Cholesterolaemic effects of the saturated fatty acids of
palm oil
Pramod Khosla and K. C. Hayes
Abstract
Dietary saturated fats are implicated as a major risk factor
in hypercholesterolaemia and cardiovascular disease.
Palm oil is a major source of the world’s supply of oils and
fats, but because of its relatively high content of saturated
fatty acids (principally palmitic acid), its consumption has
come under intense scrutiny over the last decade owing to
potential health implications. Based on studies carried out
more than thirty years ago, the hypothesis was developed
that lauric, myristic, and palmitic acid were the three
principal cholesterol-raising saturated fatty acids. Since
palmitic acid is the most abundant fatty acid in the diet,
the cholesterol-raising effect of all saturated fatty acids was
accordingly assigned to it. However, recent studies from
both humans and experimental animals suggest that not
all saturated fatty acids are cholesterol-raising. When all
dietary fatty acids are equalized, with the exception of the
two being tested, palmitic acid appears to have no impact on
the plasma cholesterol in normocholesterolaemic subjects
when dietary cholesterol intake is below a certain critical
level (400 mg per day). Only when cholesterol consumption
exceeds this level, or when hypercholesterolaemic subjects
are studied, does palmitic acid appear to increase the
plasma cholesterol. These differential effects of palmitic
acid on plasma cholesterol are thought to reflect differences
in LDL-receptor status. Collectively these data imply that,
for most of the world’s population, palm oil would be an
inexpensive and readily metabolized source of dietary
energy with minimal impact on cholesterol metabolism.
Introduction
A substantial body of data implicates dietary saturated
fat as one of the risk factors in hypercholesterolaemia and
cardiovascular disease [1, 2]. However, the debate over
what constitutes the “ideal” fat and, more specifically, its
fatty acid profile has generated much controversy and
confusion among both scientists and laymen. The subject
is complicated further by economics. Since dietary fat is
derived invariably from the consumption of various oils
and meat and dairy products, advice from the scientific
Food and Nutrition Bulletin, vol. 15, no. 2 © 1994, The United Nations University.
community affects production and distribution trends,
and, in certain instances, specific national interests.
Palm oil is a major contributor to the world’s supply of
fats and oils and is arguably the most cost-effective source
of edible fat. Because it has a relatively high content of
saturated fatty acids compared with most other oils, the
principal one being palmitic acid, the growing presence
of palm oil in the world market-place has been the
focus of much discussion over the last decade. Although
palm oil (with other so-called tropical oils) has typically
represented less than 3% of the total fat consumed in
the United States, it is a major source of dietary fat in
Latin American, South-East Asia, China, India and
Pakistan, parts of West Asia, and Africa. Thus, emerging
evidence on its metabolic impact based on carefully
constructed scientific studies both in animals and in
clinical settings will have far-reaching consequences
affecting two-thirds of the world population. Due in part
to palm oil’s potential as a cost-effective source of fat in
human nutrition, the scientific community must guard
against intentional or unintentional bias and maintain
a responsible perspective when reporting its findings or
making recommendations concerning consumption of
the oil.
It is apparent from recent data on lipoprotein
metabolism in humans and animals that focusing
on specific fat classes (saturated, mono-unsaturated,
polyunsaturated) is a gross over simplification of the
effect of dietary fat on cholesterol metabolism, including
plasma lipoproteins. Even a superficial analysis of some
of the so-called saturated fats (e.g., palm oil, lard, tallow,
butter, coconut oil) reveals that they have distinct profiles
(table 1) and empirically exert different metabolic
effects. Accordingly, research in recent years has shifted
toward elucidating the effects of specific dietary fatty
acids in triglycerides, as opposed to specific classes
of fats, on plasma lipids and lipoprotein metabolism.
Detailed reviews on palm oil per se have been published
recently [3-5]. Our purpose is to summarize the current
knowledge concerning its impact on lipid metabolism
from the perspective of its fatty acid profile.
1
2 Cholesterolaemic effects of the saturated fatty acids of palm oil

