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Plant Foods for Human Nutrition 57: 319341, 2002.

2002 Kluwer Academic Publishers. Printed in the Netherlands.

Palm oil: Biochemical, physiological, nutritional,


hematological, and toxicological aspects: A review

D.O. EDEM
Department of Chemistry and Biochemistry, University of Uyo, Uyo, Akwa Ibom State,
Nigeria

Abstract. The link between dietary fats and cardiovascular diseases has necessitated a grow-
ing research interest in palm oil, the second largest consumed vegetable oil in the world.
Palm oil, obtained from a tropical plant, Elaeis guineensis contains 50% saturated fatty acids,
yet it does not promote atherosclerosis and arterial thrombosis. The saturated fatty acid to
unsaturated fatty acid ratio of palm oil is close to unity and it contains a high amount of the
antioxidants, -carotene, and vitamin E. Although palm oil-based diets induce a higher blood
cholesterol level than do corn, soybean, safflower seed, and sunflower oils, the consumption
of palm oil causes the endogenous cholesterol level to drop. This phenomenon seems to arise
from the presence of the tocotrienols and the peculiar isomeric position of its fatty acids. The
benefits of palm oil to health include reduction in risk of arterial thrombosis and atheroscler-
osis, inhibition of endogenous cholesterol biosynthesis, platelet aggregation, and reduction in
blood pressure. Palm oil has been used in the fresh state and/or at various levels of oxidation.
Oxidation is a result of processing the oil for various culinary purposes. However, a consid-
erable amount of the commonly used palm oil is in the oxidized state, which poses potential
dangers to the biochemical and physiological functions of the body. Unlike fresh palm oil,
oxidized palm oil induces an adverse lipid profile, reproductive toxicity and toxicity of the
kidney, lung, liver, and heart. This may be as a result of the generation of toxicants brought on
by oxidation. In contrast to oxidized palm oil, red or refined palm oil at moderate levels in the
diet of experimental animals promotes efficient utilization of nutrients, favorable body weight
gains, induction of hepatic drug metabolizing enzymes, adequate hemoglobinization of red
cells and improvement of immune function. However, high palm oil levels in the diet induce
toxicity to the liver as shown by loss of cellular radial architecture and cell size reductions
which are corroborated by alanine transaminase to aspartate transaminase ratios which are
higher than unity. The consumption of moderate amounts of palm oil and reduction in the
level of oxidation may reduce the health risk believed to be associated with the consumption
of palm oil. Red palm oil, by virtue of its -carotene content, may protect against vitamin A
deficiency and certain forms of cancer.

Key words: Biochemical, Hematological, Nutritional, Palm Oil, Physiological, Toxicological

Introduction

Palm oil is a lipid extracted from the fleshy orange-red mesocarp of the fruits
of the oil palm tree (Elaeis guineensis) which contain 45% to 55% oil. The oil
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palm tree has an unbranched stem and belongs to the Palmae family. The tree,
which can grow to a height of 20 to 30 meters, has an economic life span of 25
to 30 years [1]. The female bunch produced can weigh as much as 3040 kg
and contain up to 2000 fruitlets which are black in color when young, turning
to orange-red when ripe [1]. The oil palm is important in the sociocultural
activities of inhabitants of the area in which it grows. The importance is
demonstrated by the fact that no part of the plant is wasted, as every part
of the tree has economic importance [2]. The trunk is used as timber and a
local fuel source while the ash produced by burning the dead trees is rich
in potassium oxide, used in local soap production [3]. The leaf rib is used
for fencing and shed-making and the fibers are used to make rope [4]. The
leaves are used for thatching and the petiole for fencing and protecting the
tops of mud walls. Palm wine, a sweet drink (containing 4.3 g sucrose/100 ml
and 3.4 g glucose/100 ml) obtained by tapping the male inflorescence is an
important source of B complex vitamins in the diet of inhabitants in the parts
of Africa where it grows [5]. Oil palm gives the highest yield of oil per unit
of any crop. Two distinct oils are produced by oil palms (i.e. palm kernel oil
and palm oil), both of which are important in world trade [5]. Palm kernel
oil (PKO) is the minor oil obtained from the seed of the palm fruit which
contains about 50% oil. It is a hard, light yellow oil (resembling coconut oil
in taste and odor), which contains a higher proportion of the saturated lauric
and myristic acids [5, 6]. It is used in edible fats, confectioneries and baked
goods, ice creams, mayonnaise, manufacture of toilet soaps, soap powders
and detergents. The pressed cake (19.5% protein) after oil extraction from
the kernels is an important livestock feed.
Crude (red) palm oil is the fresh oil obtained from the mesocarp before
refining. It is produced in palm oil mills; the fractionation and refining of
crude palm oil take place in palm oil refineries. Palm olein and super olein
are the fractions obtained from refining, bleaching and deodorization of palm
oil. This fractionation brings about an increase in monounsaturated oleic acid
with the concomittant reduction of palmitic acid, the major saturated fatty
acid [7, 8]. Palm oil contains a high proportion of palmitic acid as well
as considerable quantities of oleic and linoleic acids which give it a higher
unsaturated fatty acid content than coconut oil and PKO [912]. Red palm oil
(RPO) contains 50% saturated, 40% monounsaturated and 10% polyunsatur-
ated fatty acids [13]. Palm oil is a raw material used for the production of
cosmetics, waxes, lubricants and toothpaste in addition to being used as a tra-
ditional antidote to cyanide toxicity [14]. Throughout the world, 90% of palm
oil is used for edible purposes (e.g., margarine, deep fat frying, shortening,
ice creams, cocoa butter substitutes in chocolate); the remaining 10% is used
for soap and oleochemical manufacturing (fatty acids, methyl esters, fatty
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nitrogenous derivatives, surfactants and detergents) [1, 15]. Recently, palm


oil-based printing ink has been produced in a collaborative project between
the Palm Oil Research Institute of Malaysia (PORIM) and Coates Brothers
[16]. This ink has properties that are superior to conventional petroleum oil-
based ink. Of all vegetable oils, palm oil has the greatest versatility in terms
of usage [15].

Palm oil: Characteristics and potentials

Palm oil, with a world production of 11.356 million tons in 19891991,


accounted for 18.6% of the total world vegetable oil production of 61.409
million tons. It was next only to soybean oil with a world production of 16.130
million tons which accounted for 26.2% of total vegetable oil production in
the same period [17]. Palm oil is cheaper than groundnut oil, corn oil or
soybean oil. Palm oil is light yellow to orange-red in color depending on
the amount of carotenoids present, the level of oxidation by lipoxygenases
in bruised fruit stored for various periods before processing and the oxid-
ation catalyzed by iron during processing and bulking. The oil possesses
some characteristics that are important in determining its incorporation into
food products [10,18]. These characteristic include: (a) a high solid glyceride
content giving required consistency without hydrogenation, (b) resistance to
oxidation and therefore, long shelf life (c) high melting point triglycerides
together with relatively low solids content at 10 C, which is helpful in for-
mulation of products with a wide plastic range, that are suitable for hot cli-
mates and some industrial applications, (d) a competitive price, (e) use in
limited quantities in margarine specifying a high polyunsaturated fatty acid
(PUFA) level because of its linoleic acid content (1011%), (f) relatively slow
melting properties because of the wide plastic range and (g) slow crystalliz-
ation properties capable of leading to structural hardness and a tendency for
recrystallization.
Palm oil may be fractionated into two major fractions: a liquid oil (65
70%) palm olein (m.p. 1820 C) and a solid fraction (3035%) stearin (m.p.
4850 C) [19]. More sophisticated processing can provide other fractions
such as mid-fraction and the double fractionated palm olein (super olein).
Palm mid-fraction, which has properties somewhere between olein and ste-
arin, contains 60% palmitic and 40% oleic acid, and is used as a cocoa-butter
equivalent. Palm olein and super olein are more unsaturated [20,21] Palm
olein compares well with groundnut oil and deteriorates less rapidly than
many other vegetable oils such as sunflower oil and soybean oil [22]. Red
palm oil (RPO) and refined palm olein (REFPO) have good oxidative stability
due to the presence of natural antioxidants (tocopherol and tocotrienols) and
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Table 1. Physicochemical properties of palm oil and its fractions

