European Journal of Clinical Nutrition (2001) 55, 748–754
ß 2001 Nature Publishing Group All rights reserved 0954–3007/01 $15.00
www.nature.com/ejcn
Original Communication
Effects of palm oil and dietary cholesterol on plasma lipoproteins:
results from a dietary crossover trial in free-living subjects
LE Bautista1,2*, OF Herrán and C Serrano2
1
Instituto Colombiano de Investigación Biomédica, Universidad Industrial de Santander, Bucanamanga, Columbia; and 2Fundación
Cardiovascular del Oriente Colombiano, Bucanamanga, Columbia
Objective: To study the effects of palm oil (PO) and egg consumption (E) on plasma lipoproteins.
Design: Randomized crossover trial.
Setting: Free-living subjects.
Subjects: Twenty-eight healthy male students aged 20 – 34 y.
Interventions: Four typical Colombian diets (10 878 kJ=day; 57% energy in carbohydrates, 12% energy in
proteins and 31% energy in fats) were consumed for 4 weeks. The HPOLC diet was high in PO (8.8% energy as
palmitic acid, PA) and low in eggs (181.2 mg=kJ of dietary cholesterol, DC); the HPOHC diet was high in PO and
high in eggs (866.1 mg=kJ of DC); the MPOMC diet was moderate in PO (6.3% energy as PA) and moderate in
eggs (581.6 mg=kJ of DC); and the LOPOMC diet had no PO and was moderate in eggs (543.9 mg=kJ of DC).
Main outcome: Total (TC), low density (LDL-c), and high density lipoprotein cholesterol (HDL-c), and
triacylglycerols (TAG) were measured on a pool of three fasting blood samples collected in consecutive days
the last week of each diet.
Results: Comparison of the HPOHC and HPOLC diets showed increases in TC and LDL-c of 0.21 (P ¼ 0.01), and
0.16 mmol=l (P ¼ 0.05). Comparison of LOPOMC and MPOMC diets showed increases in TC and LDL-c of 0.39
(P < 0.001), and 0.38 mmol=l (P < 0.001), respectively. No significant changes in HDL-c or TAG were observed.
Conclusions: Our findings suggest that non-extreme short-term changes in PO and DC consumption lead to
significant elevations in plasma TC and LDL-c.
Sponsorship: CENIPALMA, Fundación Cardiovascular del Oriente Colombiano, Universidad Industrial de
Santander.
Descriptors: dietary fats; dietary cholesterol; palm oil; lipoproteins; cross-over studies
European Journal of Clinical Nutrition (2001) 55, 748–754
Introduction
During the last three decades, death rates from coronary
heart disease (CHD) have tripled and cardiovascular diseases have become the main cause of death in the Colombian population (Pabón Rodriguez, 1993). These changes
may be partially due to changes in population dietary
*Correspondence: LE Bautista, Uniformed Services University of the
Health Sciences (USUHS), PMB – Division of Epi and Biostat, Room
A1039, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, USA.
E-mail: [email protected]
Guarantor: LE Bautista.
Contributors: LEB was responsible for study design, supervision of the
running of the study, statistical analysis, and writing of the paper. OFH
designed the diets used in the study, supervised food preparation and
consumption, and participated in the writing of the paper. CS was in
charge of laboratory analysis and data quality, and participated in the
writing of the paper.
Received 24 April 2000; revised 5 February 2001;
accepted 5 February 2001
patterns. In this period, palm oil has become the main
source of edible fats contributing up to 80% of all fat
consumed by this population. Also, it is well known that
elevated plasma total cholesterol (TC), low density lipoprotein cholesterol (LDL-c) and triacylglycerols (TAG), as
well as low levels of high density lipoprotein cholesterol
(HDL-c) are risk factors for CHD and that they are
influenced and can be modified by the type and amount
of dietary fats (Ascherio & Willett, 1995).
