Health Effects of Palm Oil

Abstract

Increasingly, over the past 40 years, the conception of diet has undergone major changes. Many of these changes involve changes in dietary intake of fats and oils. There has been an increasing consumption of partially hydrogenated trans-vegetable oils and a decreasing intake of lauric acid-containing oils. Although popular literature usually attribute an increased risk of coronary heart disease (CHD) to elevated levels of serum cholesterol, which in turn are thought to derive from an increased dietary intake of saturated fats and cholesterol. The palm oil and palm kernel oil are high in saturated fatty acids, about 50% and 80% respectively and are esterified with glycerol. In developing countries, vegetable oils are replacing animal fats because of the cost and health concerns. It is reassuring to know that the consumption of palm oil as a source of dietary fat does not pose any additional risks for coronary artery disease when consumed in realistic amounts as part of a healthy diet.

Full text

© Kamla-Raj 2009 J Hum Ecol, 26(3): 197-203 (2009)
Health Effects of Palm Oil
Sutapa Mukherjee and Analava Mitra
School of Medical Science and Technology, Indian Institute of Technology,
Kharagpur 721 302, West Bengal, India
E-mail: amitra@smst.iitkgp.ernet.in
KEYWORDS Saturated Fats. Palm Oil. Cholesterol. Coronary Heart Disease
ABSTRACT Increasingly, over the past 40 years, the conception of diet has undergone major changes. Many of
these changes involve changes in dietary intake of fats and oils. There has been an increasing consumption of
partially hydrogenated trans- vegetable oils and a decreasing intake of lauric acid-containing oils. Although popular
literature usually attribute an increased risk of coronary heart disease (CHD) to elevated levels of serum cholesterol,
which in turn are thought to derive from an increased dietary intake of saturated fats and cholesterol. The palm oil
and palm kernel oil are high in saturated fatty acids, about 50% and 80% respectively and are esterified with glycerol.
In developing countries, vegetable oils are replacing animal fats because of the cost and health concerns. It is
reassuring to know that the consumption of palm oil as a source of dietary fat does not pose any additional risks for
coronary artery disease when consumed in realistic amounts as part of a healthy diet.
INTRODUCTION
Palm oil has been used in food preparation
for over 5,000 years. Palm oil, obtained from the
fruit of the oil palm tree, is the most widely
produced edible vegetable oil in the world and
it’s nutritional and health attributes have been
well documented (Chandrasekharan et al. 2000).
According to the Malaysian Oil Palm Statistics
in 2005 (http: //www.tocotrienol.org/en/index/
news/58.html), it surpassed soybean oil as the
most widely produced vegetable oil in the world.
Palm oil is currently enjoying strong appeal
worldwide as a cooking aid because it is free of
artery-clogging trans-fats. Besides being cleaner
and more stable, cooking with palm oil leaves the
kitchen becomes less greasy and easy to clean.
It is consumed worldwide as cooking oil, in
making of margarine and shortening, apart from
being used as an ingredient in fat blends and a
vast array of food products. In the United States,
palm oil’s principal edible use is as an ingredient
in prepared foods (primarily baked goods). Food
manufacturers choose palm oil because it has a
distinct quality, requires little or no hydro-
genation, and prolongs the shelf life of different
products (Anonymous 2003).
The palm fruit (Elaeis Guineensis) is the source
of both palm oil (extracted from palm fruit) and
palm kernel oil (extracted from the fruit seeds).
Babassu oil is extracted from the kernels of the
Babassu palm. Malaysia and Indonesia account
for 83 percent of production and 89 percent of
global exports. Oil Palm is grown as an industrial
plantation crop, often (especially in Indonesia)
on newly cleared rainforest or peat-swamp forests
rather than on already degraded land or disused
agricultural land. In Malaysia, the area devoted
to Oil Palm has increased 12-fold to 13,500 square
miles. The vast plantations that grow Oil Palm
trees have contributed to the destruction of the
rainforest and wildlife of Southeast Asia (http: //
en.wikipedia.org/wiki/Palm_oil).