Palm oil Palm olein Palm stearin

Melting point ( C) 34.2 21.6 44.556.2


Relative density
(50 C/water at 25 C) 0.890.92 0.910.92 0.880.89
Refractive index () 1.46 1.47 1.45
Moisture and
impurities (%) 0.1 0.1 00.15
Iodine value 4755.83 55.061.54 21.649.4
Saponification value
(mg KOH/g) 196208.2 189198.0 193206
Unsaponifiable matter
(%) 0.010.5 0.0010.5 0.11.0

Sources: [1, 2, 23, 24].

the absence of linolenic acid. The physicochemical properties of palm oil and
its fractions are outlined in Table 1.

Chemical composition of palm oil

The fatty acid composition of palm oil, compared with other edible vegetable
oils consumed by humans, is shown in Table 2. The major difference between
palm oil and other oils is the higher proportion of palmitic acid. There are only
minor differences in the fatty acid composition of palm oil due to geograph-
ical region. Table 3 information shows the fatty acid composition of RPO
and its fractions. Palm olein, super olein and RPO share the same major fatty
acids e.g. palmitic, oleic and linoleic acids. However, palm olein and super
olein have more oleic and linoleic acids but less palmitic acid than does palm
stearin. In fact, palm olein and super olein are more unsaturated. Because of
the semisolid texture of palm oil at room temperature, hydrogenation is not
necessary. However other oils such as soybean or rapeseed are hydrogenated
during the manufacture of margarine. Hydrogenation leads to the production
of appreciable quantities of trans fatty acids that have uncertain health effects
[26]. Palm oil and its fraction contain less than 1.5% of the hypercholester-
olemic lauric and myristic acids. In palm oil, 1723% of the palmitic acid
(16:0) is in the sn-2 position while most of the saturated myristic (14:0),
and stearic (18:0) acids are in the sn-1,3-configuration [27] suggesting the
reason for a low thrombotic tendency of palm oil since the usual precursors
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Table 2. Fatty acid composition of palm oil and other vegetable oils

Fatty acid Red Palm Coconut Soybean Groundnut Cotton Corn Sunflower
palm kernel seed

Caproic 6:0 0.2 0.5


Caprylic 8:0 3.3 8.0
Capric 10:0 3.5 6.4
Lauric 12:0 0.2 47.8 48.5 Trace
Myristic 14:0 1.1 16.3 17.6 0.1 0.1 0.8
Palmitic 16:0 44.0 8.5 8.4 11.0 11.6 23.7 12.2 6.5
Stearic 8:0 4.5 2.4 2.5 4.0 3.1 2.6 2.2 4.5
Oleic 18:1 39.2 15.4 6.5 23.4 48.5 18.4 27.5 21.1
Linoleic 18:2 10.1 2.4 1.5 53.2 31.4 53.0 57.0 66.2
Linolenic 18:3 0.4 7.8 0.1 0.9
Arachidic 20:0 0.1 0.1 1.5 0.3 0.1 0.3
Saturates 49.9 82.1 91.9 15.1 16.3 27.4 14.5 11.3
Monounsaturates 39.2 15.4 6.5 23.4 48.5 18.4 27.5 21.1
Polyunsaturates 10.5 2.4 1.5 61.0 31.4 53.1 57.9 66.2

Source: [9].

Table 3. Fatty acid composition of palm oil and its fractions

Fatty acid Red palm oil Palm olein Super olein Palm stearin

12:0 00.2 0.10.2 0.4 0.10.2


14:0 0.81.3 0.91.0 1.4 1.01.3
16:0 43.146.3 39.540.8 31.5 46.568.9
16:1 Trace0.3 Trace0.2 Trace0.2
18:0 4.05.5 3.94.4 3.2 4.45.5
18:1 36.740.8 42.743.9 49.2 19.938.4
18:2 9.411.9 10.611.4 13.7 4.19.3
18:3 0.10.4 00.4 0.3 0.10.2
20:0 0.10.4 0.10.3 0.4 0.10.3
Saturates 50.2 45.8 36.6 52.176.2
Monounsaturates 39.2 42.5 49.2 19.938.6
Polyunsaturates 10.5 11.6 14.0 4.29.5

Sources: [9, 25].


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for desaturation and elongation in the four fatty acid families are essentially
the fatty acids in the 2-position.
Palm oil and its fractions contain tocopherols. It is especially rich in -
tocotrienol. These substances, which are physiologically active as vitamin E,
are useful natural antioxidants [28, 29]. They delay the time when oxidation
in the oil will have proceeded far enough to produce noticeable off-flavors
and/or odors [19]. Furthermore, they possess free radical scavenger proper-
ties, serving to protect biological systems against oxidative and carcinogenic
stress [3033], in addition to inhibiting cholesterol biosynthesis and platelet
aggregation [34, 35].
The characteristic color of crude palm oil is due to the abundance of
carotenoids (500700 mg/L). Alpha and -carotenes are the major compon-
ents with -carotene, lycopene and xanthophylls present in smaller amounts.
Most of the carotene is destroyed during the refining, bleaching and deodor-
ization processes, which traditionally produce the light colored oils preferred
by most consumers [10].
The total sterol content of palm oil ranges from 364491 mg/L. The major
sterols in palm oil are -sitosterol (281.8 mg/L), campesterol (110.97 mg/L)
and stigmasterol (55.97 mg/L). Sterols do not have any detrimental effects,
but serve as a minor dietary source for steroidal hormones [1]. Crude palm
oil is low in phospholipids (5130 mg/L), which function as antioxidant syn-
ergists in the presence of vitamin E [1, 28]. The presence of phenolic com-
pounds (<100 mg/L) is responsible for the initial darkening of palm oil dur-
ing frying [36] and this coloration is unrelated to the deterioration of the oil
[10]. Crude palm oil may contain 10% or more free fatty acids depending on
handling. Other possible impurities in palm oil are tannins, trace flavonoids,
terpenoids, aliphatic alcohols, hydrocarbons, ketones, wax esters and methyl
esters. Refining reduces the levels of sterols, hydrocarbons and the already
mentioned volatile impurities [19, 28].