Palm oil is the most important edible source of palmitic
acid (C16:0), one of the main saturated fatty acids (SFAs)
in the human diet. Several studies have shown that dietary
palmitic acid (DPA) has a hypercholesterolemic effect,
particularly when compared with polyunsaturated fatty
acids (PUFAs; Keys et al, 1957; Keys et al, 1965a,c;
Laine et al, 1982; Mattson & Grundy, 1985; Anonymous,
1990; Ng et al, 1991; Denke & Grundy, 1992). Nevertheless, these studies have been questioned (Reiser, 1973;
Anonymous, 1987, 1990) because they were too short, had
Effects of palm oil and dietary cholesterol
LE Bautista et al
749
small sample size (Laine et al, 1982; Mattson & Grundy,
1985; Ng et al, 1991; Denke & Grundy, 1992), and the
diets used had an unusually high fat content (Keys et al,
1965b; Laine et al, 1982; Mattson & Grundy, 1985; Denke
& Grundy, 1992) and cholesterol (Laine et al, 1982;
Mattson & Grundy, 1985; Ng et al, 1991; Denke &
Grundy, 1992). Also, there is evidence that the hypercholesterolemic effect of SFAs depends on the amount of fat
and cholesterol in the diet (Laine et al, 1982; Wolf &
Grundy, 1983; Baudet et al, 1984; Schonfeld et al, 1982).
Some studies have shown that the effect of the degree of
saturation of dietary fats is increased in high cholesterol
diets (National Diet – Heart Study Research Group, 1968;
Durrington et al, 1977; Laine et al, 1982; Wolf & Grundy,
1983), while it is not important in low-cholesterol
(100 mg=day) diets (Wolf & Grundy, 1983). The fact that
the hypercholesterolemic effects of SFAs could depend on
diet composition makes it difficult to extrapolate study
results among populations with different types of diets.
Moreover, other studies (Baudet et al, 1984; Marzuki et al,
1991; Hornstra et al, 1991; Sundram et al, 1992) have
failed to show a hypercholesterolemic effect of DPA when
compared to PUFAs such as linoleic acid. Due to the
uncertainty regarding the hypercholesterolemic effects of
DPA, and the fact that those effects may depend on diet
composition, we carried out an experimental study to
ascertain the short-term effects of increased dietary cholesterol (DC) and DPA consumption among normal subjects,
following their daily activities and taking their typical diet.
We were particularly interested in the effect of high-DC as
compared to a low-DC in the context of high-PA diet, as
well as in the effect of moderate-PA as compared to lowPA in the context of a moderate-DC diet, because these
patterns are typical in the studied population.
Methods
We carried out a double-blind 44 dietary crossover trial.
Twenty-eight male university students (20 to 34-y-old)
were randomly assigned to the four diet sequences (seven
students per diet group) of a randomly selected 44
standard Latin square. A standard square was deemed
appropriate because the duration of each diet made carryover effects and diet sequence irrelevant. All the students
were living in a university residence and consumed their
three meals per day at the university cafeteria, including the
weekend. None had any evidence of physical or psychiatric
disease and all had normal blood pressure, fasting glycemia
and blood coagulation tests. The study was approved by the
Research Ethics Committee of the Universidad Industrial
de Santander, School of Medicine, and informed consent
was obtained from all participants.
Diets were composed of solid food, prepared in the
university kitchen by trained personnel, and consumed adlibidum on site. Breakfast included fresh fruits, whole milk
drinks, cereal, eggs and cheese, while lunch and dinner
included fresh fruits, beans, green salad, rice, red meat,
poultry, fish, yucca root, and plantain. Four different diets
were used, all of them with 2600 calories=day, 57% energy
from carbohydrates, 12% energy from proteins, and 31%
energy from fats. The high palm oil – low cholesterol diet
(HPOLC) was high in DPA (8.8% energy) and low in DC
(181.2 mg=kJ). The high palm oil – high cholesterol diet
(HPOHC) was high in DPA (8.8% energy) and high in DC
(866.1 mg=kJ). The moderate palm oil – moderate cholesterol diet (MPOMC) had a moderate content of DPA (6.3%
energy) and DC (581.6 mg=kJ). Finally, the low palm oil –
moderate cholesterol diet (LPOMC) had virtually no DPA
and a moderate amount of DC (543.9 mg=kJ). Changes in
DC were mostly due to the addition of one egg=day to the
diet and changes in DPA were due to replacement of
sunflower oil (5.1% DPA; 3.5% other SFAs; 57.7% oleic
acid; 15.6% linoleic acid; and 0.9% other non-SFAs) by
palm oil (43.8% DPA; 6.2% other SFAs, 38.9% oleic acid;
10.6% linoleic acid; and 0.4% other non-SFAs).
