Content uploaded by Mario John Soares
Author content
All content in this area was uploaded by Mario John Soares
Content may be subject to copyright.
Substitution of saturated with monounsaturated fat in a 4-week
diet affects body weight and composition of overweight and
obese men
L. S. Piers
1
*, Karen Z. Walker
2
, Rachel M. Stoney
3
, Mario J. Soares
4
and Kerin O’Dea
1
1
Menzies School of Health Research, Casuarina, Northern Territory, Australia
2
Nutrition and Dietetics, Department of Medicine, Monash University, Monash Medical Centre, Clayton, Victoria,
Australia
3
The Nutrition Department, The Alfred Hospital, Prahran, Victoria, Australia
4
Department of Nutrition, Dietetics and Food Science, Curtin University of Technology, School of Public Health,
Perth, Western Australia, Australia
(Received 1 August 2002 – Revised 11 April 2003 – Accepted 29 May 2003)
A randomised crossover study of eight overweight or obese men (aged 24 –49 years, BMI 25·5–31·3 kg/m
2
), who followed two diets for 4
weeks each, was performed to determine whether substitution of saturated fat with monounsaturated fat affects body weight and compo-
sition. Subjects were provided with all food and beverages as modules (selected ad libitum) of constant macronutrient composition, but
differing energy content. The % total energy from saturated fat, monounsaturated fat and polyunsaturated fat was 24, 13 and 3 % respect-
ively on the saturated fatty acid (SFA)-rich diet and 11, 22 and 7 % respectively on the monounsaturated fatty acid (MUFA)-rich diet.
MUFA accounted for about 80 % of the unsaturated fats consumed on both diets. Body composition, blood pressure, energy expenditure
(resting and postprandial metabolic rates, substrate oxidation rate, physical activity), serum lipids, the fatty acid profile of serum choles-
teryl esters and plasma glucose and insulin concentrations were measured before and after each diet period. Significant (P# 0·05) differ-
ences in total cholesterol and the fatty acid composition of serum cholesteryl esters provided evidence of dietary adherence. The men had a
lower weight (2 2·1 (
SE 0·4) kg, P¼ 0·0015) and fat mass (22·6 (SE 0·6) kg, P¼0·0034) at the end of the MUFA-rich diet as compared
with values at the end of the SFA-rich diet. No significant differences were detected in energy or fat intake, energy expenditure, substrate
oxidation rates or self-reported physical activity. Substituting dietary saturated with unsaturated fat, predominantly MUFA, can induce a
small but significant loss of body weight and fat mass without a significant change in total energy or fat intake.
Obesity: Dietary fat: Weight loss: Body composition: Energy expenditure
Despite their established health benefits, diets with a high
monounsaturated fatty acid (MUFA) content are often not
promoted due to concerns that their relatively high dietary
total fat content might promote obesity (Garg, 1994; deLor-
geril & Salen, 2000), as fat per se not only forms highly
palatable and energy-rich foods (Blundell & MacDiarmid,
1997), but is also efficiently stored in the body (Stubbs,
1998). Although population and intervention studies have
suggested the importance of high-fat diets in the promotion
of obesity (Lissner & Heitmann, 1995), a consensus estab-
lishing the relationship between a high fat intake and obesity
has not yet been established (Bray & Popkin, 1998; Willet,
2002). Recent evidence implicates saturated fatty acids
(SFA), rather than the unsaturated fats, in the development
of obesity, due to the greater propensity for SFA to be stored
in adipose tissue rather than being oxidised (Storlien et al.
1998, 2001). Studies using indirect calorimetry in human
volunteers have indicated that polyunsaturated fatty acids
(PUFA) are better oxidised than SFA in both normal
weight (Jones & Schoeller, 1988) and obese men (Jones
et al. 1992). Fewer studies, however, examine the fate of
the nutritionally important MUFA. Jones et al. (1985),
using stable isotope-labelled fatty acids of similar chain
length, demonstrated that monounsaturated oleic acid
(18 : 1) is more readily oxidised than saturated stearic acid
(18 : 0) or polyunsaturated linoleic acid (18 : 2) (stearic:lino-
leic:oleic oxidation ratio 1·0:4·5:14·0). We too have pre-
viously reported a greater postprandial fat oxidation rate
(P, 0·05) in fourteen men after consumption of a breakfast
meal rich in MUFA, as compared with a SFA-rich meal
(Piers et al. 2002). Together, these results indicate that the
predominance of certain fatty acids in a given dietary fat
* Corresponding author: Dr L. S. Piers, present address, Health Surveillance and Evaluation Section, Rural and Regional Health and Aged Care Services,
Department ofHuman Services, Level 18, 120 SpencerStreet, Melbourne, Victoria 3000, Australia,fax þ 613 9637 4763, email leonard.piers@dhs.vic.gov.au
Abbreviations: CE, cholesteryl ester; EE, energy expenditure; FM, fat mass; MUFA, monounsaturated fatty acid; PUFA, polyunsaturated fatty acid; SFA,
saturated fatty acid.
British Journal of Nutrition (2003), 90, 717–727 DOI: 10.1079/BJN2003948
q The Authors 2003
influences its in vivo partitioning between oxidation and
storage.