TABLE 1. Fatty acid composition of so-called saturated fats (percentages)

  12:0 14:0 16:0 18:0 18:1 18:2 18:3

Lard 0.1 1.4-1.7 23.1-28.3 11.7-24.0 29.7-45.3 8.1-12.6 0.7-1.2
Tallow 0.1 2.7-4.8 20.9-28.9 7.0-26.5 30.4-48.0 0.6- 1.8 0.3-0.7
Butter 2.9 10.8 26.9 12.1 28.5 3.2 -
Coconut oil 47.8 18.1 8.9 2.7 6.4 1.6 -
Cocoa butter - 0.1 26.3 33.8 34.4 3.1 -
Palm kernel oil 46.3-51.1 14.3-16.8 6.5-8.9 1.6-2.6 13.2-16.4 2.2-3.4 -
Crude palm oil 0.1 -1.0 0.9-1.5 41.8-46.8 4.2-5.1 37.3-40.8 9.1 -11.0 0.0-0.6
Palm olein 0.1-1.1 0.9-1.4 37.9-41.7 4.0-4.8 40.7-43.9 10.4-13.4 0.1-0.6
Palm stearin 0.1-0.6 1.1-1.9 47.2-73.8 4.4-5.6 15.6-37.0 3.2-9.8 0.1-0.6
Both RDB and red palm oils have fatty acid compositions similar to that of crude palm oil.

