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.
Food and Nutrition Bulletin, vol. 15, no. 2 © 1994, The United Nations University.
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.
1
2
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
A critical review of the cholesterolaemic effects of palm oil
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
Predicted
  Observed Keys Hegsted
equation [3] equation [8]
Palm olein - 36 - 26a - 33
Corn oil - 68 - 49 - 58
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.
Tony Ng Kock Wai 3

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

Test fat and trial Total cholesterol LDL cholesterol HDL cholesterol Tri glycerides
Palm oila
1 -13 -32 10 -17
2 -14 -26 -17 -5
3 -5 5 0 7
4 - 12 - 14 - 13 11
Desi gheeb
1 4 -4 2 12
2 7 6 11 -4
3 13 -4 6 7
4 16 37 -3 26
Vanaspatic
1 - 0.5 - 15 25 18
2 -9 19 0 - 15
3 -4 7 9 0.6
4 11 42 10 25
Cottonseed oild
1 11 3 -13 5
2 0.9 37 25 - 12
3 -4 0 17 5
4 35 4 16 38
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
4
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
TABLE 3. Comparative cholesterolaemic effects of palmitic acid (16:0) versus myristic acid (14:0) + lauric acid (12:0)
in monkeys
PUFA: PUFA: PUFA
Fat blend
MUFA SFA (mg/dl)
DF1 0.23 0.12 9.4
DF2 1.16 0.38 16.4
DF3 1.07 0.29 14.1
DF4 1.20 0.36 17.2
DF5 2.47 1.04 29.9
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
A critical review of the cholesterolaemic effects of palm oil
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.
14:0 + Total choles
16:0 LDL:HDL
12:0 terol (mg/dl)
66 11 232 ± 10 1.23 ± 0.1
33 8 205 11 0.95 ± 0.1
19 25 203 ± 10 0.98 ± 0.1
1 40 183 ±9 0.89 ± 0.1
1 23 173 ±9 0.77 ± 0.05
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].
Tony Ng Kock Wai
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.
5
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 α-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
6
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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