Effects of dietary coconut oil, butter and safflower oil on plasma
lipids, lipoproteins and lathosterol levels
, W Sutherland
, J Mann
, S de Jong
, A Chisholm
and M Skeaff
Human Nutrition and
Medicine, University of Otago, Dunedin, New Zealand
Objective: The aim of this present study was to determine plasma levels of lathosterol, lipids, lipoproteins and
apolipoproteins during diets rich in butter, coconut fat and saf¯ower oil.
Design: The study consisted of sequential six week periods of diets rich in butter, coconut fat then saf¯ower oil
and measurements were made at baseline and at week 4 in each diet period.
Subjects: Forty-one healthy Paci®c island polynesians living in New Zealand participated in the trial.
Interventions: Subjects were supplied with some foods rich in the test fats and were given detailed dietary
advice which was reinforced regularly.
Results: Plasma lathosterol concentration (P < 0.001), the ratio plasma lathosterol/cholesterol (P 0.04), low
density lipoprotein (LDL) cholesterol (P < 0.001) and apoB (P < 0.001) levels were signi®cantly different
among the diets and were signi®cantly lower during coconut and saf¯ower oil diets compared with butter diets.
Plasma total cholesterol, HDL cholesterol and apoA-levels were also signi®cantly (P 0.001) different among
the diets and were not signi®cantly different between buffer and coconut diets.
Conclusions: These data suggest that cholesterol synthesis is lower during diets rich in coconut fat and saf¯ower
oil compared with diets rich in butter and might be associated with lower production rates of apoB-containing
Sponsorship: The study was supported by the Health Research Council of New Zealand and the Anderson
Descriptors: diet; fat type; lathosterol; lipoproteins; polynesians
Diets rich in saturated fatty acids (SAFA) raise plasma
cholesterol and low density lipoprotein (LDL) cholesterol
levels compared with diets rich in polyunsaturated fatty
acids (PUFA). Saturated fatty acids with different chain
lengths vary in their hypercholesterolemic effect in the
order of increasing potency myristate, palmitate and laurate
(Denke & Grundy, 1992; Zock et al, 1994; Cox et al,
1995). Differences in plasma LDL cholesterol when these
fatty acids are predominant in the diet are theoretically due
to differences in the rates of very low density lipoprotein
(VLDL) production and conversion to LDL or the catabol-
ism of LDL by hepatic receptors or both. There is limited
evidence that diets rich in palmitic acid stimulate the
production of very low density lipoproteins (VLDL) and
LDL (Cortese et al, 1983). The rate of VLDL secretion
from the liver is closely linked to cholesterol synthesis rates
in normolipidemic subjects (Watts et al, 1995). Whether
cholesterol synthesis varies during diets rich in SAFA of
different chain lengths has not been widely studied.
The effect of changing the quality of dietary fat on
cholesterol synthesis is controversial. While several studies
have indicated that whole-body cholesterol synthesis is
unchanged (Shepherd et al, 1980; Spritz et al, 1965;
Grundy & Ahrens, 1970; Nestel et al, 1976) others have
documented decreased (Glatz & Katan, 1993) and
increased (Jones et al, 1994) rates when PUFA replace
SAFA in the diet. A suggested (Glatz & Katan, 1993)
explanation for these varying ®ndings is that the gas
chromatographic (GC) separation of faecal plant sterols
and endogenous sterols, a vital step in the cholesterol
balance method of measuring cholesterol synthesis, may
not have been achieved in the earlier studies before the
advent of capillary GC. Cholesterol balance estimates
whole body cholesterol synthesis as the difference between
dietary intake and excretion of cholesterol and its metabo-
lites in the faeces in the steady state. In view of the
technical dif®culties and the requirement for steady-state
conditions in the cholesterol balance technique, alternative
methods for measuring cholesterol synthesis have been
Plasma lathosterol levels and the ratio plasma latho-
sterol/cholesterol have been established as excellent indices
of cholesterol synthesis. They correlate closely with human
hepatic 3-hydroxy-3-methylglutaryl Coenzyme A (HMG
CoA) reductase activity, the rate limiting step in cholesterol
rkhem et al, 1987) and with whole-body
cholesterol synthesis rates measured by cholesterol balance
(Kempen et al, 1988). Also, levels of the sterol are
decreased when cholesterol synthesis is reduced during
treatment with drugs that inhibit the HMG CoA reductase
enzyme (Kempen et al, 1988) and are increased under
conditions of increased cholesterol synthesis (Miettinen,
1985). Lathosterol is a cholesterol precursor that is formed
after the rate-limiting step in cholesterol biosynthesis and
`leaks' from cells at rates which are proportional to
rates of cellular cholesterol synthesis. Plasma lipoproteins
are acceptors for precursor sterols released from cells.