PALM OIL
Composition of Palm Oil
The palm oil and palm kernel oil are high in
saturated fatty acids, about 50% and 80%
respectively and esterified with glycerol. The Oil
palm gives its name to the 16 carbon saturated
fatty acid palmitic acid; monounsaturated oleic
acid is also a constituent of palm oil while palm
kernel oil contains mainly lauric acid. Palm oil is
the largest natural source of tocotrienol. Palm oil
is also high in vitamin K and dietary magnesium.
Napalm derives its name from naphthenic acid,
palmitic acid and pyrotechnics or simply from a
recipe using naphtha and palm oil. Table 1 shows
fatty acids composition of palm oil and palm kernel
oil. Palm oil contained about 10% linoleic acid,
which is an unsaturated omega-6 fatty acid.
Linoleic acid is one of the two essential fatty acids
that humans require. Palm oil also contains small
amounts of squalene (possible cholesterol lower-

198 ANALAVA MITRA AND SUTAPA MUKHERJEE
ing and anti-cancer properties) and ubiquinone
(energy booster). Besides Red palm oil is also
rich in co-enzyme Q10.
Antioxidants in Palm Oil
Effects of Carotenoids: Crude palm oil is
considered to be the richest natural source of
carotenoids (about 15 times more than in carrots).
The human body uses carotenoids as Vitamin A.
Carotenoids also enhance immune function by a
variety of mechanisms, and can improve
cardiovascular health. Carotenoids also play an
important potential role by acting as biological
antioxidants, protecting cells and tissues from the
damaging effect of free radicals. When on being
exposed to pollutants in cigarette smoke, industrial
pollution, stress, unbalanced diets, pesticide and
insecticide residues in food and water, and many
other negative environmental influences, one is
also exposed to free radicals. A build-up of free
radicals in the body is associated with degenerative
diseases such as heart disease and cancer, as well
as general ageing. It is, therefore, in one’s own
best interest to ensure that to eat a diet rich in
antioxidants that will prevent the damage that is
done to bodies by free radicals. Red palm oil is a
form of processed palm oil (deacidified and
deodorised) which retains 80% of the original
carotenoids, making it a remarkable source of
Vitamin A. These natural antioxidants act as buffers
against free radicals and are believed to play a
protective role in cellular ageing, atherosclerosis,
cancer, arthritis, and Alzheimer’s disease.
Effects of Tocopherols and Tocotrienols: In
fact, no other vegetable oil has as much Vitamin E
as compared to palm oil (Chow 1992). Natural
vitamin E exists in eight different forms or isomers,
four tocopherols and four tocotrienols. Natural
palm oil contains alpha, beta, gamma, and delta-
tocopherols and alpha, beta, gamma, and delta-
tocotrienols. Tocotrienols in Vitamin E have been
found to have antioxidant and anti-cancer
activities. Tocotrienols by its action on liver
enzymes lowers blood cholesterol levels without
reduction in good cholesterol (High Density
Lipoprotein or HDL). Its antioxidant properties
bring many benefits to the human body, such as
preventing skin aging, preventing fat oxidation,
reducing blood pressure etc. Human studies have
shown that palm tocotrienols have the ability to
reverse blockage of the carotid artery and platelet
aggregation (the clumping together of cells)
thereby reducing the risk of stroke, arteriosclerosis,
and ischaemic heart diseases. Palm tocotrienols
have been shown to be protective after a strenuous
bout of exercise by preventing protein oxidation
and lipid peroxidation. Tocotrienol-rich fraction of
palm oil is capable of protecting brain against
oxidative damage and thereby from the ensuing
adverse alterations that accompany aging. Lipid
peroxides in blood vessels and plasma show a
positive correlation with blood pressure. The
antioxidant ability of gamma-tocotrienol may
prevent development of increased blood pressure
by reducing lipid peroxides and enhancing the total
antioxidant status, including superoxide dismutase
activity. Melanoma, also on the increase, can be
inhibited with the delta fraction of tocotrienols.