The four groups of students received the diets in the
following sequence. Group 1, HPOHC, MPOMC, LPOMC,
HPOLC; Group 2, MPOMC, LPOMC, HPOLC, HPOHC;
Group 3, LPOMC, HPOLC, HPOHC, MPOMC; and Group
4, HPOLC, HPOHC, MPOMC, LPOMC. Each diet was
consumed for 4 weeks and foods consumed outside the
study were recorded by the participants and its nutrient
content was estimated using Colombian food composition
tables (Instituto Colombiano de Bienestar Familiar (ICBF),
1992; Quintero et al, 1990). A daily diet compliance record
was kept by the staff of the study. All participants were
instructed to continue with their regular activities throughout the trial and they had no knowledge of the specific diet
being consumed at any study period.
During the last week of each diet period each subject
was weighted and his blood pressure was measured. Also,
three 12 h fasting venous blood samples were drawn from
each subject in consecutive days of the last week of each
diet period. Blood samples were processed and plasma was
stored at 720 C. Plasma lipids measurements were carried
out in a pool of the three plasma samples, in order to reduce
day-to-day variability in cholesterol levels. Plasma lipoprotein measurements followed the standard protocol of the
Lipid Research Clinics Program (Lipid Research Clinics
Program, 1974). To reduce laboratory-related variability,
blood samples were analyzed in batches and measurements
were repeated in a 10% random sample of all participants,
for quality control. Lipid measurements were carried out
without knowledge of the type of diet the subject was
eating.
The effects of the experimental diets on lipid concentration were estimated by using the methodology of basic
contrasts suggested by Senn (1993). Mean average changes
in plasma lipids concentration were calculated and paired ttest and analysis of variance (ANOVA) were used to
evaluate their statistical significance. Multiple linear
regression was used to explore possible associations
between participant’s baseline characteristics and response
to each experimental diet. To assess the effects of the
European Journal of Clinical Nutrition
Effects of palm oil and dietary cholesterol
LE Bautista et al
750
controlled diets on the variability of the change in lipids
concentration, we calculated the coefficient of variation for
each basic contrast. Pearson correlation coefficients were
used to quantify the potential association between the
response to DPA and the response to DC.
Results
Twenty-eight male subjects were enrolled in the study
(mean age 24.6 y; 95% CI, 23.5, 25.8). Only one of them
had total cholesterol levels over 6.21 mmol=l, but eight
(28.6%) had cholesterol levels between 5.17 and
6.21 mmol=l. Mean TC, LDL-c, HDL-c and TAG were
4.80 mmol=l (95% CI, 4.50, 5.11), 3.35 (95% CI, 3.09,
3.62), 0.93 (95% CI, 0.86, 1.01), and 1.12 (95% CI, 0.96,
1.29) mmol=l, respectively. After randomization, baseline
TC, LDL-c and TAG were higher in Groups 1 and 2 than in
Groups 3 and 4 (Table 1). However, these differences were
not statistically significant and did not compromise the
validity of our results because each subject acted as his own
control. There were no drop-outs and participants consumed 90% of all meals provided in the study. Foods
consumed most frequently outside the study diets were
bottled drinks, bread and sweets. Diet compliance was
similar in the four diet-sequence groups and for all diets.
Only one out of 140 blood lipids measurements was
missing. Plasma lipid measurements were carried out in a
pool of three blood samples 80% of the time, in a pool of
two samples 17% of the time, and in one sample 3% of the
time.
Changes in plasma lipoproteins due to changes in DC
were estimated by contrasting lipoprotein levels at the end
of the HPOHC diet and the HPOLC diet. Similarly,
changes in lipoprotein profile associated with DPA were
estimated by comparing plasma lipoprotein levels at the
end of the LPOMC diet and the MPOMC diet. There was a
non significant average reduction of 1.1 kg in body weight
during the study period (P ¼ 0.09).