Correspondence: Dr W Sutherland, Department of Medicine, Dunedin
School of Medicine, PO Box 913, Dunedin, New Zealand.
Received 4 December 1997; revised 24 April 1998; accepted 9 May 1998
European Journal of Clinical Nutrition (1998) 52, 650±654
ß 1998 Stockton Press. All rights reserved 0954±3007/98 $12.00
Consequently, the ratio plasma lathosterol/cholesterol has
been frequently used to correct for the effect of varying
numbers of lipoprotein acceptors on plasma lathosterol
levels. When PUFA are substituted for SAFA in the diet
plasma latho-sterol levels and the ratio lathosterol/choles-
terol are reduced (Glatz & Katan, 1993) suggesting that
cholesterol synthesis is also reduced.
The aim of the present study was to determine the effect
of diets rich in coconut fat, butter and saf¯ower oil on
plasma levels of lathosterol. The study was conducted in
Paci®c Islanders because these types of diets have parti-
cular relevance in that population. Traditionally, they eat
diets rich in coconut fat but on migration to New Zealand
they increase their intake of other types of fat (Stanhope
et al, 1981).
Subjects and methods
Forty-seven Paci®c Islanders from two Paci®c Island
churches in Dunedin, New Zealand were recruited. Six
subjects dropped out immediately after initial screening and
41 subjects started the dietary phase of the study. The 41
subjects included 24 men and 17 women ages 19±72 y (31
Western Samoans and 10 Cook Islanders) with plasma
cholesterol levels between 4.2 mmol/l and 7.5 mmol/l and
plasma triglycerides less than 3 mmol/l. None was receiv-
ing drugs known to in¯uence lipid metabolism. Character-
istics of the subjects at baseline are shown in Table 1. All
subjects gave informed consent and the study was approved
by the Ethics committee of the Otago Area Health Board.
The study included a run in period of six weeks followed
by three consecutive six week periods when diets rich in
butter (butter diet), coconut fat (coconut diet) then saf-
¯ower oil (saf¯ower diet) were consumed without washout
periods between the experimental diet periods. A sequen-
tial study design rather than the preferred randomized
crossover design was used to encourage compliance with
the diets because participants frequently ate communally
within the church group. During the run in period partici-
pants completed a food frequency questionnaire to assess
their usual food and nutrient intake and a health question-
naire. Body weight was measured and fasted venous blood
samples were taken on two occasions during the baseline
period and at weeks four and six of each diet period.
Plasma lipids and HDL cholesterol levels were measured in
all blood samples collected. Plasma lathosterol, very low
density lipoprotein (VLDL) cholesterol and apolipopro-
teins A±I, A±II and B were measured on one occasion
during the baseline period and at the four-week point of
each diet period. An earlier study from our laboratories
(Cox et al, 1995) suggested that plasma lipid and lipo-
protein levels had attained equilibrium by four weeks after
a change in the type of fat in the diet.
The experimental diets were designed to provide approxi-
mately 17% protein, 47% carbohydrate and 36% fat as a
fraction of total energy intake. Target values for fat intake
based on an 8.4 MJ/d diet were 84 g total fat for all diets
and including; 39 g fat from butter plus fat from palmitic
acid-rich foods to give an intake of approximately 17 g
palmitic acid (butter diet); 39 g fat from coconut oil to give
an intake of approximately 17 g lauric acid (coconut diet);
and 24 g fat from saf¯ower oil to give an intake of
approximately 17 g linoleic acid (saf¯ower diet). Calcu-
lated intakes of myristic acid and linoleic acid were
approximately similar in the coconut and butter diets. To
encourage dietary compliance, participants were supplied
with butter and cream during the butter diet, coconut
cream, coconut oil and monounsaturated margarine
during the coconut diet and saf¯ower oil and polyunsatu-
rated margarine during the saf¯ower diet. Specially baked
bread including similar amounts of butter, coconut oil or
saf¯ower oil were supplied to the study participants during
the appropriate diet period. Egg yolk was added to the
coconut diet and the saf¯ower diet to maintain approxi-
mately similar cholesterol intake (250±300 mg/d) during
the experimental diets. Subjects assigned to the butter diet
were instructed to eat butter, cream, butter bread, cheese,
meat, ®sh, chicken, fruit and vegetables, rice, noodles, full
cream milk and milk products and were instructed not to
eat coconut cream or products, margarine and cooking oils.