Dietary fats and serum cholesterol
Cardiovascular disease accounts for almost half a
million deaths annually in the United States. One of the
most easily measured indicators of risk is the serum or
plasma cholesterol concentration, specifically the level
of low-density lipoprotein (LDL) cholesterol, called the
“bad” cholesterol. An elevated level of LDL cholesterol
is a major risk factor. Conversely, an elevated level of
high-density lipoprotein (HDL) cholesterol (the “good”
cholesterol) is believed to confer protection. Hence, in
any individual with elevated cholesterol, the primary goal
is to lower the LDL cholesterol level to reduce the risk of
cardiovascular disease. Although this objective may be
achieved by drug therapy, one of the first interventions
is dietary modification. Since 1908 we have known that
diet affects serum cholesterol levels and, in the case of
laboratory animals, the ability to develop atherosclerosis
[6]. Although numerous dietary factors have been
implicated on the basis of epidemiological studies, the
single most important variable that has come under the
most scrutiny is fat.
Saturated, mono-unsaturated, and
polyunsaturated fats
Classification of fats has typically been based on their
constituent fatty acids. Hence, fats in which the fatty
acids with no double bonds (those most frequently
encountered are 1218°C, lauric, myristic, palmitic, and
stearic respectively) represent more than 50% of the total
fatty acids are referred to as saturated; those in which
the majority of total fatty acids have one double bond
(usually oleic acid) are designated mono-unsaturated;
and those in which fatty acids with two or more double
bonds are the majority (usually linoleic acid) are referred
to as polyunsaturated. Therefore, although two different
fats may both be referred to as saturated, they may
have distinctly different fatty acid profiles-for example,
coconut oil, rich in lauric and myristic acid; palm oil, rich
in palmitic acid; and cocoa butter, rich in stearic acid.
The two most abundant fatty acids in nature are oleic and
palmitic, which raises serious doubts that either would be
considered detrimental to normal metabolic processes.
Since the 1950s numerous studies both in humans
and in animals have investigated the effects of dietary
fat saturation on cholesterolaemia [1, 2, 7-11]. The
human studies were complicated by numerous variables,
including the age and sex of the subjects, whether
they were carried out in a metabolic ward or had
free-living subjects, whether the subjects consumed
liquid-formula diets or solid diets, and so on. The
general consensus emerged, however, that saturated fats
were twice as effective in elevating serum cholesterol
as polyunsaturated fats were in lowering it. Mono-
unsaturated fats were considered neutral (i.e., as having
no effect on serum cholesterol). These observations led
to a massive introduction of polyunsaturated fats in the
marketplace from the 1950s, which doubled the typical
polyunsaturated consumption between 1940 and 1985
from 2.5% to 5.5% of energy (en%) [12]. This rise in
intake was associated with a peak in serum cholesterol
and a decline in coronary heart disease [1].
Regression equations
Two independent research groups [8, 10] translated
these early results into mathematical regression
equations that have been used to predict the average
change in serum cholesterol that might be expected for
a given change in the percentage of energy consumed
from a specific class of fatty acids. In addition, the
equations included a cholesterol-elevating contribution
Pramod Khosla et al.
from dietary cholesterol itself. These early studies also
assigned essentially equal cholesterol-raising power
to three saturated fatty acids, 12:0, 14:0, and 16:0,
whereas the saturated fatty acids 10:0 and 18:0 were
considered neutral. Even though an initial study and
regression analysis showed myristic acid (14:0) to be
four times as potent as palmitic acid (16:0) in raising
serum cholesterol [5], a subsequent study with modified
(transesterified) fat led to a revised opinion and to the
labelling of 12:0, 14:0, and 16:0 saturated fatty acids as
equivalent [13]. The fact that palmitic acid is the most
abundant fatty acid in the food supply has meant that
the cholesterol-raising property of all saturated fats has
generally been attributed to their palmitic acid content.
By the same argument, because myristic acid (and lauric
acid) typically represent less than 2% of the energy in
the American diet, their cholesterol-raising potential
has been overlooked or dismissed as having any impact
of consequence.
These studies focused on types of fats and oils, from
which inferences were made about fatty acids and their
ability to raise and lower serum cholesterol. We now
have substantially more information about lipoprotein
metabolism. This is important because the LDL:HDL
ratio appears to be critical to the atherogenic potential
of the lipoproteins. In theory it is conceivable that a
proper balance in the fats (i.e., fatty acids) consumed
will greatly enhance the circulating lipoprotein profile.
In addition, the discovery of the LDL receptor [14]
revealed a complex metabolic pathway that must be
appreciated to understand fully the impact that dietary
fatty acids have on lipoprotein metabolism. Although
regression equations [9,10] have proved useful in
attempts to sort out the saturated and unsaturated fatty
acid effects on serum cholesterol among populations,
they provide minimal information on how dietary fat
effects lipoprotein metabolism, especially as it pertains
to individuals. Also, it is now apparent that over the full
range of potential 18:2 intakes (1-30 en %) the resulting
decrease in plasma cholesterol may be non-linear.
Is mono-unsaturated fat as good as
polyunsaturated fat?
In recent years a series of reports have suggested that
the cholesterol-lowering potential of mono-unsaturated
fat compares favourably with that of polyunsaturates,
lowering LDL without lowering HDL [15,16]. This
claim is surprising in light of data indicating that
monounsaturated fatty acids are relatively neutral. We
3
believe that total substitution with a mono-unsaturated
fat in the experimental settings (which seldom occurs
in Western diets because other fatty acids are present)
does two important things: it potentially removes all
the myristic acid from the diet, and it supplies more
than enough 18:2 (about 4 en%) to maximize the LDL-
receptor efficiency in the absence of 14:0 [16]. Our data
suggest that 18:1 is not as effective as 18:2 when either
14:0 or cholesterol has down-regulated the receptors at a
fatty acid intake below this critical 18:2 threshold.
In addition, on the basis of the above premise and
as discussed previously [17, 18], it follows that any
data obtained with a ratio of dietary polyunsaturated
to saturated fat outside the normal range in the human
diet (0.2-1.0) is likely to generate spurious results for
the reasons stated. That is why feeding all the fat as
safflower oil or coconut oil is not a legitimate, practical,
or clinically meaningful evaluation of a saturated or
polyunsaturated fat effect. Clearly, to derive valid
information about the physiological impact of dietary
fat, and specifically fatty acids, it should be fed at the
levels that the body normally encounters.
Is palmitic acid cholesterol-elevating?
In an initial study with three different species of monkeys
[19], tallow and lard (as saturated fats) were not much
more cholesterolaemic than corn oil (a polyunsaturated
fat) and were less so than other saturated fats, coconut
oil or butter, even though both lard and tallow contain
appreciable amounts of saturated fatty acids. Analysis
revealed distinctly different profiles of the saturated
fatty acids. This prompted us to question the generally
held belief that the 12-16°C fatty acids were equivalent
in terms of their cholesterol-raising ability. On further
investigation with diets using blends of oils in which
total saturated, mono-unsaturated, and polyunsaturated
fatty acids were held constant, the exchange of dietary
16:0 for 12:0 + 14:0 [20] caused a decrease in the plasma
cholesterol (table 2). This result clearly suggested that
palmitic acid was not cholesterolaemic but neutral
under those conditions, and that the widely held belief
that all saturated fatty acids are the same was invalid.
In a collaborative study, the same result was obtained
in normocholesterolaemic humans, even with 300 mg
of cholesterol in the diet [21]. Essentially similar results
were obtained for hamsters fed blends of fats to control
for specific fatty acids. Furthermore, the HDL cholesterol
and the mRNA abundance for the LDL receptor were
increased by 16:0 [22].
4
TABLE 2. Effect of exchanging 16:0 for 12:0 + 14:0 on lipid values in 21 monkeys of three species fed cholesterol-free
purified
Fatty acid (% of
 