When applied topically, vitamin E/tocotrienols is
quickly absorbed into the deep layers of the skin.
Gamma- and delta-tocotrienols derived from palm
oil exhibit a strong activity against tumor
promotion by inhibiting Epstein- Barr virus. The
delta and gamma factions of tocotrienols can inhibit
certain types of cancer, including both the
estrogen- positive and estrogen-negative breast
cancer cells. The inhibition of the growth of breast
cancer cells by palm tocotrienols could have
extraordinarily important clinical implications on
world health. Not only can the palm tocotrienols
prevent the growth of these unwanted cells, but
they can also do this in the presence as well as in
the absence of estradiol, thereby protecting against
both hormone-related and other kinds of breast
cancer. It is interesting to note that tocotrienols
can inhibit or even kill normal cells, but only in
extremely high amounts — just as most any
Palm Oil
Saturated acids- Palmitic (C16) 44.3%, Stearic (C18) 4.6%,
Myristic (C14) 1.0%
Mono Unsaturated acids- Oleic (C18) 38.7%
Poly Unsaturated acids- Linoleic (C18) 10.5%
Other/Unknown - 0.9%
Table 1: Fatty acids composition of palm oil and palm kernel oil (Chow 1992)
Palm Kernel Oil
Saturated acids- Lauric (C12) 48.2%, Myristic (C14) 16.2%,
Palmitic (C16) 8.4%, Capric (C10) 3.4%, Caprylic
(C8) 3.3%, Stearic (C18) 2.5%
Mono Unsaturated acids-Oleic (C18) 15.3%
Poly Unsaturated acids-Linoleic (C18) 2.3%
Other/Unknown 0.4%

199
HEALTH EFFECTS OF PALM OIL
beneficial substance can be detrimental in excessive
quantity. Malignant cells, on the other hand, are
very sensitive to tocotrienols. In fact, the more
cancerous the cell, the more susceptible it is to the
destructive effects of tocotrienol, so very little is
required to accomplish its favorable role of cancer-
cell annihilation (Ebong et al. 1999).
Benefits of Palm Oil
Palm oil is consumed in the fresh state and/or
at various levels of oxidation. Feeding experiments
in various animal species and humans have
highlighted the beneficial role of fresh palm oil to
health. These benefits include reduction in the
risk of arterial thrombosis and atherosclerosis,
inhibition of cholesterol biosynthesis and platelet
aggregation, and reduction in blood pressure.
However, on being used in the oxidized state
possesses potential dangers to the physiological
and biochemical functions of the body. Oxidized
palm oil induces an adverse effect on plasma lipid
profile, free fatty acids, phospholipids and
cerebrosides. Additionally, oxidized palm oil
induces reproductive toxicity and organ toxicity
particularly of the kidneys, lungs, liver and heart.
Available evidence suggests that at least part of
the oxidized oil impact on health is due to
generation of toxicants due to oxidation. The
reduction of the dietary level of oxidized oil and/
or the level of oxidation may reduce the health
risk (Ebong et al. 1999).
A study by a group of researchers in China
comparing palm, soybean, peanut oils and lard
showed that palm oil actually increased the levels
of good cholesterol and reduced the levels of
bad cholesterol in the blood (Zhang et al. 1997
cited by Koh 2007). A study by Hornstra in 1990
also showed similar results. Zhang et al. (1997)
found that in normo and hypercholesterolemic
subjects, the use of palm oil in the diet should be
safe and will not increase the risk of Cerebro
Vascular Disease (CVD). Toxicological and phar-
macological studies show that supplementation
with palm tocotrienols up to 2,500 milligrams per
day per kilogram of body weight does not
produce any significant side effects. Although
higher levels can be used for therapeutic
purposes, those who want to enhance their
antioxidant intake can use 30 to 50 milligrams of
tocotrienols daily. Additional phyto-nutrients,
designed by some of our best formulators,
provide synergy for the palm tocotrienols (http: /
/www.bettykamen.com/newsletters/palmoil.htm).