Those assigned to the coconut diet were instructed to eat
coconut cream, coconut bread, monounsaturated margarine,
coconut, ®sh, meat cheese, chicken, fruit and vegetables,
rice, noodles, trim milk and other low fat dairy products
and not to eat butter, cream, other margarines, chicken skin,
deep-fried takeway foods and vegetable oils. Those
assigned to the saf¯ower diet were instructed to eat poly-
unsaturated margarine, saf¯ower oil, saf¯ower bread,
cheese, meat, ®sh, chicken, fruit and vegetables, rice,
noodles, trim milk, low fat dairy products and not to eat
butter, cream, coconut cream and products, cream, reduced
fat cream and deep-fried takeaway foods. Prior to commen-
cing the experimental diets and during each appointment
for blood sampling a dietitian provided detailed dietary
instructions which were reinforced during group sessions
throughout the study. Dietary instruction included ways to
incorporate the test fats in the diet and foods to eat and
foods to avoid during each experimental diet. Menus were
suggested and recipes were provided. Dietary compliance
was assessed from the plasma triglyeride fatty acid com-
position at week 4 of each diet period. All contact with
study participants took place on Sunday mornings in the
church hall after church service.
Table 1 Characteristics of the subjects at baseline
Variable n 21 n 16
Age (y) 35 (9) 39 (9)
Body mass index (kg/m
) 29.7 (3.5) 26.8 (5.4)
Fasting blood glucose (mmol/l) 5.12 (0.82) 5.66 (1.56)
Plasma lipids (mmol/l)
Total cholesterol 5.47 (0.89) 5.55 (1.05)
VLDL cholesterol 0.38 (0.27) 0.30 (0.13)
LDL cholesterol 3.50 (0.85) 3.64 (0.95)
HDL cholesterol 1.07 (0.26) 1.13 (0.17)
Triglycerides 1.98 (1.61) 1.50 (0.49)
Plasma apolipoproteins (g/l)
A±I 1.19 (0.19) 1.24 (0.17)
A±II 0.32 (0.09) 0.34 (0.05)
B 0.76 (0.22) 0.78 (0.19)
Lathosterol (mmol/mmol cholesterol) 1.14 (0.41) 1.14 (0.47)
Values are mean (s.d.).
Abbreviations: VLDL, very low density lipoproteins; LDL, low density
lipoproteins; HDL, high density lipoproteins.
Dietary fat type and lathosterol levels
Subjects fasted overnight and at approximately midday the
following day (Sunday) venous blood was taken into tubes
containing EDTA. Plasma was separated by low speed
centrifugation of blood at 4
C. VLDL was separated by
ultracentrifugation of plasma according to the Lipid
Research Clinics' protocol (Lipid Research Clinics' Pro-
gram, 1974). HDL cholesterol was measured in the super-
natant after precipitation of apoB-containing lipoproteins
with phosphotungstate and magnesium ions (Assman et al,
1983). Cholesterol (coef®cient of variation 1.6%) and
triglycerides were measured in plasma and plasma frac-
tions using commercial enzymatic kits (Boehringer Man-
nheim, Germany). Plasma apoA±I, and B were measured
by immunoturbidimetry using commercial kits (Boehrin-
ger Mannheim, Germany) and apoA±II was measured by a
modi®cation of a published method (Siedel et al, 1988).
Plasma lathosterol levels were measured by gas±liquid
chromatography as described previously (Sutherland et
al, 1991) and values were also expressed as mmol/mmol
plasma cholesterol to correct for varying numbers of
lipoprotein acceptor particles for the sterol in plasma.
The coef®cient of variation for the lathosterol measure-
ment was typically 4%. Plasma samples for lathosterol
measurement were stored at 780
C until the end of the
study and all samples from an individual were measured
on the same day. Plasma triglyceride fatty acid composi-
tion was also measured by gas±liquid chromatography
(Cox et al, 1995).