Red palm oil and its nutritional significance

Throughout the world, 90% of the palm oil produced is used for edible pur-
poses [15]. In culinary practice, palm oil is used extensively for frying (be-
cause of low foaming properties due to the absence of lauric glycerides),
stews and for preparing soups [2, 37].
Red palm oil is the richest food source of carotenoids. The characteristic
color of RPO is due to the abundance of these carotenoids (500700 mg/L)
in the crude oil [10]. The carotenoids, together with vitamin E, ascorbic acid,
enzymes and proteins, are members of the biological antioxidant network [30,
38] converting highly reactive radicals ( OH) and free fatty peroxy radicals
325

Figure 1. Conversion of -carotene to retinal [52, 53].

to less active species, thus protecting against oxidative damage to cells [39].
Besides providing high energy density in the diet, RPO is a rich natural source
of -carotene: 375 mg/g [13]. Beta-carotene is the most abundant carotenoid
which can be converted to vitamin A, which plays an important role in the
visual process, differentiation of cellular epithelium and genetic regulation.
Furthermore, it is an antioxidant that destroys singlet oxygen and free rad-
icals [13, 30, 3843]. Beta-carotene is oxidatively cleaved by -carotene
15, 15 dioxygenase, in the intestine, into two molecules of vitamin A, an
isoprenoid compound with a 6-membered carboxylic ring and an 11-carbon
side chain [44]. Alpha and -carotenes each yield one molecule of vitamin
A. Vitamin A is required for normal development and growth [45]. It plays a
role in many metabolic processes in many cells, but its best known function
326

Figure 2. Structure of vitamin A and some of its metabolites.

is in the eye as an important participant in the visual process. Vitamin A


plays a part in reproduction through the synthesis of sexual steroids [40], dif-
ferentiation of cellular epithelium [4648], regulation of cell division, genetic
regulation, enhancement of immune response [41, 42, 4951] and in all stages
(differentiation, health and growth) of lung development [51]. Two important
327

metabolites of vitamin A are retinal (retinaldehyde), the active element of


visual pigment, and retinoic acid, an intracellular messenger that modulates
cell differentiation. Figure 1 is a depiction of the cleavage of -carotene into
retinal. The structure of vitamin A and some of its metabolites are shown in
Figure 2.
Red palm oil is a rich source of vitamin E, which is about 559 to 1000 ppm
[8, 29, 54]. Vitamin E (tocopherols and tocotrienols) acts as a potent an-
tioxidant serving to protect cellular membranes from free radical-catalyzed
lipid peroxidation [55]. The predominant palm oil vitamin Es are tocotrienols
which are unsaturated analogues of tocopherol. The tocopherols constitute
1822% of the vitamin Es content of palm oil while the tocotrienols constitute
7882% [29]. Palm oil is the only vegetable oil available on the world market
in appreciable quantities that is rich in tocotrienols [10, 56]. The tocotrienols
have been reported to be natural inhibitors of cholesterol synthesis [35, 57].
The tocopherols and tocotrienols promote an antithrombotic state by redu-
cing platelet aggregation and modulating prostanoid synthesis [34, 35, 58,
59]. They have also been highlighted in the prevention and therapy of certain
forms of cancers [54, 6063].
Furthermore, RPO has a near ideal unsaturated fatty acid to saturated
fatty acid ratio in that it contains saturated fatty acids and unsaturated fatty
acids at about equal levels [1,9,13,25]. The presence of significant amounts
of -carotene (provitamin A) and vitamin E [64] coupled with the minimal
contents of linoleic (211%) and linolenic (0.10.2%) acids make palm oil
one of the most oxidatively stable dietary oils in the world [65, 66].
Palm oil is consumed in the fresh state and/or at various levels of oxida-
tion. When the fresh oil is subjected to several rounds of heating at high tem-
peratures (about 150 C), it becomes oxidized and the color becomes darker.
Uncontrolled oxidation leads to peroxidation. Many of the resulting oxidative
products are cytotoxic. Oxidized oil has been reported to cause hyperlip-
idemia, thrombocytopenia, platelet aggregation, increased basal metabolic
rate (BMR) and tissue damage [67, 68].

Palm oil in the diet and health aspects

Studies on cardiovascular disease (CVD), one of the leading causes of death


in many countries, have focused on ways of reducing plasma cholesterol by
nutritional means [69]. Diet is very important in controlling blood lipids. The
type and amount of fat present in a diet is one of the factors that plays a
role in the regulation of blood pressure and incidence of hypertension. Chain
length and degree of saturation of dietary fatty acids alter plasma cholesterol
concentrations by their effects on the synthesis, processing and catabolism
328

of plasma lipoproteins, resulting in profiles that significantly modify CVD


risk [70, 71]. Saturated fatty acids have been identified as the major dietary
causes of atherosclerosis [72]. Atherosclerosis is characterized by the depos-
ition of cholesterol esters and other lipids (triacylglycerols included) in the
connective tissue of the arterial walls. Of the serum lipids, cholesterol has
been the most investigated in the relationship between raised serum lipids
and the incidence of coronary heart disease (CHD) and atherosclerosis. Cho-
lesterol, transported in lipoproteins, mainly low density lipoprotein (LDL) in
the plasma [73], is a major risk factor for the progression of atherosclerosis
[74]. High cholesterol levels, particularly elevated LDL levels, clearly predis-
pose middle-aged men [75, 76] to CHD. Saturated fatty acids (SFA) increase
plasma LDL concentrations [77, 78]. The consumption of SFA leads to an
increase in blood pressure [79].
Palm oil has been a major target of avoid saturated fat campaigns by
virtue of the fact that saturated fats elevate cholesterol levels, thus questioning
its use in food products [10]. Palm oil contains both saturated and unsaturated
fatty acids (in nearly equal amounts) which have opposing effects on the
cardiovascular system.

Palm oil and tissue/plasma lipids

The hypocholesterolemic effect of polyunsaturated fatty acids (PUFA) and


monounsaturated fatty acids (MUFA) relative to SFA has been documented
in humans and animals [8083]. It has also been demonstrated that palm oil
consumption results in serum cholesterol concentrations which are higher
than after administration of highly unsaturated corn, sunflower seed, soybean
and sunflower seed oils [84, 85]. However, the cholesterol level after the palm
oil consumption period was lower than at the start of the studies [86]. Isong
[2], in her biochemical and nutritional studies with rats fed thermally oxidized
palm oil (TPO), observed that tissue total cholesterol, free fatty acids (FFA),
phospholipids and cerebroside levels were significantly elevated in TPO-fed
rats as a result of oxidative toxicity. The organs most affected by alterations
in lipid levels included kidneys, brains, lungs, liver and the heart. However,
chronic feeding of red palm oil did not raise the tissue levels of phospholipids
in various organs or cerebroside in the brain; neither were FFA contents of
brain and testes elevated in rats [67].
Hornstra & Sundram [87] demonstrated that the maximal replacement of
the habitual fats in the Dutch diet with palm oil in a group of 40 male vo-
lunteers (in a double blind crossover design consisting of two periods of six
weeks feeding) had no significant effect on blood cholesterol; the levels were
190 mg/dL for Dutch blend and 191 mg/dL for palm oil diet. Furthermore,
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refined palm olein (REFPO)-enriched diets caused 1315% reductions in the