Controversies of Palm Oil
For many years now, it has been established
that the primary cholesterol-elevating fatty acids
are the saturated fatty acids with 12 (lauric acid),
14 (myristic acid) and 16 (palmitic acid) carbon
atoms with a concomitant increase in the risk of
coronary heart disease. The World Health
Organization in its report (2003) states that there
is convincing evidence that palmitic oil
consumption contributes to an increased risk of
developing of cardiovascular diseases.
In the past, palm oil was attacked as “satura-
ted” since it contains 44% palmitic acid and 5%
stearic acid, and thereby allegedly raises blood
cholesterol and increases the risk of cardio-
vascular disease. However, a sizeable and growing
body of scientific evidence indicates that palm
oil’s effect on blood cholesterol is relatively
neutral when compared to other fats and oils. Palm
oil raises plasma cholesterol only when an excess
of dietary cholesterol is presented in the diet. Two
meta-analysis have examined the effect of palmitic
acid (found in palm oil) on serum cholesterol. In a
1997 study based on 134 clinical studies, British
researchers concluded that, compared to
carbohydrates, palmitic acid raises blood
cholesterol levels (Clarke et al. 1997). In 2003,
Dutch scientists conducted a meta-analysis of
35 clinical studies (Mensink et al. 2003) and
examined what many experts consider the best
indicator of heart-disease risk: the ratio of total
cholesterol to HDL cholesterol (Institute of
Medicine, National Academies 2002). Palmitic
acid increased the total: HDL cholesterol ratio
more than other saturated fatty acids, including
lauric acid and myristic acid, which are abundant
in palm kernel oil and coconut oil; the other highly
saturated tropical oil (Enig 1993). Palm oil
increases the total: HDL cholesterol ratio more
than the average U.S. or British dietary fat (Jensen
et al. 1999; Keys et al. 1957). That finding indicates
that, in terms of blood cholesterol, palm oil is
somewhat more harmful than the average U.S.
dietary fat and much more harmful than such
liquid oils as olive, soy, and canola. The World
Health Organization has stated that there is
“convincing evidence” that palmitic acid
increases the risk of cardiovascular disease
(World Health Organization 2003).
A number of pre-1990 human feeding studies

200 ANALAVA MITRA AND SUTAPA MUKHERJEE
reported that palm oil diets resulted in lower serum
cholesterol levels than pre-study values. Indeed,
scientists concluded that these studies, although
not specifically designed to study palm oil, have
revealed that a palm oil diet lowered plasma
cholesterol compared with the starting periods
during which the subjects were eating their
habitual Western diets. These conclusions were
questioned because the studies were not desi-
gned to measure the effects of palm oil. But
subsequent studies, specifically designed to
evaluate palm oil, confirmed that palm oil’s impact
on serum lipid and lipoprotein profiles compares
favorably to corn oil, lightly hydrogenated soybean
oil, and olive oil. Thus, palm oil’s impact on serum
lipids is more like a monounsaturated than
saturated oil. Palm oil contains a high percentage
of monounsaturates (40%). Palm oil’s saturated
fatty acids are palmitic (44%) and stearic (5%),
which do not appear to elevate blood cholesterol
in people with cholesterol levels within normal
ranges. Palm oil stimulates the synthesis of
protective HDL cholesterol and removal of harmful
Low Density Lipoprotein (LDL) cholesterol. Palm
oil is rich in vitamin E, (particularly tocotrienols),
which appear to reduce serum cholesterol
concentrations (Ebong et al. 1999).
Ancel Keys is largely responsible for starting
the anti-saturated fat agenda in the United States.
From 1953 to 1957 Keys made a series of state-
ments regarding the atherogenicity of fats. These
pronouncements were: “All fats raise serum
cholesterol; Nearly half of total fat comes from
vegetable fats and oils; No difference between
animal and vegetable fats in effect on Coronary
Heart Disease (CHD) (1953); Type of fat makes no
difference; Need to reduce margarine and
shortening (1956); All fats are comparable;
Saturated fats raise and polyunsaturated fats lower
serum cholesterol; Hydrogenated vegetable fats
are the problem; Animal fats are the problem.”