Analyses were carried out on values from the four week
points in the diet periods. Data from the three diet periods
were compared by ANOVA and when a signi®cant effect
of diet was detected paired t-tests were used to compare
values between pairs of diets. Two-tailed tests of signi®-
cance were used and a P value of less than 0.05 was
considered to be statistically signi®cant.
Forty-one subjects completed the study and four subjects
did not have plasma lathosterol levels measured for tech-
nical reasons and their data were excluded from the present
report. Body weight (mean s.d.) did not change signi®-
cantly during the study (baseline: 91.7 15.2 kg; 4-week
values: butter: 92.5 16.1 kg; coconut: 92.6 16.4 kg, saf-
¯ower: 92.2 16.2 kg).
Table 2 shows plasma lathosterol/cholesterol ratio in
subjects during the dietary intervention periods. In the total
study group, the ratio was signi®cantly different among the
diet periods and was signi®cantly lower during diets rich in
coconut fat and saf¯ower oil compared with diets rich in
butter. Similarly, mean ( s.d.) plasma lathosterol concen-
tration was signi®cantly (P 0.0006, repeated measures
ANOVA) different among the diet periods (butter:
6.86 2.72 mmol/l; coconut: 5.83 1.86 mmol/l; saf¯ower
oil: 5.62 2.38 mmol/l).
Plasma levels of LDL cholesterol and apoB were sig-
ni®cantly lower and plasma triglyceride concentration was
lower at a marginal level of signi®cance at four weeks
during the coconut diet compared with the butter diet.
Plasma cholesterol, LDL cholesterol, HDL cholesterol,
apoA±I and apoB were signi®cantly lower during the saf-
¯ower diet compared with both the butter diet and the
coconut diet. These results are summarised in Table 3.
Plasma cholesterol and triglycerides levels did not change
signi®cantly between weeks four and six in the study. The
pattern of plasma lipid, lipoprotein and apolipoprotein
levels was similar in men and women during the diets.
Age was not correlated signi®cantly with plasma choles-
terol (r 0.231) and log ratio plasma lathosterol/choles-
terol (r 0.173) at baseline and during the study.
Plasma triglyceride lauric acid content was signi®cantly
(P < 0.05) higher during the coconut diet and the content of
linoleic acid was signi®cantly higher during the saf¯ower
diet compared with other diets. Plasma triglyceride content
of myristic acid and palmitic acid were not signi®cantly
different between the diet periods. These results are sum-
marised in Table 4.
In an earlier randomised study in moderately hypercholes-
terolemic subjects we reported that plasma cholesterol and
LDL cholesterol levels were lower during diets rich in
coconut fat and were lower still during diets rich in saf-
¯ower oil compared with diets rich in butter (Cox et al,
1995). The present data con®rm these ®ndings for plasma
LDL cholesterol in healthy subjects. Plasma cholesterol
levels were not clearly lower in spite of reduced LDL
cholesterol levels because levels of plasma HDL choles-
terol and VLDL cholesterol tended to increase when coco-
nut fat replaced butter in the diet. We also report that
plasma lathosterol and the ratio plasma lathosterol/
Table 2 Plasma lathosterol to cholesterol ratio on subjects during butter,
coconut, and saf¯ower oil diets
All subjects Men Women
n 37 n 21 n 16
Diet mmol/mmol cholesterol
Butter 1.24 (0.24)
1.22 (0.49) 1.27 (0.39)
Coconut 1.09 (0.34)
1.04 (0.39) 1.11 (0.36)
Saf¯ower 1.14 (0.49)
1.11 (0.57) 1.19 (0.41)
0.04 0.08 0.56
Values are mean (s.d.).
Values with different superscripts are signi®cantly different by paired
t-test (P < 0.05).
Repeated measures analysis of variances on log-transformed data.
Table 3 Plasma lipids, lipoproteins and apolipoproteins in the subjects
during butter, coconut and saf¯ower diets
Butter Coconut Saf¯ower P
TC (mmol/l) 5.61 (0.96)
VLDL-C (mmol/l) 0.34 (0.18) 0.41 (0.36) 0.45 (0.45) 0.31
LDL-C (mmol/l) 4.08 (0.89)
HDL-C (mmol/l) 1.16 (0.24)
TG (mmol/l) 1.86 (0.89) 1.61 (0.93) 1.77 (1.25) 0.18
ApoA±I (g/l) 1.23 (0.18)
ApoA±II (g/l) 0.34 (0.08) 0.35 (0.08) 0.35 (0.08) 0.31
ApoB (g/l) 1.00 (0.22)
Values are mean (s.d.).