The increase in DC resulted in a significant rise in TC
and LDL-c: 0.21 mmol=l (P ¼ 0.009) and 0.16 mmol=l
(P ¼ 0.047), respectively (Table 2). However, the highcholesterol diet did not result in significant increases in
HDL-c nor in TAG: 0.03 mmol=l (P ¼ 0.095) and
0.04 mmol=l (P ¼ 0.390), respectively. Overall, changes in
TC associated with DC intake showed a large variability,
ranging from 70.41 to 1.19 mmol=l (Figure 1). Nine
(33.3%) subjects showed no increase or even a decrease
in TC, while 10 (37.0%) showed increases greater than
0.26 mmol=l. The standard deviation of the mean TC
change was 0.39 mmol=l and the coefficient of variation
was 184.1%. The variability in LDL-c change was similar
to that in TC. LDL-c change varied from 70.62 to
1.24 mmol=l, the standard deviation of the mean change
Table 1 Baseline participant’s characteristics after random assignment to the four diet sequences
Diet sequence groupsa
Characteristic
Age (y)
Weight (kg)
Total cholesterol (mmol=l)
HDL cholesterol (mmol=l)
LDL cholesterol (mmol=l)
Triacylglycerols (mmol=l)
All
1
2
3
4
P-value
24.6
62.0
4.80
0.93
3.35
1.12
25.3
63.4
5.04
0.93
3.59
1.13
25.6
63.3
5.07
1.01
3.45
1.31
23.4
58.9
4.57
0.92
3.15
1.10
24.3
63.0
4.53
0.87
3.22
0.94
0.55
0.60
0.56
0.61
0.63
0.53
a
Group 1: (high palm oil þ high cholesterol), (moderate palm oil þ moderate cholesterol), (low palm oil þ moderate
cholesterol), and (high palm oil þ low cholesterol).
Group 2: (moderate palm oil þ moderate cholesterol), (low palm oil þ moderate cholesterol), (high palm oil þ low
cholesterol), and (high palm oil þ high cholesterol).
Group 3: (low palm oil þ moderate cholesterol), (high palm oil þ low cholesterol), (high palm oil þ high cholesterol),
and (moderate palm oil þ moderate cholesterol).
Group 4: (high palm oil þ low cholesterol), (moderate palm oil þ high cholesterol), (moderate palm oil þ moderate
cholesterol), and (low palm oil þ moderate cholesterol).
Table 2 Changes in plasma lipids associated with changes in dietary cholesterol and palmitic acid content in the diet
Dietary contrast
Plasma lipid
High vs low cholesterol
Total cholesterol
LDL cholesterol
HDL cholesterol
Triacylglycerols
Total cholesterol
LDL cholesterol
HDL cholesterol
Triacylglycerols
High vs low palm oil
European Journal of Clinical Nutrition
Change (mmol=l)
0.21
0.16
0.03
0.04
0.39
0.38
0.03
70.05
95% confidence interval
(0.07,
(0.002,
(70.006,
(70.06,
(0.19,
(0.21,
(70.006,
(70.002,
0.36)
0.32)
0.08)
0.15)
0.59)
0.55)
0.07)
0.07)
P-value
0.009
0.047
0.095
0.390
< 0.001
< 0.001
0.097
0.405
Effects of palm oil and dietary cholesterol
LE Bautista et al
751
Figure 1
diet.
Changes in total cholesterol associated with a high colesterol
was 0.40 mmol=l and the coefficient of variation was
249.7%.
Consumption of the high-DPA diet resulted in increases
of 0.39 mmol=l in TC (P < 0.001) and 0.38 mmol=l in
LDL-c (P < 0.001). Neither HDL-c nor TAG were significantly affected by the high DPA diet (Table 2). The
response to DPA was very variable, ranging from 70.49 to
1.50 mmol=l. Two participants (7.1%) lowered their TC by
0.21 mmol=l or more, 11 (39.3%) had changes between
70.23 and 0.23 mmol=l and 15 (53.6%) had increase
0.26 mmol=l (Figure 2). The standard deviation of TC
changes was 0.51 mmol=l and the coefficient of variation
was 129.7%. Results for LDL-c were similar as those
for TC.
DC and DPA effects on blood lipoprotein profile were
independent of diet sequence (P ¼ 0.24). However, the
subject’s response to DC tend to be correlated to the
response to DPA, as shown by a Pearson correlation
coefficient of 0.46 (P ¼ 0.02). Similar results were found
for LDL-c (correlation coefficient ¼ 0.41, P ¼ 0.03).
Finally, age, sex, and initial weight did not modify the
effect of a higher consumption of DC or DPA on plasma
lipids. Nevertheless, subjects with higher baseline cholesterol levels were more responsive to the high DPA diet
(Figure 2). Each increment of one mg=dl of baseline TC
resulted in an additional change of 0.006 mmol=l in the
effect of DPA on TC (P ¼ 0.048). On the contrary, baseline
Figure 2
diet.