total)
Diet 12:0 14:0 16:0
A 23.8 9.6 8.6
B 13.4 5.8 25.1
C 0.2 1.0 40.3
Adapted from ret 20.
Diets were formulated to give identical levels of total
saturated, mono-unsaturated, and polyunsaturated fatty
acids, with 16:0 increased at the expense of 12:0 + 14:0 in
going from diet A to C.
Values are mean ± SEM.
* Means in the same column sharing an asterisk are
significantly different.
In a subsequent study [23], monkeys were fed diets
rich in either 12:0 + 14:0 or 16:0 + 18:1 and simultaneously
injected with homologous 125I-VLDL and 131I-LDL to
assess apo B (and therefore very low-density lipoprotein
[VLDL] and LDL) metabolism. Analysis of apo B specific
activity data showed that monkeys fed the 16:0 + 18:1-
rich diet had increases in the pool size of VLDL apo B
and its transport rate and decreases in the pool size of
LDL apo B and its total transport rate. The irreversible
fractionated catabolic rate (FCR) for VLDL apo B and
LDL apo B was similar between dietary groups (table 3).
Although the total apo B and VLDL apo B transport rates
were increased, LDL apo B concentration was reduced
because of a decrease in the mass and proportion of
LDL apo B derived independently of VLDL catabolism.
This study further suggested that 16:0 is unlike 12:0 or
14:0, and clearly indicated that saturation of dietary fat
has distinct effects on the transport of LDL apo B from
VLDL-dependent and -independent pathways.
These studies [20, 22, 23] used cholesterol-free diets
and normocholesterolaemic animals, and the results
suggested that 12:0 + 14:0 is more cholesterolaemic
than 16:0, and that 16:0 and 18:1 are neutral in terms
of their effects on plasma cholesterol, as originally
suggested [9]. A reappraisal of the literature, especially
reports that developed the notion that palmitic acid was
a cholesterol-elevating fatty acid, revealed two telling
points. First, most studies used patients with mild
(>220 mg/dl) to severe (>250 mg/dl)
hypercholesterolaemia [9, 15], and many employed a
design in which fat was fed in a background of dietary
cholesterol. Thus, studies in both hypercholesterolaemic
Cholesterolaemic effects of the saturated fatty acids of palm oil
Cholesterol (mg/dl plasma)
Total LDL HDL LDL: HDL
205 ± 11* 92 ± 8* 99 ± 4* 0.95 ± 0.08
203 ± 10 87 ±7 96 ± 6 0.98 ± 0.09
183 ± 9* 79 ± 6* 86 ± 6* 0.89 ± 0.07
human subjects [15] and non-human primates fed
cholesterol-containing diets [24] suggested 16:0 was
hypercholesterolaemic compared with 18:1.
In both these situations some degree of down-regulation
of the LDL receptor would be expected [14]. Since the
LDL receptor, in addition to clearing circulating LDL, is
responsible for clearing VLDL remnants [2, 25], when its
activity is compromised it will fail to clear VLDL remnants.
Consequently, the latter would be further metabolized
to lead to an expanded LDL pool. However, when LDL
receptor activity is not compromised by cholesterol
feeding or other environmental-genetic interactions, as
in our rhesus study [23], no expansion of the LDL pool
occurs, since VLDL remnants are effectively removed to
preclude their conversion to LDL. As a consequence, no
elevation in plasma cholesterol was apparent when 16:0
was fed [19, 20, 22, 23].
As a working hypothesis, we suspected that in cases
of normal LDL-receptor activity (i.e., in the absence of
dietary cholesterol), 16:0 and 18:1 would exert similar
effects on receptor-mediated LDL clearance. To test this,
normocholesterolaemic cebus monkeys fed diets rich in
16:0,18:1, or 18:2 without cholesterol, were coinjected
with radiolabelled native and methylated LDL (table 4).
Receptor-mediated LDL clearance was similar for all
three diets [26]. The total cholesterol was lower in cebus
fed the 18:2-rich diet, but this was totally attributable to
decreased HDL. The LDL concentrations and clearance
were similar for all three diets. In fact, the 16:0-rich diet
produced the lowest LDL:HDL ratio, significantly better
than 18:2-rich diet, supporting our previous finding in
hamsters [22] that 16:0 may be the saturated fatty acid
responsible for the rise in HDL associated with saturated
fat consumption. On the basis of our cebus data [26],
we exchanged 16:0 for 18:1 in normocholesterolaemic
humans (7 en%) and again observed no differences in
LDL or HDL or total cholesterol, whereas increasing
12:0 + 14:0 caused a significant rise in LDL and total
cholesterol [27], just as in our earlier monkey study [20].
Pramod Khosla et al. 5

