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A critical review of the cholesterolaemic effects of palm oil

Tony Ng Kock Wai

Abstract

This paper reviews recent reports of the cholesterolaemic effects of palm oil. The evidence indicates that the substitution of palm oil or its lipid fractions for the usual fats in the diet does not result in an elevation of total serum cholesterol in lean, normocholesterolaemic individuals with a cholesterol intake of less than 300 mg per day. When threshold dietary levels of linoleic acid (18:2) are met, they tend to counter the cholesterol-raising effects of the 12- and 16-carbon saturated fatty acids. In view of this, the use of a cholesterol saturated-fat index to measure the hypercholesterolaemic and atherogenic potential of foods can be misleading, particularly when applied to palm oil. Nutritionists and health professionals need to keep abreast of recent knowledge on the cholesterolaemic impact of dietary fats and fatty acids.

Introduction

The health hazards of excessive intake of dietary fats, especially those rich in saturated fatty acids and derived from animal sources such as milk fat (butter, cream), lard, and tallow, have often been highlighted in the scientific media and the popular press. As a result, all saturated fats, whether animal or vegetable in origin, have been discredited. The tropical oils in particular, namely palm oil, palm kernel oil, and coconut oil, have been major targets of health campaigns against the wider consumption of saturated fats [1, 2].

Consequently, palm oil's image has suffered greatly in recent years. The allegation that it raises total serum cholesterol, thereby increasing the risk of coronary heart disease, unfortunately was not based on actual experimental studies but on extrapolation of the Keys equation [3] to palm oil. In actual fact, not a single properly controlled human feeding study investigating the cholesterolaemic effects of palm oil could be found in the literature before 1987.

Adverse publicity and coincident research on the effects of dietary mono-unsaturates [4, 5] and stearic acid [6] spurred intensive research on palm oil worldwide. This article provides a critical examination of the cholesterolaemic effects of palm oil reported in some selected studies, with particular emphasis on new data that have emerged over the last five years or so.

Selected studies

One of the earliest human feeding studies in this area compared the effects on the serum lipid profile of typical Malaysian diets prepared with palm olein, corn oil, and coconut oil [7]. These oils supplied 22% kcal (approximately 75% of total fat calories) to three matched groups of healthy, normolipidaemic volunteers (61 men, 22 women), 20-34 years old, living at a student hostel. In this double-blind trial, one group received a coconut-palm-coconut dietary sequence during three five-week feeding periods; the second group, coconut-corn-coconut; and the third group, coconut oil (hypercholesterolaemic control). All daily meals were provided at the hostel canteen, and individual food consumption was meticulously recorded.

The switch from coconut oil to palm olein or corn oil significantly reduced the concentrations of total serum cholesterol ( - 19% and - 36% respectively; see fig. 1), low-density lipoprotein (LDL) cholesterol ( - 20%, - 42%), and high-density lipoprotein (HDL) cholesterol ( - 20%, - 26%). Whereas the entry-level LDL:HDL ratio was not appreciably altered by coconut oil, it was decreased 8% by palm olein and 25% by corn oil. Thus, it was evident that the cholesterolaemic effects of palm olein were intermediate between those of coconut oil and corn oil, and that palm olein was distinctly hypocholesterolaemic compared with coconut oil. As such, palm olein should not be placed in the same group as coconut oil.

FIG. 1. Total serum cholesterol in three groups of subjects fed palm olein, corn oil, or coconut oil as the main dietary fat. 0% represents the mean entry level, 170 mg/dl. Values in parentheses are absolute levels in mg/dl. (Source: Ref. 7)

In the switch of the test oils, the authors also noted that the reductions in total serum cholesterol with palm olein (-36 mg/dl) and corn oil ( - 68 mg/dl) were appreciably greater than predicted (table 1), particularly than the prediction obtained by the Keys equation [3]. However, when 16:0 for the palm olein period was omitted from the equation (i.e., 16:0 was treated as neutral), the predicted value fit the observed response perfectly ( - 36 versus -37 mg/dl). A major criticism of this study is that too many five-week periods were allocated to the hypercholesterolaemic control, while only one five-week dietary period was assigned to the test oil, palm olein.

In another study [9], 110 high school boys 16-17 years old ate a typical test diet of Malaysian foods cooked in palm olein for five weeks. After a six-week washout period during which the subjects reverted to their habitual diets at the school canteen, they were given a similar test diet cooked with soybean oil for a further five weeks. Neither palm olein nor soy-bean oil appreciably altered the baseline values for total plasma cholesterol, LDL and HDL cholesterol, and apolipoprotein A1 and apo B. However, apo B values were significantly depressed by soy-bean oil compared with the palm olein, and the soy-bean oil unexpectedly raised plasma triglyceride values significantly above the baseline.