Changes in total cholesterol associated wity a high palm oil
TC had no significant influence (P ¼ 0.11) on the effect of
DC on TC (Figure 1).
Discussion
Our results show that non-extreme short term changes in
DPA and DC consumption lead to significant elevations in
plasma TC and LDL-c. On the other hand, plasma HDL-c
and TAG changed very little in response to DPA or DC.
These results are consistent with results from previous
studies (Keys et al 1957, 1965a – c; Hegsted et al, 1965;
Roberts et al, 1981; Tan et al, 1980; Sacks et al, 1984;
McMurry et al, 1982; Mattson & Grundy, 1985; Laine
et al, 1982; Anonymous, 1990; Ng et al, 1991; Denke &
Grundy, 1992), even though our study was conducted with
typical diets, among free-living subjects who continued
their regular daily activities.
We should keep in mind that the observed effects
occurred in young males taking a diet with 31% energy
coming from fat. The rise in TC associated to increased DC
intake was similar to the expected change predicted using
Keys’ formula (Keys et al, 1965a). Similarly, TC changes
in response to DPA were consistent with the expected
change according to Keys’ studies (Keys et al, 1957).
Not all study subjects experienced an increase in plasma
lipids when challenged with DC or DPA. The existence of
European Journal of Clinical Nutrition
Effects of palm oil and dietary cholesterol
LE Bautista et al
752
hypo- and hyper-responders to DC seems to be individually
determined, but the classification of subjects in either group
compromises the diet-independent within-person variability
of serum cholesterol (Katan & Beynen, 1992). On the other
hand, it is known that hypo- and hyper-responders to
dietary fats do exist, but total insensitivity of serum
cholesterol is usually due to random fluctuations and it is
not a fixed characteristic of the subject (Katan & Beynen,
1992). Although the accurate identification of hypo- and
hyper-responders to DC and DPA is of practical interest for
dietary advice, no feasible test is currently available to
accomplish this task.
Moreover, we found that subjects who have an accentuated response to DC tend to be also hyper-responsive to
DPA. The correlation between DC and DPA responses
observed in our study (r ¼ 0.46, P ¼ 0.02) was similar to
that reported in previous experimental studies (r ¼ 0.50,
n ¼ 23; P < 0.05, Katan et al, 1988; Katan & Beynen,
1992). Although Katan & Beynen (1987) have reported
that subjects who were hyper-responsive to DC had
higher levels of TC than subjects who were hyporesponders, we did not find such a relationship in our
study. However, TC response to DPA was related to baseline TC levels. This suggests that subjects with hypercholesterolemia are even more sensible to DPA than those who
are normocholesterolemic.
Changes due to DC and DPA were very variable, but the
response to DPA was less so than the response to DC. This is
consistent with the fact that the consumption of fatty acids
explains most of the variability in plasma cholesterol levels
(Hegsted et al, 1965). The exact mechanism by which SFAs
increment plasma cholesterol has not been establish, but there
is some evidence that this effect is mediated by suppression of
the LDL receptor (Grundy & Vega, 1990).
Our results contradict those of other studies (Baudet
et al, 1984; Marzuki et al, 1991; Hornstra et al, 1991;
Sundram et al, 1992) that reported a neutral DPA effect.
The absence of a DPA effect in Marzuki’s study (Marzuki
et al, 1991) could be due to random error because only one
blood sample was used to measure plasma cholesterol.
Also, the palm oil used by Baudet et al (1984) had a low
concentration of palmitic acid (22%) and a high concentration of oleic acid (58%), which could result in lower plasma
cholesterol levels due to the effect of the monounsaturated
fatty acid.
Moreover, in the studies of Hornstra et al (1991) and
Sundram et al (1992), the control diet was the usual diet of
the participants and was very similar to the experimental
diet in fatty acid proportional composition. Therefore, their
results could not be considered as valid evidence of a
hypocholesterolemic or even neutral effect of DPA when
compared with polyunsaturated fatty acids.