TABLE 3. VLDL and LDL kinetic values in rhesus monkeys fed cholesterol-free diets rich in 12:0 + 14:0 or 16:0 + 18:1

Transport to LDL/ Direct

Pool Size FCR (pools/ Transport rate Direct removal
Diet from VLDLa Production
(mg/kg) hr) (mg/kg/hr) (mg/kg/hr)
(mg/kg/hr) (mg/kg/hr)
VLDL apo B
12:0 + 14:0 2.5 ± 1.8 0.28 ± 0.17 0.53 ± 0.17 0.47 ± 0.17 0.06 ± 0.06  
        (89% ± 6) (11% ± 6)  
16:0 + 18:1 6.8 ± 2.2* 0.28 ± 0.10 1.77 ± 0.39* 1.62 ± 0.37* 0.15 ± 0.04*  
        (91% ± 2) (9% ± 2)  
LDL apo B
12:0 + 14:0 14.4 ± 3.1 0.036 ± 0.008 0.50 ± 0.03   0.062 ± 0.06 0.435 ± 0.05
          (12% ± 11) (88% ± 11)
16:0 + 18:1 7.0 ± 2.1* 0.033 ± 0.003 0.23 ± 0.08*   0.147 ± 0.04* 0.085 ±0.06*
          (65% ± 11) (35% ± 16)
Adapted from ref. 23.
Values are the mean ± SD of four monkeys per dietary group.
a. Values in the VLDL rows are transport to LDL; those in the LDL rows, from VLDL.
* Significantly different from the 12:0 + 14:0-rich diet.