Important limitations in the study design and protocol that somewhat weakened the validity of this otherwise interesting study were the non-randomization of the test-fat sequence, the lack of a hypercholesterolaemic control group, the failure to provide information on the fatty acid profile of the experimental diets as well as the kilocalories attributed to the test fats, and the relatively young age of the subjects, as adults would have been more appropriate.

TABLE 1. Observed versus predicted responses of total serum cholesterol (mg/dl) when coconut oil is replaced by palm olein or corn oil as the major dietary fat

Adapted from ref. 7.
a. 37 when 16:0 is considered neutral.

The effects of diets enriched with palm oil, desi ghee (butter fat), a blend of hydrogenated soy-bean oil and palm oil (65:35), or hydrogenated cottonseed oil, supplying 30%-33% kcal as fat energy, were compared in Pakistan [10]. About 117 subjects or more were randomly divided into four groups, each of which underwent a 10-day preparatory period (during which the normal diet was consumed) before being assigned a different test fat for 60 days. The trial was repeated three times, with the groups interchanging the test fats, so that by the end of the experiment every group had eaten each diet.

The palm oil diet had pronounced hypocholesterolaemic effects that were not exhibited by the other three test fats (table 2). Although the results were consistent with the non-hypercholesterolaemic action of palm oil reported in other human studies [7, 9], this study can be criticized on several grounds. The four groups of subjects were not initially matched for their lipid values, and no mention was made as to the degree of dietary compliance during the rather long 60-day feeding periods.

TABLE 2. Mean percentage change in serum lipid values for four feeding trials

Source: Ref. 10.

a. Refined, bleached, and deodorized.
b. Butter fat.
c. Hydrogenated soy-bean oil and palm oil.
d. Hydrogenated.

In two separate double-blind, randomized, crossover (no washout period) experiments, 21 free-living, healthy adult Australians ate potato crisps fried in either palm olein or canola oil for two to three weeks [11]. The palm olein, but not the canola oil, caused a mean 3% rise in total cholesterol, due predominantly to a 10% rise in HDL cholesterol, compared with the typical Australian diet. The test fats consumed (53 g for men, 35 g for women) approximated 50% of total dietary fat. These findings represent a rare report on the beneficial impact of palm olein on HDL cholesterol levels in humans, although a similar finding was reported earlier in an animal model [12]. Unfortunately, the authors were not able to confirm this interesting finding, as the canola oil used in their second study was contaminated by palm olein at factory source.

The effects of dietary palm oil, hydrogenated canola oil, and soy-bean oil (incorporated into sauces, pastries, cakes, biscuits, etc. at 26% kcal, or 65% of total fat) on indexes of cardiovascular risk were compared in free-living healthy subjects [13]. The three test oils did not differ greatly in their overall effect on plasma risk profiles. Beneficial effects were seen with the palm oil diet, such as significantly reduced plasma triglycerides and a tendency toward increased HDL cholesterol.

The non-hypercholesterolaemic effect of a palm oil-enriched diet was also reported in an American study conducted on 13 healthy men, 22-43 years old, randomized to receive three dietary periods of palm oil, hydrogenated soy-bean oil, and coconut oil, separated by washout periods of two weeks during which ad libitum diets were ingested [14]. The test fats, which were incorporated into muffins or cookies, each contributed 17.5% kcal, equivalent to 50% of total dietary fat. This study, although conducted on a small number of subjects, served to drive home an important point, namely, that half the fats in a typical American diet can be replaced with palm oil (representing a twentyfold increase in palm oil) with no detrimental cholesterolaemic effects.

The cholesterolaemic effects of a Dutch diet were compared with one in which there was a maximum replacement (approximately 70% of total fat) of the habitual fats with palm oil in 40 free-living volunteers, 19-45 years old, using a double-blind, crossover design [15]. Palm oil caused no significant change in the concentrations of total cholesterol, LDL cholesterol, and total triglycerides but raised HDL₂ cholesterol and apo A1 and lowered the LDL triglycerides and apo B significantly. The palm oil diet contained significantly lower cholesterol but higher 16:0 and 18:2 acids than the control diet (with no change in the ratio of polyunsaturated to saturated fatty acids). These differences could be expected, since the study design did not maintain constant levels of specific dietary constituents, and in this respect was somewhat similar to the American study [14].