More recently published studies have failed to find a
hypercholesterolemic effect of PO (de Bosh et al, 1996;
Choudhury et al, 1995; Ghafoorunissa et al, 1995; Mutalib
et al, 1999). Results from de Bosch et al (1996) can be
questioned because her experiments were not randomized,
no other measure for control of potential confounders was
European Journal of Clinical Nutrition
used, and no information regarding compliance nor data
quality control are provided to the reader. Thus, her
conclusion that there are no adverse influences of PO on
plasma lipoprotein profile seems to be unfounded.
Similarly, in a crossover trial among free-living young
adults, Choudhury et al (1995) did not find a hypercholesterolemic effect of palmolein when compared with olive
oil. However, they replaced only half of the usual individualized dietary fat intake by palmolein or olive oil,
corresponding to 17% of total dietary fat intake. Moreover,
study subjects prepared their own food and were instructed
to exclude from their diets fat sources such as butter,
margarine, eggs and cooking oils, making the study diets
unrealistic. On the contrary, only one type of cooking oil
(palm or sunflower oil) was used in our study, and food
preparation was strictly standardized. The low percentage
of total dietary fat intake change in the Choudhury study
and the lack of direct control over other fat sources may
explain why palmolein consumption did not result in
increased cholesterol levels.
In another dietary crossover trial comparing groundnut
oil with PO, Ghafoorunissa et al (1995) found no increase
in TC, LDL-c or HDL-c associated with consumption of the
PO diet. However, their study included only 12 subjects
and plasma lipoprotein measurements were based on a
single blood sample taken at the end of each diet period.
The small sample size and the use of a single blood sample
resulted in large variability in the measurement of plasma
lipids and low power to detect between-diet differences.
For example, mean TC for the group consuming the PO
diet was 155 mg=dl, but the 95% confidence interval was
very wide, from 137.9 to 172.1 mg=dl (our calculation).
Finally, based on the results of a parallel experimental
design, Mutalib et al (1999) reported that changes in TC
and LDL-c associated to a diet with 26% energy from PO
(15 subjects) were similar to those in a ‘wild’ control group
of 10 subjects receiving their usual diet, with 3% energy
from PO. However, design and interpretation issues make
questionable their conclusion. Their data actually showed
an increase in TC and LDL-c of 0.41 mmol=l in the PO diet
group, and a pooled increase of 0.25 mmol=l in the control
group (calculated from Table 2 of Mutalib et al, 1999).
Moreover, due to the large variability in the response to
dietary PO and the small sample size used, it is likely that
both groups were not comparable regarding factors related
to the response to dietary PO. Furthermore, they had no real
data on the nutrient content of the control diet. Assuming
that the content of PO in the control diet was 3% of energy
depended on the unlikely fact that 10 non-randomly
selected subjects were a representative sample of the
Scottish population regarding characteristics of the diet.
Since sources of potential error were tightly controlled,
it is unlikely that our study results were biased. Because
diet sequences were randomly assigned and each subject
acted as his own control, selection bias can be ruled out.
Measurement errors were also unlikely because laboratory
tests were carried out without knowledge of the type of diet
being consumed and were based on a pool of multiple
Effects of palm oil and dietary cholesterol
LE Bautista et al
753
blood samples to reduce individual day-to-day variability in
plasma cholesterol levels.
Although it is well known that changes in plasma
cholesterol associated with changes in the diet are stable
after the third week in the same diet, extrapolation of our
results to long-term effects is compromised because each
diet lasted only one month. Another study limitation is the
lack of measurements of other plasma lipid fractions such
as lipoprotein(a) and HDL-c subfractions.
The effects of DPA and DC observed in this study may
have important implications in dietary counseling. Considering that experimental and observational cohort studies
have shown that a 1% reduction in TC yields a 2% reduction
in the long term risk of coronary heart disease (Lipids
Research Clinics Program, 1984; Stamler et al, 1986; Law
et al, 1994), the hypercholesterolemic effect of DPA (8%
change) and DC (4% change) observed in our study could
result in a significantly higher risk of atherosclerosis and
cardiovascular diseases in this population. Since no suitable
tests to distinguish between responders and non-responders
to PA or DC are currently available, restriction in the
consumption of palm oil and eggs in subjects at high risk
of coronary heart disease may be advisable
Acknowledgements —We thank Dr Patricio López for reviewing and
helping to edit the final manuscript.
References
Anonymous (1987): New findings on palm oil. Nutr. Rev. 45, 205 – 207.
