal of Clinical Nutrition]. All rights reserved.
to the top