Recently, an editorial by Harvard’s Walter Willett,
in the American Journal of Public Health (1990)
acknowledged that even though “the focus of
dietary recommendations is usually a reduction of
saturated fat intake, no relation between saturated
fat intake and risk of CHD was observed in the
most informative prospective study to date.”
Another editorial, this time by Framingham’s
William P. Castelli in the Archives of Internal
Medicine (1992), declared for the record that “...in
Framingham, Mass, the more saturated fat one ate,
the more cholesterol one ate, the more calories one
ate, the lower the person’s serum cholesterol... the
opposite of what the equations provided by
Hegsted et al. (1965) and Keys et al. (1957) would
predict...” Castelli (1992) further admitted that “...in
Framingham, for example, we found that the people
who ate the most cholesterol, ate the most
saturated fat, ate the most calories, weighed the
least, and were the most physically active”.
Dietary fat and CHD
Dietary fat is principally composed of triacy-
lglycerol (TAG). Therefore, following digestion
of a meal, there is a significant increase in the
plasma TAG concentration. Prospective epide-
miological studies show that plasma TAG,
especially the non-fasting level is an important
factor in the pathogenesis of coronary heart
disease (CHD) (Roche 2000). A positive corre-
lation between plasma TAG levels and CHD risk
has been found in women, diabetics, the Japanese
and those with elevated LDL or decreased HDLC
levels (Betterbridge 1999; Mann 1993). An Israeli
study suggests that elevated plasma TAG levels
are an independent risk factor for mortality among
CHD patients (Vogel et al. 1997). Elevation of
post-prandial TAG rich plasma lipoproteins and
suppression of HDL-C concentrations are
considered potentially atherogenic (Patsch 1994).
Several clinical studies have shown that elevated
levels of TAG rich lipoprotein and its remnants
during the post-prandial phase of lipid metabolism
are related to the presence and progress of coro-
nary atherosclerosis (Cohn 1994; Roche and
Gibney 1995). Atherosclerosis and thrombosis are
the two key patho-physiological processes, which
lead to the development of CHD. An excessive
postprandial TAG response to a meal high in fat
can be due to over production of TAG rich
lipoproteins to inadequate lipolysis or to
abnormalities in the metabolism of remnant
lipoproteins. In the latter instance, the remnant
lipoproteins will accumulate in the circulation. In
this situation, chylomicrons remain in the
circulation longer and interact with both LDL and
HDL. Chylomicrons give their TAGs to the LDLs,
which become smaller and denser, and more
atherogenic (Patsch 1994). The HDLs also become
over enriched with TAGs. The resultant HDLs are
more susceptible to catabolism, whereby the liver
removes the cardio protective HDL fraction from
the circulation. These chylomicron remnants are a
component of the atherosclerotic plaque; therefore

201
HEALTH EFFECTS OF PALM OIL
excessive chylomicron remnant concentrations
promote the process of atherogenesis (Slyper
1992). It is known that the quantity of dietary fat
increases postprandial lipemia in a dose dependent
manner and that the production and clearance of
lipoproteins and lipoprotein derived remnants are
affected by the composition of the diets. A
prothrombotic state is produced by elevated
post-prandial lipemia because a high con-
centration of TAG rich lipoprotein in the circulation
activates coagulation factor VII (FVII). There are
indications that dietary fat intake is a major
determinant of factor VII activity (FVIIc).