Abbreviations: TC, total cholesterol; VLDL-C, very low density
lipoprotein cholesterol; LDL-C, low density lipoprotein; HDL-C, high
density lipoprotein; TG, triglycerides; Apo, apolipoprotein.
Values in the same row with different superscripts are signi®cantly
different by paired t-test (P < 0.01).
Dietary fat type and lathosterol levels
cholesterol were lower which may indicate lower choles-
terol synthesis during diets in coconut fat and saf¯ower oil
compared with diets rich in butter.
Since this study was conducted in free-living individuals
reduced compliance with experimental diet regimen could
have potentially in¯uenced results. Participants were given
detailed dietary advice and supplies of the test fats and
special breads baked using these fats. Furthermore, they
were contacted frequently to reinforce dietary instructions.
Plasma triglyceride fatty acid composition which showed
highest levels of lauric acid during the coconut diet, highest
levels of linoleic acid during the saf¯ower oil diet and a
trend toward highest levels of stearic acid during the butter
diet suggests that on average subjects complied satisfacto-
rily with dietary instructions.
Glatz & Katan (1993) have reported a higher ratio
plasma lathosterol/cholesterol and a higher rate of whole
body cholesterol synthesis in subjects consuming diets rich
in saturated fat compared with polyunsaturated fats. Our
data in the present study and in an earlier study (Cox et al,
1996) are in accord with this ®nding. Also, the magnitude
of the differences in the ratio plasma lathosterol/cholesterol
(0.10 mol/mol) and mean plasma cholesterol concentration
(0.52 mmol/l) between the butter diet and the diet rich in
saf¯ower oil are approximately in proportion to the corre-
sponding differences (ratio plasma lathosterol/cholesterol,
0.21 mol/mol; mean plasma cholesterol, 0.93 mmol/l)
reported between SAFA and PUFA diets (Glatz & Katan,
1993). These ®ndings suggest that the average magnitude
of the decrease in cholesterol synthesis may predict the
average magnitude of the decrease in plasma cholesterol
levels when PUFA replaces SAFA in the diet.
It has been postulated previously that the higher rate of
cholesterol synthesis during diets rich in SAFA may be due
to increased synthesis and secretion of VLDL from the liver
(Glatz & Katan, 1993). Synthesis of VLDL is a major drain
on the hepatic cholesterol pool (Shepherd & Packard, 1988)
and apparently activates cholesterol synthesis to maintain a
suf®cient supply of the sterol for lipoprotein synthesis (Goh
& Heimberg, 1979). A close correlation between choles-
terol synthesis rates and VLDL-apoB secretion in normo-
lipidaemic subjects (Watts et al, 1995) is in line with a link
between VLDL production and cholesterol synthesis.
In the present study, the lower ratio plasma lathosterol/
cholesterol suggests that cholesterol synthesis is reduced
during diets rich in coconut fat compared with those rich in
butter. The mechanism underlying a lower rate of choles-
terol synthesis in response to dietary coconut fat is unre-
solved by our data. Conceivably, synthesis and secretion of
VLDL may be decreased which could lead to reduced
requirement for hepatic cholesterol and in turn decreased
cholesterol synthesis. In rhesus monkeys, the production
rate of VLDL-apoB was 3-fold lower in animals fed a diet
rich in coconut fat compared with those fed a diet rich in
palmitic acid in the form of palm oil ((Khosla & Hayes,
1991). However, the effect of a diet rich in coconut fat on
VLDL secretion in humans has not been reported.
On the other hand, it is possible that a lower rate of
cholesterol synthesis during diets rich in coconut fat may
reduce hepatic secretion of VLDL-apoB rather than the
reverse. There is evidence that cholesterol synthesis may be
an important determinant of VLDL-apoB production. The
correlation between cholesterol synthesis and VLDL-apoB
secretion reported previously may indicate that cholesterol
synthesis is a determinant of VLDL production (Watts et
al, 1995). Also, Arad and coworkers (1992) have reported
that inhibition of HMG CoA reductase activity, the rate-
limiting step in cholesterol biosynthesis, by lovastatin
treatment appears to reduce the assembly and secretion of
VLDL in subjects with hyperlipidemia. Lastly, rates of
cholesteryl ester synthesis and apoB secretion are closely
coupled in cultured HepG2 cells incubated with fatty acids
(Cian¯one et al, 1990).