levels of serum cholesterol of four groups of human volunteers in Pakistan in
contrast to diets enriched with butter ghee, vanaspati or hydrogenated cotton
seed oil [88].
Long term dietary supplementation of standard dry rat food with 12%
chemically refined palm oil (in Hooded-Wistar rats) caused significant inhib-
ition of myocardial thromboxane A2 , similar to that by a 1:1 blend of sheep
fat and fish oil [89]. The effects of diets containing palm olein (REFPO),
corn oil (CO) and coconut oil (CNO) in three groups of adult volunteers
in Malaysia were compared by Ng et al. [90]. Each dietary fat was con-
sumed for five weeks, with the test fat contributing 30% the energy of the
test diets. These workers observed that CNO increased serum while REFPO
and CO reduced serum cholesterol levels, but CO gave a higher reduction
than REFPO. Marzuki et al. [91] observed that plasma cholesterol levels (in
110 student volunteers) during a REFPO dietary period (149 mg/dL) were
comparable to those of a soybean oil period (153 mg/dL). The effects of the
tocotrienol-enriched fraction (palm vitee) on serum lipids of hypercholester-
olemic human subjects (serum cholesterol> 294 mg/dL) were evaluated by
Qureshi et al. [35]. Significant reductions in total cholesterol (31%), LDL-
cholesterol (8%) and thromboxane (25%) were found on administration of
palm vitee for 8 weeks.
Nutritional evaluation of palm oil in weanling rats revealed amounts
of serum and tissue cholesterol and triglycerides in crude palm oil-fed and
REFPO-fed rats that were comparable to groundnut oil-fed rats [23]. The
influence of positional distribution of fatty acids in palm oil on blood lipids of
rats was studied using native palm oil (NPO) and interesterified (randomized)
palm oil (IPO) [27]. Two groups of rats were fed 26% fat as NPO or IPO for 4
months. It was observed that rats fed IPO had higher plasma total cholesterol,
triglyceride and FFA levels than those fed NPO diets, but HDL-cholesterol
of IPO-fed rats was lower than that of NPO-fed rats. Also, lipidemia was
significantly affected only by dietary fatty acids at the sn-2 position; the
usual precursors for elongation and desaturation were essentially fatty acids
in this position. Thus, it was suggested that the physiological and eventually
the pathological effects of a dietary triacylglycerol depends not only on its
fatty acid composition, but also on its stereochemical configuration. Plasma
LDL concentrations are increased by high fat diets [92]. Increasing the fat
contents of palm oil containing diets led to a dose-dependent increase in
plasma total and LDL-cholesterol concentrations [24]. Consumption of palm
oil in normal diets reduces plasma cholesterol level and is, thus, safe to the
consumer. High levels of palm oil (about 30% of the diet) may be a risk
330

factor for cardiovascular diseases by significantly reducing HDL-cholesterol


and elevating LDL-cholesterol concentrations.

Palm oil and blood pressure

Saturated fats such as beef tallow, coconut oil and oxidized oil cause an
increase in blood pressure [79,93,94] while ingestion of PUFA and MUFA
containing fats have the opposite effect [9597]. Palm oil does not contain
much lauric acid, which is known to raise plasma lipid SFA levels. A recent
study with regard to the effect of palm oil diets on mean arterial pressure
(MAP) of rats provides evidence that diets containing 15% (w/w) RPO fed
for 18 weeks did not raise blood pressure [94]. Saturated fatty acids enhance
contractile responses of blood vessels to vasoactive agents and increase vas-
cular resistance [98100]. Unsaturated fatty acids relax blood vessels causing
an increased production of vasodilatory prostaglandins PGF1 and PGI2 , thus
exhibiting their antihypertensive effects [97, 101106]. Palm oil seems to
have a protective effect on the endothelium of the blood vessels. Owu et
al. [100] found no increase in -adrenergic stimulation nor attenuation in
endothelium-dependent relaxation in blood vessels obtained from rats fed
RPO when compared with vessels of animals that received normal rat chow;
neither were there functional changes in aortic smooth muscle in response to
voltage-operated calcium channels for contraction.

Palm oil, arterial thrombosis, and platelet function

Hyperlipidemia, associated with hypercoagulability of platelets, is an import-


ant cause of thrombosis [107]. Arterial thrombosis is an important risk factor
in cardiovascular disease (CVD). Fats and oils influence platelet aggregation,
an early stage in the formation of thrombosis (a clot in the arteries).
The thrombosis tendency is higher, with a higher amount of SFA in the
diet; it is lower when the PUFA content of the oils in the diets is higher
[108]. Saturated fats increase platelet aggregation and thrombosis [109] while
polyunsaturated oils have the opposite effect [86, 110]. Platelet aggregation,
arterial thrombosis tendency, thromboxane A2 and thromboxane to prosta-
cyclin ratios have been found to be decreased by palm oil diets [35, 55, 86,
89, 111, 112]. However, platelet aggregability and thrombocytopenia were in-
creased by TPO diets [67]. Interesterification of palm oil resulted in increased
thrombin (177%) and ADP (30%) induced platelet aggregation [27].
331

Palm oil and enzyme activities/tumorigenesis

The activities of lipogenic and some glycolytic enzymes of the liver are elev-
ated by highly saturated fats [113]. Palm oil, because of its rich contents of -
carotene, vitamin E and induction of some drug metabolizing enzymes such
as glutathione-S-transferase, aminopyrine N-demethylase and ethoxyresoru-
fin-O-deethylase [31, 32], seems to have some protective effect against ox-
idative damage [63] and tumorigenesis [114]. Rukmini [13] observed signi-
ficant inhibition of microsomal 3-hydroxy-3-methyl glutaryl CoA reductase
activity in rats fed RPO and REFPO indicating reduced synthesis of endogen-
ous cholesterol. Thermally oxidized palm oil (TPO), which is more saturated
than RPO, caused a significant increase in the activities of serum alkaline
phosphatase (ALP), aspartate transaminase (AST) and alanine transaminase
(ALT) when compared with those of a control diet [115]. The activities of
ALT in rats fed RPO diets were comparable to those of the control group.
Ngah et al. [63] reported that plasma and hepatic -glutamyl transpeptidase
activities were significantly lower in rats fed a diet containing 0.7 mg of a
tocotrienol-enriched isolate of palm oil, leading to a reduction in the severity
of 2-acetylaminofluorene induced hepatocarcinogenesis. A more recent study
by Edem [24] indicated dose-dependent decreases in the plasma activities
of lipase, ALT, AST and ALT/AST ratios when the concentration of dietary
palm oils were increased; however there were also increases in ALP following
increases in concentration of oil in the diet.

Palm oil and basal metabolic rate

Basal metabolic rate (BMR) is a measure of energy expenditure of the body


at rest. Since fats have twice the energy value of proteins or carbohydrates
[116], BMR is influenced by fats. Osim et al. [68] studied the effect of RPO
and TPO on BMR by administering commercial stock feed (control) diets
supplemented (15% by weight) with RPO and TPO to rats for 14 weeks. It
was found that while RPO raised BMR by only 5% over the control, TPO
raised BMR by 21% over the control (1.50 ml/hr/g). Thus RPO, whose BMR
elevation effects was intermediate between the highly saturated oxidized TPO
and the control diets was observed to be more beneficial to the body with
respect to overall heat production.
332

Palm oil and reproductive capacity

Isong et al. [117] reported on reproductive performance of albino rats fed di-
ets containing rat pellets supplemented at 15% (by weight) with TPO. Inges-
tion of oxidized oil was characterized by reproductive toxicity, the features of
which included functional changes in the testes of male animals [118], gesta-
tion resorption syndrome in female rats, discoloration of the uterus, ovary and
testes [119], delays in gestation, reduced fertility and embryo fetal toxicity
[117]. The findings of Isong et al. [117] indicated that RPO neither delayed
gestational periods, nor reduced pregnancy rates and litter sizes, but the symp-
toms of reproductive toxicity were exhibited in TPO-fed rats. These authors
thus suggested that RPO exerted its effects on reproductive capacity by im-
proving the efficiency of protein biosynthesis or utilization in such a way that
was favorable to sex hormone function. It is also likely that RPO provided
vitamin A which is known to play a part in reproduction through the synthesis
of sexual steroids [40], embryogenesis and spermatogenesis [120]. Edem [24]
observed significance increases in plasma vitamin A concentrations of rats
fed diets containing RPO.