TABLE 4. LDL kinetic values in cebus monkeys fed cholesterol-free diets rich in 18:2,18:1, or 16:0

LDL apo B FCR (pools/days) Transport

 
(mg/kg) Total Non-receptor Receptor (mg/kg/day)
18:2 20 ± 3 1.29 ± 0.14 0.48 ± 0.05 0.81 ± 0.15 25 ± 5
      (39 ± 8) (61 ± 8)  
18:1 20 ± 4 1.38 ± 0.20 0.47 ± 0.09 0.91 ± 0.21 22 ± 7
      (36 ± 7) (64 ± 7)  
16:0 21 ± 3 1.21 ± 0.15 0.41 ± 0.09 0.81 ± 0.15 26 ± 5
      (34 ± 7) (66 ± 7)  
Adapted from ref. 26.

Values are the mean ± SD of nine monkeys per dietary
group. Figures in parentheses represent the percentage
of the total FCR that is attributable to non-receptor- or
receptor-mediated pathways.
Using accumulated data from the feeding of 16
different cholesterol-free fat blends, we generated
regression equations (of the type originally developed
by Hegsted) for the fatty acid impact on the plasma
cholesterol response in our cebus monkeys [28].
The dietary 14:0 and 18:2 intakes alone were able
to explain almost 92% of the observed variation in
plasma cholesterol, with 16:0 and 18:1 appearing to be
neutral. In view of our working hypothesis concerning
the importance of the LDL receptor, we decided to re-
examine the report in which the entire dietary fatty
acid profile (not just saturated versus polyunsaturated)
was published together with the cholesterol response
in a large number of dietary manipulations (36 diets)
using the same people [9]. Just as originally reported
for all 36 diets, we found that 14:0 was four times as
cholesterolaemic as 16:0, with 18:2 the only fatty acid that
lowered cholesterol. However, based on our hypothesis
that 16:0 was neutral when LDL-receptor activity
was not compromised (e.g., by dietary cholesterol),
we analysed the data at low (<= 300 mg) or high
(>400 mg) cholesterol intakes. In the 17 human diets in
which cholesterol intake was 300 mg or less, 85% of the
observed variation in serum cholesterol could be explained
solely on the basis of 14:0 and 18:2. However, in the 19
human diets containing more than 400 mg cholesterol,
16:0 appeared slightly cholesterolaemic. We now also have
accumulated data from normocholesterolaemic gerbils
fed a total of 33 cholesterol-free diets [29]. Again, 14 0
and 18:2 explain almost 90% of the observed variation
in plasma cholesterol. Including dietary 16:0 and 18:1 in
the regression failed to improve the predictability of the
regression on the cholesterol response.
6
As an additional test of our hypothesis, we recently fed
normocholesterolaemic cebus monkeys cholesterol-free
diets rich in 16:0, 18:1, or equivalent amounts of 16:0 +
18:1. Again, no differences were noted in plasma lipid or
LDL and HDL kinetic values among the groups [30]. Only
when LDL receptors were down-regulated with dietary
cholesterol (0.3% w/w) was a hypercholesterolaemic
effect of 16:0 apparent (authors’ personal observation),
similar to the observations of others in monkeys fed
similar diets [24].
Summary
Palmitic acid is best considered a transitional fatty acid;
no apparent abnormality in cholesterol metabolism
develops when energy flow is normal and fat is
transported and cleared under normal physiological
circumstances. Circumstances may develop, however, as
in hypercholesterolaemic persons, wherein lipoprotein
production or clearance becomes impaired, such as
obesity and hyperinsulinaemia where compromised
LDL-receptor activity is a factor. In such individuals
palmitic acid may add to the cholesterolaemia because
it represents the primary stimulus for fat transport as
triglycerides among the fatty acids, thereby contributing
to the pool of lipoproteins that must subsequently
be subjected to an impaired clearance process. Only
then does 16:0 appear to have a negative impact on
cholesterol metabolism [31, 32]. The inference is that
for most of the world’s population, in whom adequate
energy consumption and not energy storage (adiposity)
is the problem, palm oil represents an ideal, inexpensive,
highly palatable source of energy in the food supply.
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