It is unlikely that lathosterol in the diet in¯uenced
appreciably the differences in plasma lathosterol and the
ratio lathosterol/cholesterol during this study. Eggs, which
appear to be the main source of lathosterol in the diet
(Duane, 1995), were added to the diets rich in coconut fat
and saf¯ower oil during which plasma lathosterol levels
and the ratio lathosterol/cholesterol were lower compared
with the butter diets. Furthermore, cholesterol (egg) intake
was maintained low and in a range which probably has
little in¯uence on plasma lathosterol levels.
Since LDL is derived from the intravascular hydrolysis of
VLDL, any decrease in VLDL±apoB secretion could, in
theory, contribute to the lower plasma LDL cholesterol
levels during diets rich in cocount fat compared with diets
rich in butter. However, Watts and coworkers have reported
that plasma LDL cholesterol concentration and VLDL±apoB
secretion rates in normolipidemic men are not correlated
(Watts et al, 1995) which suggests that VLDL±apoB secre-
tion rate may not be a major determinant of plasma LDL
cholesterol levels in man. An increase in LDL receptor
number is probably an important mechanism by which
reduction of dietary saturated fat reduces plasma LDL
cholesterol levels (Mustad et al, 1997). While hepatic LDL
receptor activity (and plasma cholesterol levels) is similar in
hamsters fed diets rich in lauric acid or palmitic acid
(Woollett et al, 1992), the effect of substituting butter with
coconut fat in the diet on LDL receptor numbers in man has
not been determined. Reduced intake of SAFA may lead to
higher numbers of LDL receptors (Mustad et al, 1997) which
may contribute substantially to lower plasma cholesterol and
LDL cholesterol levels during diets rich in saf¯ower oil
compared with those rich in coconut fat (and butter) in the
present study. However, the ratio plasma lathosterol/choles-
terol was similar during these diets which suggests that the
decrease in plasma cholesterol levels when dietary saf¯ower
oil replaced coconut fat is not linked to cholesterol synthesis
or associated metabolic pathways.
Table 4 Plasma triglyceride fatty acid composition in subjects during
butter, coconut and saf¯ower diets
Fatty acid Butter Coconut Saf¯ower
(mol%) (n 18) (n 18) (n 18)
C12:0 0.29 (0.36)
C14:0 3.18 (1.12) 2.95 (0.78) 2.74 (0.85)
C14:1 0.21 (0.18) 0.52 (0.87) 0.32 (0.37)
C16:0 29.95 (2.89) 29.20 (2.87) 29.90 (3.26)
C16:1 4.77 (0.87) 5.35 (0.85)
C18:0 6.34 (1.40) 5.30 (1.32) 5.67 (2.47)
C18:1 n-9 42.21 (4.34)
C18:2 n-6 7.46 (3.14)
C18:3 n-6 0.11 (0.10)
C18:3 n-3 0.08 (0.14)
C20:4 n-6 0.18 (0.09)
C22:6 n-3 0.27 (0.42) 0.15 (0.23) 0.34 (0.30)
Values are mean (s.d.).
Values in the same row with different superscripts are signi®cantly
different by paired t-test (P < 0.05).
Dietary fat type and lathosterol levels
There are limitations to the present ®ndings. Subjects
were not randomized into diet groups and a sequential
study design was used. Therefore, it could be argued that
order of the diets and changes with time including regres-
sion to the mean could affect the results. However, it is
unlikely that these factors were in¯uential because similar
changes in plasma lipids, lipoproteins and apolipoproteins
were recorded in our previous study in subjects who
consumed diets rich in coconut fat, butter and saf¯ower
oil in a randomised cross-over design (Cox et al, 1995). In
the present study, the switch from diets rich in butter to
coconut fat diets (the main comparison) without a washout
period would tend to minimize the effects of this change in
dietary fat on measured variables.
Our data suggest that cholesterol synthesis is reduced
leading to lower plasma lathosterol levels when butter is
replaced by coconut fat in the diet. The mechanism under-
lying this change and its relationship to changes in lipo-
protein metabolism when the composition of dietary fat is
altered remains to be determined.
AcknowledgementsÐThe authors greatly appreciate the cooperation of
participants in the study and the excellent technical and research assistance
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