Palm oil and nutrient utilization

The stimulation of efficient utilization of cassava-based diets by rabbits fed


palm oil has been reported by Fomunyam et al. [121]. These workers ob-
served that the growth traits of rabbits fed palm oil supplemented cassava
diets (with Stylosanthes guyanensis as part of the dietary protein) were com-
parable to those of a corn-based standard rabbit ration containing 8% fish
meal. Digestion, absorption and utilization of refined palm oil, palm olein and
palm stearin in the rat have been studied [122]. It was observed that refined
palm oil and its fractionation products (at 10%20% of the diet) were easily
digested, well absorbed and efficiently utilized for growth, with digestibilities
ranging from 94.2% (palm stearin) to 96.4% (palm olein).
Palm oil promotes the intestinal uptake of amino acids, even when the
amino acids are present as a mixture, by modifying the intestinal epithelium
for better uptake [123]. In terms of absorbed amino acids, palm oil improves
the metabolism of the sulphur containing amino acids [14].
Crude palm oil and refined palm olein at 10% (w/w) of the diet had no
adverse effects on growth rate, feed efficiency, protein efficiency ratio, net
protein utilization, digestibility, fat absorption, nitrogen balance, and phos-
phorus and calcium retention of rats [23]. Nutrient absorption studies [24]
revealed that protein, fat, carbohydrate and mineral absorption in rats fed 10%
palm oil-supplemented diets were comparable to those of rats fed the normal
333

commercial rat chow. However the effective absorption of protein, carbo-


hydrate, fat, calcium, sodium, potassium, magnesium, copper and manganese
decreased with increasing level of test dietary palm oils.

Palm oil, organ weight, and tissue morphology

Fats and oils, since they form a part of the membrane architecture of various
cells, exert some degree of influence on body/organ weight and morphology
of tissues. An early study by Abaelu et al. [123] in experimental animals
reported that a 3-week palm oil feeding resulted in lower body weights and
lower weight gains than feeding a highly unsaturated oil. However, more
recent studies, lasting for 414 weeks, have shown that diets containing mod-
erate amounts of RPO have no adverse effects on body weight and tissue
morphology [23, 24, 68]; but TPO caused tissue damage and reduction in
organ weights [2, 68]. Thermoxidized palm oil, in addition to causing re-
ductions in organ weights, caused congestion and interstitial hemorrhage in
the lung, congestion of hepatic sinusoids, degenerative changes in the central
zone of hepatic lobules and partial tubular atrophy of the kidney.
The amount and quantity of food consumed by experimental animals great-
ly influence growth responses [124]. Fat contributes to the palatability and
enhances satiety of food [125, 126]. Palatability of food leads to a greater
consumption of the latter. When moderate amounts of fat are added to the
diet, caloric consumption is more frequently increased than decreased [127].
However food intake is depressed when high amounts of fat are added to the
diet. Animals fed diets containing 30% (w/w) palm oil had lower total body
weights and body weight gain when compared with those fed 10% palm oil-
supplemented diets. Increasing the oil contents of the diets induced significant
reductions in body and organ weights of the test animals [24]. Furthermore,
palm oil at the level of 30% of the diet induced toxicity to the liver, caused
reduction in liver cell size and loss of cellular radial architecture, as corrobor-
ated by alanine transaminase to aspartate transaminase ratio (which is higher
than unity) [24]. These changes which are likely to be a consequence of the
caloric character of the diets, could be ascribed to the presence of some toxic
species probably generated by auto oxidative processes in the oil. Also, the
dilution of the protein content of the test diets by high oil concentration may
have imposed some protein imbalance. These could have been responsible
for inadequate amounts of protein being retained for the synthesis of cell
components. While animals fed 10% palm oil diets had normal tissue mor-
phology, those fed 20% palm oil-enriched diets had mild cell size reductions
and distortions of cellular architecture. Thus, consumption of palm oil at
334

normal amounts in a diet had no adverse effects on body weights and organ
morphology.

Palm oil Hematological aspects

There is paucity of information regarding the effect of palm oil consumption


on blood hematology. A recent study [24] indicates mild reductions in total
white blood cell counts when the levels of palm oil in the experimental diets
were increased. Palm oil at a 30% level of supplementation significantly re-
duced platelet counts; a reduction which may be reflective of aggregability
of platelets. The variations in hemoglobin concentrations and packed cell
volume were not significant. The mean corpuscular hemoglobin concentra-
tion (a useful index of the average hemoglobin concentration of the red cells
[128]) indicated adequate hemoglobinization of red blood cells in the test
animals fed palm oil diets. Thus at 1020% levels, palm oil consumption has
no negative impact or immune function; neither does it enhance aggregability
of platelets, but promotes hemoglobinization of red blood cells.

Summary and conclusion

There is considerable concern about the role of dietary fats in human and
animal nutrition. Palm oil contains almost equal amounts of saturated and
unsaturated fatty acids. It contains negligible amounts of the hypercholes-
terolemic fatty acids, lauric (12:0) and myristic acid (14:0). It is moderately
rich in the hypocholesterolemic monounsaturated oleic acid (18:1) and has
adequate amounts of linoleic acid (18:2 6). Besides, it is very rich in
-carotene (provitamin A) and vitamin E.
Animal experiments and human studies have shown that palm oil, al-
though it contains 50% saturated fatty acids, does not behave as a saturated
oil. It is beneficial to the body in terms of low heat production and has no
adverse effects on the body weight and morphology of various tissues at
levels normally consumed in the diet. Anomalous behavior is a function of
the tocopherol and tocotrienol contents of the non-triglyceride or unsaponifi-
able fraction of the oil. The high content of tocotrienols may be particularly
relevant to these observations. Palm oil reduces the blood levels of total cho-
lesterol, triglycerides, LDL-cholesterol, thrombotic eicosanoids (oxygenated
metabolites of arachidonic acid and eicosapentaenoic acid) implicated in sev-
eral pathophysiological processes of the cardiovascular system. Palm oil is
beneficial by reducing blood pressure and thrombotic tendency of platelets
while offering protection against oxidative damage of the liver and other
335

organs. It reduces the risk of atherosclerosis, enhances intestinal uptake of


proteins and metabolism of sulphur amino acids, and promotes reproductive
capacity.
The -carotene of palm oil may be important to correct vitamin A defi-
ciency (a public health problem of many developing countries) in addition to
protecting against certain forms of cancer. From the foregoing, it can be seen
that palm oil (at moderate levels) is completely safe and non-toxic, easily di-
gestible, efficiently utilized and well absorbed; a very stable and good quality
oil which does not contain trans fatty acids. In addition to reducing the risk of
CVD, it is a rich source of -carotene, which can prevent nutritionally caused
blindness and is protective against carcinogens. The tocotrienols, which are
present more in palm oil than in many other oils, inhibit cholesterol biosyn-
thesis, platelet aggregation and lengthens the life-span of cancerous animals.
Many of the properties and effects attributed to palm oil are believed to be
mediated through its major triglyceride and minor non-glyceride components,
but also by the peculiar stereochemical configuration or fatty acid isomeric
position. Therefore, palm oil is a completely safe and nutritive edible oil with
nutritionally beneficial properties.
While palm oil may have its positive attributes, a considerable amount of
it is used in a form other than its fresh state. The practice of heating palm oil
in the presence of food condiments increases the possibility for deteriorative
changes in the oil, including oxidation and the formation of toxic by-products.
Some food vendors as well as domestic applications used palm oil heated in-
termittently (TPO) without discarding. This practice needs to be discouraged
in view of the potential dangers of increasing the oxidative status of the oil
several times with each heating cycle. It is recommended that small portion
of heated palm oil should be used for not more than a maximum of two to
three times in order to delay oxidation to some extent.