Anonymous (1990): Saturated fatty acids in vegetable oils. Council on
Scientific Affairs. J.A.M.A. 263, 693 – 695.
Ascherio A & Willett W (1995): New directions in dietary studies of
coronary heart disease. J. Nutr. 125, 647S – 655S.
Baudet MF, Dachet C, Lasserre M, Esteva O & Jacotot B (1984):
Modification in the composition and metabolic properties of human
low density and high density lipoproteins by different dietary fats.
J. Lipid Res. 25, 456 – 468.
Choudhury N, Truswell AS & McNeil Y (1995): Comparison of plasma
lipids and vitamin E in young and middle-aged subjects on potato crisps
fried in palmolein and highly oleic sunflower oil. Am. J. Clin. Nutr. 61,
1043 – 1051.
de Bosch NB, Bosch V & Apitz R (1996): Dietary fatty acids in atherothrombogenesis: influence of palm oil ingestion. Haemostasis 26, 46 –
54.
Denke MA & Grundy SM (1992): Comparison of effects of lauric acid and
palmitic acid on plasma lipids and lipoproteins. Am. J. Clin. Nutr. 56,
895 – 898.
Durrington PN, Bolton CH, Hartog M, Hartog M, Angelinetta R, Emmett P
& Furniss S (1977): The effect of a low-cholesterol, high-polyunsaturate diet on serum lipids levels, apolipoprotein B levels and trygliceride
fatty acid composition. Atherosclerosis 27, 465 – 475.
Ghafoorunissa, Reddy V & Sesikaran B (1995) Palmolein and groundnut
oil have comparable effects on blood lipids and platelet aggregation in
healthy Indian subjects. Lipids 30, 1163 – 1169.
Grundy SM & Vega GL (1990): Causes of high blood cholesterol.
Circulation 81, 412 – 427.
Hegsted DM, McGandy RB, Myers ML & Stare FJ (1965): Quantitative
effects of dietary fat on serum cholesterol in man. Am. J. Clin. Nutr. 17,
281 – 295.
Hornstra G, Van Houwelingen AC, Kester AD & Sundram K (1991): A plam
oil-enriched diet lowers serum lipoprotein(a) in normocholesterolemic
volunteers. [Letter]. Atherosclerosis 90, 91 – 93.
Instituto Colombiano de Bienestar Familiar (ICBF) (1992): Tabla de
composición de alimentos colombianos. Santa Fé de Bogota: Ministerio
de Salud.
Katan MB, Berns MAM, Glatz JFC, Knuiman JT, Nobels A & De Vries
JHM (1988): Congruence of individual responsiveness to dietary
cholesterol and to saturated fats in humans. J. Lipid Res. 29, 883.
Katan MB & Beynen AC (1987): Characteristics of human hypo- and
hyperresponders to dietary cholesterol. Am. J. Epidemiol. 125, 387 – 399.
Katan MB & Beynen AC (1992): Hyporesponders and hyperresponders to
changes in diet. In Cholesterol and Coronary Heart Disease. The Great
Debate. Proceedings of an International Conference, ed. P Gold,
Grover S, DAK Roncari, pp 177 – 187. Park Ridge, NJ: Parthenon.
Publishing Group.
Keys A, Anderson JT & Grande F (1957): Prediction of serum cholesterol
responses of men to changes in fats in the diet. Lancet ii, 959 – 966.
Keys A, Anderson JT & Grande F (1965a): Serum cholesterol response to
changes in the diet. I. Iodine values of dietary fat versus 2S-P.
Metabolism 14, 747 – 758.
Keys A, Anderson JT & Grande F (1965b): Serum cholesterol response to
changes in the diet. II. The effect of cholesterol in the diet. Metabolism
14, 759 – 765.
Keys A, Anderson JT & Grande F (1965c): Serum cholesterol response to
changes in the diet. IV. Particular saturated fatty acids in the diet.
Metabolism 14, 776 – 787.
Laine DC, Snodgrass CM, Dawson EA, Ener MA, Kuba K, & Frantz ID Jr
(1982): Lightly hydrogenated soy oil versus other vegetable oils as a
lipid-lowering dietary constituent. Am. J. Clin. Nutr. 35, 683 – 690.
Law MR, Wald NJ & Thompson SG (1994). By how much and how
quickly does reduction in serum cholesterol concentration lower risk of
ischemic heart disease? Br. Med. J. 308, 367 – 373.