The hypercholesterolaemic effect of palmitic acid (16:0) versus myristic acid (14:0) plus lauric acid (12:0) was explored in a study [16] with three species of monkeys fed cholesterol-free diets, each containing one of five fat blends (DF1-DF5, table 3) as 31% kcal prepared from palm oil, coconut oil, soy-bean oil, and high-oleic safflower-seed oil. In DF2, DF3, and DF4, the content of 16:0, 14:0, and 12:0 varied, while the total amount of these three saturated fatty acids (SFA), polyunsaturated fatty acids (PUFA), and monounsaturated fatty acids (MUFA) was kept constant. DF1, containing a blend of coconut oil and soy-bean oil, served as the hypercholesterolaemic control, and DF5 was an American fat blend resembling that recommended by the American Heart Association.

TABLE 3. Comparative cholesterolaemic effects of palmitic acid (16:0) versus myristic acid (14:0) + lauric acid (12:0) in monkeys

Source: Ref. 16.

Switching from DF2 to DF4, with 14:0 and 12:0 acids replaced quantitatively by 16:0, resulted in a significant reduction in total cholesterol ( - 22 mg/dl; table 3). Furthermore, switching from the Heart Association diet (DF5) to DF4, with PUFA replaced by 16:0, caused a non-significant rise in total cholesterol, whereas switching from DF5 to DF3, with PUFA replaced by 14:0 + 12:0 caused a significant increase in total cholesterol (30 mg/dl). The Keys [3] and Hegsted [8] equations provided good fits for the observed data, but they predicted the response perfectly (r = .99) when 16:0 was considered neutral, and thus the hypercholesterolaemic effect of saturated fats in non-human primates probably was due primarily to the 14:0 and 12:0 and not to the 16:0.

Subsequently, 16:0-rich (palm oil source) or 14:0 + 12:0-rich (coconut oil source) diets were fed to 18 normocholesterolaemic male volunteers using a crossover design over two consecutive four-week periods [17]. Dietary levels of PUFA (3% kcal), MUFA (14% kcal), and SFA (15% kcal) were held constant during a one-to-one exchange of 10% kcal of 16:0 for 14:0 + 12:0. The 16:0-rich diet lowered total plasma cholesterol and LDL cholesterol (only marginally for the latter) and improved the LDL:HDL ratio compared with the 14:0 + 12:0-rich diet. The authors concluded that 16:0 exerts a distinctly different impact on cholesterol metabolism from that of 14:0 + 12:0 in normocholesterolaemic humans. This agreed with the findings in normocholesterolaemic monkeys [16], and may also be inferred from Hegsted's findings [8], although the latter used relatively hypercholesterolaemic subjects and found 12:0 to be close to neutral.

Since butter routinely increases cholesterol in monkeys [18] and humans [3, 8, 19], yet contains much less 12:0 than 14:0, the latter SFA would appear to be the common denominator and major contributor to the SFA-induced cholesterolaemia in two studies [16, 17], which agrees with other findings [8].

In Japan, palm oil exhibited favourable effects on cholesterolaemia and prostaglandin production compared with olive oil in a rat model [20].

Subsequently, the investigation of these effects was extended to humans [21]. Healthy, normolipidaemic subjects (20 men, 13 women), 22-41 years old, were fed either palm olein or olive oil supplying two-thirds (22% kcal) of total dietary fat, using a crossover design during two consecutive six-week dietary periods. In a one-to-one exchange of 7% kcal between 16:0 and 18:1-with dietary cholesterol below 300 ma, linoleic acid (18:2) held constant at approximately 3.0% kcal, and 14:0 + 12:0 at less than 1.0% kcal- 16:0 and 18:1 exerted equivalent effects on the serum lipid profile in normocholesterolaemic subjects. (Somewhat similar findings for 16:0 and 18:1 were demonstrated in normocholesterolaemic monkeys [16].)

The cholesterol value during palm olein consumption should have been 18-20 mg/dl higher than with olive oil according to the Keys and Hegsted regression equations, but this difference disappears in accord with the observed results when 16:0 is considered neutral. Thus this study, together with others [7, 16], offers strong support for the inference that the SFAs of palm oil, like those of cocoa butter, do not exert the hypercholesterolaemic action predicted by the classic regression equations.

Earlier human studies in which dietary 16:0 was hypercholesterolaemic relative to 18:1 [4, 5] differed from this one [21] in at least three respects. First, the diets in the earlier studies were fed as liquid formulas, which characteristically generate aberrant results [22] and have been discounted in major literature reviews [23]. Second, subjects in the previous studies were older, had greater body mass index (BMI), were relatively hypercholesterolaemic (average total cholesterol >225 mg/dl), and presumably had relatively depressed LDL-receptor activity at the time of study. Third, the percentage of energy exchanged between 16:0 and 18:1 in the earlier studies was extreme (>15% kcal) compared with the present exchange (7% kcal) or with what might be achieved through other practical manipulations of typical diets ( < 10% kcal).