References

1. Hassan AH (1988) Palm oil and health. The Planter 64 (752): 505519.
2. Isong EU (1988) Biochemical and Nutritional studies on rat fed thermally oxidized
palm oil (Elaeis guineensis). Nigeria: PhD Thesis, University of Calabar.
3. Usoro EJ (1974) The Nigerian oil palm industry. Ibadan: Ibadan University Press.
4. Vickery ML, Vickery B (1979) Plant products of tropical Africa. London: Macmillan
Press, pp 2728.
5. Purseglove JW (1983) Tropical Crops Monocotyledons, vols. 1 and 2 combined. Essex,
England: English Language Book Society and Longmans Group Ltd, pp 479510.
6. Oyenuga VA (1968) Nigerias Foods and Feeding Stuffs. 3rd edn. Ibadan: Ibadan
University Press, 99 pp.
7. MacFarlane N, Swetmen AA, Coursey DG (1984) Comparison of traditional and
industrial palm oil. Palm Oil News 28: 1117.
336

8. Chong YH, Ng TKW (1991) Effects of palm oil on cardiovascular risk Med J Malaysia
46(1): 4150.
9. Gunstone FD, Harwood JL, Padley FB (1986) The Lipid Handbook. London: Chapman
and Hall, pp 7678.
10. Cottrell RC (1991) Nutritional aspects of palm oil. Am J Clin Nutr 53: 989S1009S.
11. Satchithanandam S, Reiks M, Calvert RJ, Cassidy MM, Kritchevsky D (1993) Coconut
oil and sesame oil affect lymphatic absorption of cholesterol and fatty acids in rats. J
Nutr 123: 18521858.
12. Ayre KJ, Hulbert AJ (1996) Dietary fatty acid profile influences the composition of
skeletal muscle phospholipids in rats. J Nutr 126: 653662.
13. Rukmini C (1994) Red palm oil to combat vitamin A deficiency in developing
countries. Food Nutr Bull 15(2): 126129.
14. Umoh IB, Ayalogu EO, Oke OL (1983) Effect of different levels of palm oil and sulphur
in cassava-based diets. Food Chem 10(2): 8395.
15. Idris NA, Samsuddin S (1993) Developments in food uses of palm oil: a brief review.
Palmas 15(3): 6669.
16. Ooi TL, Ying NC, Kilfi HI, Chako YM (1994) Palm oil-based printing ink. Palmas
15(1): 7374.
17. Escobar R, Peralta F, Alpizar G (1994) Perspectives for the development of the oil palm
industry worldwide. Palmas 15(1): 5159.
18. Kheiri SA (1987) End uses of palm oil: human food. In Gunstone FD (ed), Palm Oil.
Chichester: John Wiley and Sons, pp 7183.
19. Gunstone FD, Norris FA (1983) Lipids in Foods: Chemistry, Biochemistry and
Technology. Oxford: Pergamon Press, pp 40, 141, 144146.
20. Tan BK, Oh FCH (1981) Malaysian Palm Oil: Chemical and Physical Characteristics.
PORIM Technology, Nos. 3 and 4, May 1981.
21. Tan BK (1989) Novel fractions and fats from palm and palm kernel oils. Palm Oil
Development, 11: PORIM, September 1989.
22. Bracco U, Diffenbacher A, Kolarovic L (1985) Frying performance of palm oil liquid
fractions. J Am Oil Chem Soc 58: 612.
23. Manorama R, Rukmini C (1991) Nutritional evaluation of crude palm oil in rats. Am J
Clin Nutr 53: 1031S1033S.
24. Edem DO (1999) Comparative biochemical and hematological studies on rats fed vari-
ous levels of palm oil-containing diets. Nigeria: PhD Thesis, University of Calabar,
283 pp.
25. King B, Sibley I (1984) Authenticity of edible vegetable oils and fats. Part II. Palm oil
and palm oil fractions. Surrey, UK: Leatherhead Food Research Association (LFRA
research report no 642).
26. British Nutrition Foundation (1987) Trans Fatty acids: report of the BNF Task Force,
BNF, London.
27. Renaud SC, Ruf JC, Petithory D (1995) The positional distribution of fatty acids in
palm oil and lard influences their biologic effects in rats. J Nutr 125: 229237.
28. Goh SH, Choo YM, Ong SH (1985) Minor carotenoids of palm oil. J Am Oil Chem
Soc 62: 237240.
29. Sundram K, Top AGM (1994) Vitamin E from palm oil. Its extraction and nutritional
properties. Palmas 15 (1): 7782.
30. Krinsky NI (1992) Mechanism of action of biological antioxidants. Proc Soc Exp Biol
Med 200: 248254.
337

31. Manorama R, Chinnasamy N, Rukmini C (1993) Effect of red palm oil on some hepatic
drug-metabolizing enzymes in rats. Food Chem Toxicol 31 (8): 583588.
32. Nesaretnam K, Devasagayam TP, Singh BB, Basiron Y (1993) The influence of
palm oil or its tocotrienol-rich fraction on the lipid peroxidation potential of rat liver
mitochondria and microsomes. Biochem Mol Biol Int 30 (1): 159167.
33. Diplock AT (1994) Antioxidants and disease prevention. Med Aspect Med 15: 293
376.
34. Helub BJ, Sicilia I, Mahadevappa VG (1989) Effect of tocotrienol derivatives on
collagen and ADP-induced plasma platelet aggregation. Abstracts 1989. PORIM
International Palm Oil Development Conference, September 59, Kuala Lumpur, N 9.
35. Qureshi AA, Qureshi N, Wright JJK, Shens S, Kromer G, Gapor A, Chong YH,
Dewitt G, Ong ASH, Peterson D, Bradlow BA (1991) Lowering of serum cholesterol
in hypercholesterolemic humans by tocotrienols (palm vitee). Am J Clin Nutr 53:
1021S1026S.
36. Berger KG (1987) Palm oil. Chem Ind 24: 846851.
37. Okiy DA, Oke OL (1984) A study of the effects of salt and pepper on palm oil used as
a frying medium. Food Chem 14(4): 251262.
38. Hendrich S, Lee K, Xu X, Wang H, Murphy PA (1994) Defining food components as
new nutrients. J Nutr 124: 1789S1792S.
39. Packer L (1992) Interactions among antioxidants in health and disease. Vitamin E and
the redox cycle. Proc Soc Exp Biol Med 200: 271276.
40. Alais C, Linden G (1991) Biochimie alimentaire, 2nd edition. Paris: Mason, pp 110
116.
41. Olson JA (1994a) Vitamins: The tortuous path from needs to fantasies. J Nutr 124:
1771S1776S.
42. Olson JA (1994b) Vitamin A, retinoids and carotenoids. In Shils ME, Olson JA, Shike
M (eds), Modern Nutrition in Health and Disease, 8th ed. Philadelphia, PA: Lea and
Febiger, pp 287307.
43. Gaziano JM, Hennekens CH (1993). The role of beta-carotene in the prevention of
cardiovascular disease. Ann N Y Acad Sci 691: 148155.
44. Lehninger AL, Nelson DL, Cox Mm (1993) Principles of Biochemistry, 2nd ed. New
York: Worth Publishers, pp 259262.
45. Levin MS, Davis AE (1997) Retinoic acid increases cellular retinol binding protein II
mRNA and retinol uptake in the human intestinal Caco-2 cell line. J Nutr 127: 1317.
46. Morriss-Kay G (ed) (1992) Retinoids in normal development and tetratogenesis.
Oxford: Oxford University Press.
47. Blomhoff R (ed) (1994) Vitamin A in health and disease. New York: Marcel Dekker
Inc.
48. Sporn MB, Roberts AB, Goodman DS (eds) 1994. The Retinoids, 2nd edn. New York:
Raven Press.
49. Semba RD (1994) Vitamin A, immunity and infection. Clin Infect Dis 19: 489499.
50. Bates CJ (1995) FatSoluble vitamins: Vitamin A. The Lancet 345: 3134.
51. Zachman RD (1995) Role of vitamin A in lung development. J Nutr 125: 1634S1638S.
52. Whitney EN, Hamilton EMN, Rolfes SR (1990) Understanding nutrition, 5th ed. USA:
West Publishing Co, pp 238251.
53. Gouado I (1994) Status Vitaminique A et E des populations rurales de lOuest et de
lExtreme-Nord du Cameroun. Cameroun: PhD Thesis, University of Yaounde 1.
54. Goh SH, Hew NF, Norhanom AW, Yadav M (1994) Inhibition of tumor promotion by
various palm oil tocotrienols. Int J Cancer 57: 529531.
338