Postprandial TAG rich lipoprotein enhances
postprandial FVIIc (Larsen et al. 1997). A positive
relationship between FVIIc and CHD mortality
has been demonstrated. Patients with CHD have
high levels of FVIIc. The possible mechanisms
involved could be that the plasma TAG
concentration affects the concentration and
catabolism of FVII and converts the inactive FVII
(zymogen) to FVIIa. Altering the saturated:
monounsaturated fatty acid (SFA: MUFA) ratio
of an acute test meal does not influence the
magnitude of post-prandial FVIIc (Marckman et
al. 1990; Roche and Gibney 1997). Several studies
have demonstrated that all the traditional coronary
risk factors are associated with endothelial
dysfunction, independent of the presence of CHD
(Vogel et al. 1997). It has become increasingly
clear that endothelial cells play important roles in
the maintenance of the homeostatic balance in
vivo and in the modulation of vascular function
in health and disease. Ong et al. (1999) have
reported that the consumption of a meal high in
monounsaturated fat was associated with acute
impairment of endothelial function (as measured
by flow mediated reactivity of the brachial artery)
when compared with a carbohydrate rich meal. It
is pertinent in this context to note that a study in
the US found that men with the highest level of
saturated fatty acids had the lowest incidence of
ischaemic stroke (Gillman et al. 1997). These
findings once again reaffirm that fats and oils with
different fatty acid compositions do not differ in
their acute effects on plasma TAG and FVII levels.
The present observations lend further testimony
to the merits of Palm Oil in that it is comparable to
the other oils in terms of its postprandial lipid
response and effects on prothrombotic activity
(Thomsen et al. 1999). In developing countries,
vegetable oils are replacing animal fats because
of the cost and health concerns and Palm Oil has
become one of the major edible oils in the world
(Chandrasekharan 1999). It is reassuring to know
that the consumption of Palm Oil as a source of
dietary fat does not pose any additional risks for
coronary artery disease when consumed in
realistic amounts as part of a healthy diet
(Pedersen et al. 1999).
Increasingly, over the past 40 years, the
conception of diet has undergone major changes.
Many of these changes involve changes of fats
and oils. There has been an increasing supply of
the partially hydrogenated trans-containing
vegetable oils and a decreasing amount of the
lauric acid-containing oils (Enig 1996). As a result,
there has been an increased consumption of
Tran’s fatty acids and linoleic acid and a decrease
in the consumption of lauric acid. This type of
change in diet has an effect on the fatty acids the
body has available for metabolic activities.
Although popular literature of epidemiological
studies usually attribute an increased risk of
coronary heart disease (CHD) to elevated levels
of serum cholesterol, which in turn are thought
to derive from a dietary intake of saturated fats
and cholesterol (Mann 1993). But, saturated fats
may be considered a major culprit for CHD only if
the links between serum cholesterol and CHD and
between saturated fat and serum cholesterol are
each firmly established. Decades of large-scale
tests and conclusions there from have supported
to establish the first link. In fact, this relationship
has reached the level of dogma. But the scientific
basis for these relationships has now been
challenged as resulting from large-scale mis-
interpretation and misrepresentation of the data
(Enig 1993; Mann 1993; Smith 1991; Ravnskov
1995; Roche 2000).
CONCLUSION
Epidemiological studies usually attribute an
increased risk of coronary heart disease (CHD)
to elevated levels of serum cholesterol, which in
turn are thought to derive from a dietary intake of
saturated fats and cholesterol. Dietary fat is
principally composed of triacylglycerol (TAG).
Therefore, following digestion of a meal, there is
a significant increase in the plasma TAG
concentration. Prospective epidemiological
studies show that plasma TAG, especially the non-
fasting level is an important factor in the
pathogenesis of coronary heart disease. In the
past, palm oil was attacked as “saturated” since

202 ANALAVA MITRA AND SUTAPA MUKHERJEE
it contains 44% palmitic acid and 5% stearic acid,
and thereby allegedly raises blood cholesterol and
increases the risk of cardiovascular disease.
However, a sizeable and growing body of scientific
evidence indicates that palm oil’s effect on blood
cholesterol is relatively neutral when compared to
other fats and oils. Palm oil raises plasma
cholesterol only when an excess of dietary
cholesterol is presented in the diet. Palm oil stimu-
lates the synthesis of protective HDL cholesterol
and removal of harmful LDL cholesterol. Palm oil is
rich in vitamin E, (particularly tocotrienols), which
appear to reduce serum cholesterol concentrations
and has potent anti-oxidant effects.
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