Discussion

Contrary to the predictions of the Keys [3] and Hegsted [8] equations, the evidence presented in this review indicates that the substitution of palm oil or its liquid fractions (palm olein, super olein) for habitual fats in the diet does not result in an elevation of total serum cholesterol. This appears to be so particularly under certain dietary and anthropomorphic conditions, namely, when threshold dietary levels of 18:2 are met and counter the cholesterol-raising effects of the 12- and 16-carbon SFAs [24], and in lean, normocholesterolaemic individuals with low dietary cholesterol intake ( <300 mg daily), who presumably have up-regulated LDL-receptor activity.

The typical Malaysian diet cooked in palm olein contains about 3% kcal of 18:2 [25], whereas the palm olein-rich diets in two studies [7, 21] contained about 3.5% kcal of this PUFA. In the presence of only trace amounts (approximately 0.5% kcal) of the cholesterolaemic "villain" 14:0, the dietary level of 18:2 in the above diets either approximated or exceeded threshold levels [24] required to counter the cholesterol-raising effects of the 12-and 16-carbon SFAs. This would largely explain the non-hypercholesterolaemic effects of palm olein-rich diets. The same explanation also applies to the study in which no detrimental cholesterolaemic effects were observed despite raising the level of palm oil in a typical American diet twentyfold [14].

Furthermore, at least two factors contribute to the recurrent discrepancy that has been noted [7, 21] between the cholesterolaemic response obtained with a 16:0-rich diet and the predictions generated by the Keys and Hegsted regressions. One is that the initial cholesterolaemia (i.e., LDL-receptor set point) of the study population seems to affect the response, particularly that to 16:0 [26]. This point was highlighted earlier for discrepancies observed in some studies [4, 5, 21] for the cholesterolaemic response of 16:0-rich versus 18:1-rich diets. The second factor is the failure of the classic regressions to recognize the non-linear total serum cholesterol response associated with dietary 18:2 intake [27].

Ample evidence establishes that the intramolecular fatty acid distribution in the triglycerides influences the cholesterolaemic impact of dietary fats [2, 28, 29]. An important explanation of why palm oil does not "obey" the Keys and Hegsted models is that its 16:0 content, being predominantly esterified at the a-position, does not raise blood cholesterol levels, in contrast to the 16:0 in butterfat (esterified in the ß-position), which served as the major source of 16:0 in the Keys and Hegsted studies [3, 8].

It is also noteworthy that, unlike most polyunsaturated vegetable oils, palm oil requires little or no hydrogenation before its incorporation into food products [30, 31]. This attribute puts palm oil in good light, particularly when the question of the health impact of dietary transfatty acids (formed during hydrogenation) is still controversial. Interest in the topic has recently been renewed by reports that dietary transfatty acids raise the atherogenic factors LDL [32] and lipoprotein(a) [33] and lower the protective HDL [32].

Another possible reason for the unexpected non-hypercholesterolaemic action of palm oil is that the oil is very rich in tocotrienols, the unsaturated analogue of tocopherols. They reportedly inhibit cholesterol synthesis in vivo [34], thus exerting a hypocholesterolaemic action in human [35, 36] and animal models [34, 37]. However, it must be emphasized that the ingestion of encapsulated tocotrienolrich concentrates from palm oil is quite different from eating typical diets cooked in and containing palm olein. In the latter case, some destruction of these minor components in the oil is expected during the cooking process.

Work on the influence of 16:0 and other fatty acids on apo A1 and LDL-receptor mRNA abundance represents a challenging new field, which at present is in its infancy. Available reports on the beneficial impact of 16:0 + 18:1-rich diets (palm-oil source) in this area appear to come from only one group of American investigators [38, 39]. It would appear that more work needs to be done before the full impact of the findings in this interesting area is realized.

In conclusion, the evidence presented for palm oil in this review highlights that not all dietary fats generally regarded as saturated need raise total serum cholesterol, and thus such foods have a place in our daily diet. In view of this, the use of the cholesterol/ saturated-fat index [40], a computation modified from Zilversmit's cholesterol index for foods [41], which was based on the Keys regression [3], to measure the hypercholesterolaemic and atherogenic potential of foods can be misleading, particularly when applied to palm oil. On the same point, recent efforts through CODEX channels to label the cholesterol content of foods on the basis of their total SFA content appear unjustified.

Nutritionists and health professionals, particularly physicians, have a responsibility in the area of disseminating nutrition information. It is important that they keep abreast of recent knowledge on the cholesterolaemic impact of dietary fats and fatty acids. There is certainly no need to subscribe to the "saturated-fats phobia".

Acknowledgements

The author thanks Dato' Dr. M. Jegathesan, director of the Institute for Medical Research, Kuala Lumpur, for permission to submit this paper for publication. He also acknowledges the valued comments of Dr. Chong Yoon Hin during the preparation of the manuscript.

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