55. Gapor AB, Ong ASH, Kato A, Watanabe H, Kawada T (1989) Antioxodant activities of
palm vitamin E with special reference to tocotrienols. Elaeis (The International Journal
of Oil Palm Research and Development) 1(1): 6367.
56. Gu J-Y, Tsujita A, Wakizono Y, Yamada K, Sugano M (1997) Combined effects of
sesamin with alpha-tocopherol or tocotrienols on lipid and immune indices in Brown-
Norway rats. Nutr Res 17(2): 339350.
57. Pearce BC, Parker RA, Deason ME, Qureshi AA, Wright JJ (1992) Hypocholester-
olemic activity of synthetic and natural tocotrienols. J Med Chem 35: 35953606.
58. Steiner M, Anatasi J (1975) Vitamin E and platelet aggregation. J Clin Invest 57: 732
737.
59. Chan AC, Leith MK (1981) Decreased prostacyclin synthesis in vitamin E deficient
rabbit aorta. Am J Clin Nutr 34: 23412347.
60. Comstock GW, Helzlsoeur KJ, Bush TL (1991) Prediagnostic serum levelsof caroten-
oids and vitamin E as related to subsequent cancer in Washington county, Maryland.
Am J Clin Nutr 53: 28052945.
61. Gould MN, Haag JD, Kennan WS, Tanner M, Elson C (1991) A comparison of to-
copherol and tocotrienol for the chemoprevention of chemically-induced rat mammary
tumours. Am J Clin Nutr 53: 1068510705.
62. Knekt P, Reunanen A, Jarvinen R, Seppanen R, Helivaara T, Aromaa A (1994) Anti-
oxidant Vitamin intake and coronary mortality in a longitudinal population study. Am
J Epidemiol 139(12): 11801189.
63. Ngah WZW, Jarien Z, San Mm, Marzuki A, Top GM, Shaman NA, Kadir KA (1991)
Effect of tocotrienols on hepatocarcinogenesis induced by 2-acetylaminoflourene in
rats. Am J Clin Nutr 53: 1076S1081S.
64. Packer L (1994) Vitamin E is Natures master antioxidant. Sci Am Sci Med 1(1): 5463.
65. Kocharr SL (1981) Economic Botany in the Tropics. New Delhi, India: MacMillan.
66. Loncin M (1970) Palm Oil: A Major Tropical Product. Brussels: Unilever House.
67. Osim EE, Owu DU, Isong E, Umoh IB (1992) Influence of chronic consumption of
themooxidized palm oil on platelet aggregation in the rats. Disc Innov 4(1): 8387.
68. Osim EE, Owu DU, Isong E, Umoh IB (1994) Influence of chronic consumption
of themooxidized and fresh palm oil diets on basal metabolicrate, body weight and
morphology of tissues in rats. Disc Innov 6(4): 389396.
69. Onyeneke EC, Alumanah EO (1991) The influence of cholesterol on plasma lecithin:
cholesterol acyl transferase (LCAT) activity of rat. Nig J Nutr Sci 12(1): 1417.
70. Hayes KC, Khosla P (1992) Dietary fatty acid thresholds and cholesterolemia. FASEB
J 6: 26002607.
71. McNamara DJ (1992) Dietary fatty acids, lipoproteins and cardiovascular disease. Adv
Food Nutr Res 36: 253351.
72. Gurr MI, Harwood JL (1991) Lipid Biochemistry: An Introduction. 4th ed. London:
Chapman and Hall, pp 184237.
73. Lawn RM (1992) Lipoprotein in heart disease. Sci Am 266: 2632.
74. Breslow JL (1988) Apolipoprotein genetic variation and human disease. Physiol Rev
68: 85132.
75. Stamler J, Wentworth D, Neaton J (1986) Is the relationship between serum cholesterol
and risk of death from coronary heart disease continuous and graded? J Am Med Assoc
256: 28232828.
76. Tan K, Marmot Mg, Talmud P, Humphries SE, Yudkin J, Betteridge DJ (1993)
Hypertriglyceridemia and vascular risk. Lancet 342: 781786.
339

77. Fernandez ML, Lin ECK, McNamara DJ (1992a) Regulation of guinea pig plasma low
density lipoprotein kinetics by dietary fat saturation. J Lip Res 33: 97109.
78. Fernandez ML, Lin ECK, McNamara DJ (1992b) Differential effects of saturated fatty
acids on low density lipoprotein metabolism in the guinea pig. J Lip Res 33: 1833
1842.
79. Mutanen M, Kleemola P, Valsta LM, Mensink RP, Rasanen L (1992) Lack of effect on
blood pressure by polyunsaturated and monounsaturated fat diets. Eur J Clin Nutr 46:
16.
80. Mattson FH, Grundy SM (1985) Comparison of effects of dietary saturated, monoun-
saturated and polyunsaturated fatty acids on plasma lipids and lipoproteins in man. J
Lip Res 26: 194202.
81. Fernandez ML, McNamara DJ (1994) Dietary fat saturation and chain length modulate
guinea pig hepatic cholesterol metabolism. J Nutr 124: 331339.
82. Sugano M, Imaizumi K (1991) Effect of palm oil on lipid and lipoprotein metabolism
and eicosanoid production in rats. Am J Clin Nutr 53: 1034S1038S.
83. Bonanome A, Grundy SM (1998) Effect of dietary stearic acid on plasma cholesterol
and lipoprotein levels. N Engl J Med 318: 12441248.
84. Baudet MF, Dachet C, Lasserre M, Esteva O, Jacotot B (1984) Modification in the com-
position and metabolic properties of human low density and high density lipoproteins
by different dietary fats. J Lip Res 25: 456468.
85. Grundy SM (1986) Comparison of monounsaturated fatty acids and carbohydrates for
lowering plasma cholesterol. New Eng J Med 314: 745748.
86. Hornstra G (1988) Dietary lipids and cardiovascular disease: effects of palmoil.
Oleagineux 43(2): 7581.
87. Hornstra G, Sundram K (1989) The Effect of Dietary Palm Oil on Cardiovascular Risk
in Man. Abstracts 1989. International Development Conference, September 59, N 3.
Kuala Lumpur: PORIM.
88. Khan SA, Chugtai AB, Khalid L, Jaffrey SA (1989) Comparative physiological evalu-
ation of palm oil and hydrogenated vegetable oils in Pakistan. Proceedings 1989. Palm
Oil International Development Conference, 59 September, pp 1620. Kuala Lumpur,
PORIM.
89. Abeywardena MY, McLennan PL, Charnock JS (1991) C hanges in myocardial
eicosanoid production following long term dietary lipid supplementation in rats. Am
J Clin Nutr 53: 10391041.
90. Ng TKW, Hassan K, Lim JH, Lye MS, Ishak R (1991) Non hypercholesterolemic
effects of a palm oil diet in Malaysian volunteers. Am J Clin Nutr 53: 1015S1020S.
91. Marzuki A, Arshad F, Tariq AR, Jaarin K (1991) Influence of dietary fat on plasma
lipid profiles of Malaysian adolescents. Am J Clin Nutr 53: 1010S1014S.
92. Fernandez ML, Sun DM, Montano C, McNamara DJ (1995) Carbohydrate-fat ex-
change and regulation of hepatic cholesterol and plasma lipoprotein metabolism in the
guinea pig. Metabolism 44: 855864.
93. Foley M, Ball M, Chisholm A, Duncan A, Spears G, Mann J (1992) Should mono or
poly-unsaturated fat replace saturated fat in the diet? Eur J Clin Nutr 46: 429436.
94. Osim EE, Owu DU, Etta KM (1996) Arterial pressure and lipid profile in rats following
chronic ingestion of palm oil diets. Afr J Med Sci 25 (4): 335340.
95. Deferne JL, Leeds AR (1992) The antihypertensive effect of dietary supplementation
with a 6-desaturate essential fatty acid concentrate ascompared with sunflower seed oil.
J Hum Hyperten 6: 113119.
340