Lipids Research Clinics Program (1974): Lipid Research Clinics Program.
Manual of Laboratory Operations. Bethesda, MD: National Institutes of
Health.
Lipids Research Clinics Program (1984): The Lipid Research Clinics
Coronary Primary Prevention Trial Results — reduction in incidence
of coronary heart disease. J.A.M.A. 251, 351 – 364.
Marzuki A, Arshad F, Razak TA & Jaarin K (1991): Influence of dietary
fat on plasma lipid profiles of Malaysian adolescents. Am. J. Clin. Nutr.
53, 1010S – 1014S.
Mattson FH & Grundy SM (1985): Comparison of effects of dietary
saturated, monounsaturated, and polyunsaturated fatty acids on plasma
lipids and lipoproteins in man. J. Lipid Res. 26, 194 – 202.
McMurry MP, Connor WE & Cerqueira MT (1982): Dietary cholesterol
and the plasma lipids and lipoproteins in the Tarahumara Indians: a
people habituated to a low cholesterol diet after weaning. Am. J. Clin.
Nutr. 35, 741 – 744.
Mutalib MSA, Wahle KWJ, Duthie GG, Whiting P, Peace H & Jenkinson
A (1999): The effect of dietary palm oil, hydrogenated rape and soya oil
on indices of coronary heart disease risk in healthy Scottish volunteers.
Nutr. Res. 19, 335 – 348.
National Diet – Heart Study Research Group (1968): The national dietheart study final report. Circulation 38(Suppl I), 1 – 428.
Ng TK, Hassan K, Lim JB, Lye MS & Ishak R (1991): Nonhypercholesterolemic effects of a palm-oil diet in Malaysian volunteers. Am. J. Clin.
Nutr. 53, 1015S – 1020S.
Pabón Rodrı́guez A (1993): La mortalidad en Colombia 1953 – 1991:
Bogotá: Instituto Nacional de Salud.
Quintero D, Alzate MC & Moreno S (1990): Tabla de composición de
alimentos. Medellin: Centro de Atención Nutricional.
Reiser R (1973): Saturated fat in the diet and serum cholesterol concentration:
a critical examination of the literature. Am. J. Clin. Nutr. 26, 524 – 555.
Roberts SL, McMurry MP & Connor WE (1981): Does egg feeding (ie
dietary cholesterol) affects plasma cholesterol in man? The results of a
double blind study. Am. J. Clin. Nutr. 34, 2092 – 2099.
Sacks FM, Salazar J, Miller L, Foster JM, Sutherland M, Samonds KW,
Albers JJ & Kass EH (1984): Ingestion of egg raises plasma low density
lipoproteins in free-living subjects. Lancet i, 647 – 649.
Schonfeld G, Patsch W, Rudel LL, Nelson C, Epstein M & Olson RE
(1982): Effects of dietary cholesterol and fatty acids on plasma
lipoproteins. J. Clin. Invest. 69, 1072 – 1080.
European Journal of Clinical Nutrition
Effects of palm oil and dietary cholesterol
LE Bautista et al
754
SennS (1993): Cross-over Trialsin Clinical Research. New York: John Wiley.
Stamler J, Wentworth D, Neaton JD (1986): Is the relationship between serum
cholesterol and risk of premature death from coronary heart disease
continuous and graded? Findings in 356,222 primary screnees of the
Multiple Risk Factor Intervention Trial (MRFIT). J.A.M.A. 256, 2823 –
2828.
Sundram K, Hornstra G, von Houwelingen AC & Kester AD (1992):
Replacement of dietary fat with palm oil: effect on human serum lipids,
lipoproteins and apolipoproteins. Br. J. Nutr. 68, 677 – 692.
European Journal of Clinical Nutrition
Tan MH, Dickinson MA, Albers JJ, Havel RJ, Cheung MC & Vigne JL
(1980): The effect of a high cholesterol and saturated fat diet on
serum high-density lipoprotein-cholesterol, apoprotein A-I, and apoprotein E levels in normolipidemic humans. Am. J. Clin. Nutr. 33, 2559 –
2565.
Wolf RN & Grundy SM (1983): Influence of exchanging carbohydrate for
saturated fatty acids on plasma lipids and lipoproteins in man. J. Nutr.
113, 1521 – 1528.