96. Bairati I, Roy L, Meyer F (1992) Effect of a fish oil supplement on blood pressure and
serum lipids in patients treated for coronary artery disease. Can J Cardiol 8: 4146.
97. Engler MM (1993) Comparative study of diets enriched with evening primrose, black
currant, borage or fungal oils on blood pressure and pressor responses in spontaneously
hypertensive rats. Prostaglandins Leukot. Essential Fatty Acids 49: 809814.
98. Yin K, Chu ZM, Beilin LJ (1991) Blood pressure and vascular reactivity changes in
spontaneously hypertensive rats fed fish oil. Br J Pharmacol 102: 991997.
99. Kitagawa S, Yamaguchi Y, Kunitomo M, Imaizumi N, Fujiwara M (1992) Important
of endothelium dependent relaxation in aorta from rats with arteriosclerosis induced by
excess vitamin D and a high cholesterol diet. Jpn J Pharmacol 59: 339347.
100. Owu DU, Osim EE, Orie NN, (1997) Altered responses of isolated aortic smooth
muscle following chronic ingestion of palm oil diets in rats. Afr J Med Med Sci 26:
8386.
101. Jenkins DK, Mitchell JC, Manku MS Horrobin DF (1988) Effects of different
sources of gamma-linolenic acid on the formation of essential fattyacid and prostanoid
metabolites. Med Sci Res 16: 525526.
102. Hui R, St Louis J, Falardeau P (1989) Antihypertensive properties oflinoleic acid and
fish oil omega-3 fatty acids independent of the prostaglandin system. Am J Hyperten
2: 610.
103. Engler MB (1992a) Vascular relaxation to omega-3 fatty acids: comparison to sodium
nitroprusside, nitroglycerine, papaverine and D600. Cardiovasc. Drugs Ther 6: 605
610.
104. Engler MB (1992b) Effects of omega-3, omega-6 and omega-9 fatty acids onvascular
smooth muscle tone. Eur J Pharmacol 215: 325328.
105. Engler MB (1992c) Effects of omega-3 fatty acids, docosahexaenoic and eicos-
apentaenoic acids on norepinephrine-induced contractions. Can JPhysiol Pharmacol
70: 675679.
106. Beilin LJ (1993) Dietary fats, fish and blood pressure. Ann N Y Acad Sci 683: 3545.
107. Suchiro A, Kakishita E, Nagai K (1982) The role of platelet hyperfunction in thrombus
formation in hyperlipidemia. Thromb Res 25(4): 331339.
108. Hornstra G, Lussenburg RN (1975) Relationship between the type of dietaryfatty acid
and arterial thrombosis tendency in rats. Atherosclerosis 22: 499516.
109. Lowe GD, Johnson RV, Drummond Mm, Forber CD, Prentice OR (1979) Induction of
circulating platelet aggregation in healthy subjects by a saturatedfat meal. Thromb Res
16: 565568.
110. Harker LA, Kelly AB, Hanson SR, Krupski W, Bass A, Osterud B, Fitzgerald GA,
Goodnight SH, Connor WW (1993) Interruption of vascular thrombus formation and
vascular lesion formation by dietary n-3 fattyacids in fish oil in non human primates.
Circulation 87: 10171029.
111. Rand ML, Hennsen AAHM Hornstra G (1988) Effects of dietary palm oil on arterial
thrombosis, platelet responses and platelet membrane fluidity in rats. Lipids 23(11):
10191023.
112. Abeywardena MY, McLennan PL, Charnock JS (1989) Increase in myocardial
PGI/TXA balance following long term palm oil feeding in the rat. J Molec Cell Cardiol
(Supp II) 21: 599.
113. Eder K, Kirchgessner M (1995) Zinc deficiency and activities of lipogenic and
glycolytic enzymes in livers of rats fed coconut oils or linseed oil. Lipids 30: 6369.
341

114. Sundram K, Kohr HT, Ong ASH, Pathmanathan R (1989) Effect of dietary palm oils
on mammary carcinogenesis induced by 7,12-dimethylbenzanthracene. Cancer Res 49:
14471451.
115. Owu DU, Osim EE, Ebong PE (1998) Serum liver enzymes profile of Wistar rats
following chronic consumption of fresh or oxidized palm oil diets. Acta Tropica 65:
6573.
116. Burskirk ER, Mendez J (1980) Energy: caloric requirements. In Alfin-Slater RB,
Kritchevsky D (eds), Human Nutrition V3A. New York: Plenum Press, pp 4995.
117. Isong EU, Ebong PE, Ifon ET, Umoh IB Eka OU (1997) Thermoxidized palm oil
induces reproductive toxicity in healthy and malnourished rats. Plant Foods Hum Nutr
51: 159166.
118. Krivenkova EM, Treschuk LI (1978) Morphological and functional investigation of
testes of albino rats after long term inclusion in their ration ofthermally oxidized fats.
Veprosy Pitaniya 6: 5964.
119. Giassudin ASM (1985) The role and mode of action of vitamin E andselenium: a
review. Nig J Biochem 2: 1422.
120. McArdle HJ, Ashworth CJ (1999) Micronutrients in fetal growth and development. Br
Med Bull 55(3): 499510.
121. Fomunyam RT, Adegbola AA, Oke OL (1984) The reproductive, growthand carcass
traits of rabbits fed cassava-based diets supplemented with palmoil. Food Chem 14(4):
263272.
122. Ng TKW, Khor HT, Chong YH (1988) The digestion, absorption andutilization of
refined palm oil, palm olein and palm stearin in the rat. Pertanika 11(3): 399406.
123. Abaelu AM, Okochi VI, Oyesile OO, Akinyele JO, Akinrimisi EO (1991) Nigerian
dietary oils and transport of amino acids in rat intestine. Nig J Physiol Sci 7: 3237.
124. Fashakin JB, Unokiwedi CC (1993) Nutritional evaluation of warankasi and
waragusi prepared from cow milk partially substituted with melon milk. Nig Food
J 11: 128134.
125. Newsholme EA, Calder P, Yaqoob P (1993) The regulatory, informationaland immun-
omodulatory roles of fat fuels. Am J Clin Nutr 57: (Suppl) 738S751S.
126. Mead JF, Alfin-Slater RB, Howton DR, Popjak G (1986) Lipids: Chemistry, Biochem-
istry and Nutrition. New York and London: Plenum Press, pp. 459473.
127. NRC (1978) National Research Council. Nutrient requirement of laboratory animals,
no. 10, (3rd ed). Washington DC: National Academy of Sciences, pp 5682.
128. Swash M, Mason S (1984) Hutchisons Clinical Methods 18th ed. East Sussex:
Bailliere Tindall, pp 434435.

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