We, therefore, hypothesised that if a MUFA-rich diet
were compared with a SFA-rich diet, the higher rate of
fat oxidation on the MUFA-rich diet would result in
reduced energy intake and/or the loss of body fat mass
(FM). Reduced food intake would compensate for the
greater amount of energy liberated from ingested food
high in MUFA. Loss of FM would result if the rate of
fat deposition declined while the rate of endogenous fat
mobilisation remained stable. Furthermore, on a MUFA-
rich diet, an enlarged body fat store would no longer be
required to achieve high fat oxidation rates, as would be
the case when poorly oxidisable SFA was consumed
(Flatt, 1995).
To test these hypotheses, we invited all subjects from
our previous acute study (Piers et al. 2002) to participate
in a longer intervention study examining the influence of
the type of dietary fat on energy intake, body weight and
composition. Subjects were required to consume two
diets of constant macronutrient composition and with a
fat content reflecting that of an average western diet
(about 40 % total energy), but differing in fatty acid com-
position (one being rich in SFA and the other in MUFA) in
a randomised crossover study. Each diet was consumed for
4 weeks.
Subjects and methods
Subjects
Subjects for the present study were recruited from partici-
pants of our earlier acute study investigating fat oxidation
rates by indirect calorimetry (Piers et al. 2002). As the
results of the earlier study were not available at that
time, subjects were only told that we were interested in
seeing if the consumption of two special diets, for
4 weeks each, resulted in any change in fat oxidation
rates in the longer term. Subjects remained unaware that
a change in body weight or composition might be
expected. Eight of the fourteen volunteers agreed to partici-
pate in the intervention study and the remaining men
declined due to the time commitment required. The eight
male subjects (seven of European and one of South
Asian ancestry) were aged between 24 and 49 years and
were resident in Melbourne, Victoria, Australia. Inclusion
criteria were as in the previous study (Piers et al. 2002)
including: (1) absence of clinical signs or symptoms of
chronic disease; (2) weight stability (^ 2 kg for preceding
12 months); (3) not on medication affecting body compo-
sition; (4) BMI within the range 25–32 kg/m
2
; (5) resting
diastolic blood pressure , 90 mmHg.
Study design
Subjects consumed two high-fat diets (40 % energy) of
fixed macronutrient composition. The diets were designed
to differ only in the type of fat provided, one diet
predominantly containing MUFA and the other predomi-
nantly containing SFA. In order to determine whether
total energy intake varied with the type of dietary fat
consumed, each diet was administered in a modular
form; this kept the proportion of macronutrients constant
while permitting ad libitum energy intake. The order of
administration of the diets was randomly assigned and
there was no intervening washout period. Anthropometric
measurements, body composition and blood pressure
measurements were made initially and at the end of each
diet period. Resting and postprandial metabolic rate were
also measured in response to an isoenergetic test meal of
constant macronutrient composition. However, the type
of fat in the test meal reflected the type of fat that had
been predominantly consumed in the associated diet
period. Fasting and 2 h postprandial venous blood samples
were collected on these occasions. In addition, subjects
were required to maintain a self-reported physical
activity diary daily for the entire duration of the two diet
periods.
Diets
Sources of fat for the SFA-rich diet were milk, butter,
cream, cheese and fatty meat, while fat in the MUFA-
rich diet was provided from olive oil, nuts and avocados.
Each diet comprised forty modules, paired between diets
for similar energy, protein, carbohydrate, total fat and
fibre content, and with the exception of the fat source,
based on largely similar foods. Each diet contained ten
breakfast modules (0·7– 2·2 MJ), ten lunch modules
(0·9–4·1 MJ), ten dinner modules (3·1– 5·3 MJ) and ten
snack modules (1·0– 4·2 MJ). The forty modules provided
for the SFA-rich diet contained on average (% energy):
fat 40·3 (
SD 0·8), SFA 24·4 (SD 2·6), MUFA 12·5 (SD
1·5), carbohydrate 41·9 (SD 3·7). The forty modules pro-
vided for the MUFA-rich diet were designed to contain
on average (% energy): fat 40·1 (
SD 1·1), SFA 11·0 (SD
0·9), MUFA 22·3 (SD 1·7), carbohydrate 42·2 (SD 3·6).
An exception was two paired snack modules containing
wine or beer (% energy): alcohol 19·2, fat 40·7, carbo-
hydrate 27·2. The MUFA-rich diet modules provided
slightly more dietary fibre than the SFA-rich diet modules
(3·4 (
SD 1·8) v. 2·8 (SD 1·9) g/MJ respectively). Examples
of the modules are provided in Table 1. The macronutrient
composition of each module, and the module recipe can be
obtained by contacting the corresponding author (L. S. P.).
Each week, each subject chose freely from the module
menu and could consume their chosen modules in any
order and in any quantity, each day. Modules were
always provided in excess of intake requirements. Subjects
were instructed that once the consumption of a module was
started, the entire module had to be consumed. No food
other than that provided was allowed. All food was pre-
pared under the supervision of a research dietitian at
The Kingston Centre (Cheltenham, Victoria, Australia), a
hospital for geriatric patients with large food service
facilities. Modules were given to subjects mainly in a
ready-to-eat form. Some modules required reheating
or simple cooking. Detailed storage and preparation
instructions were provided for each module. Each subject
completed, on a daily basis, a record detailing all modules
consumed each day, over the four weeks of each diet.
L. S. Piers et al.718
Breakfast meals used for postprandial studies
The SFA-rich breakfast comprised 92 g natural Swiss
muesli (Uncle Toby’s; Wahgunyah, Victoria, Australia),
57 g cream (Bulla, Regal Cream Products; Colac, Victoria,
Australia) and 275 g skimmed milk (Australian Milk Mar-
keting; Abbotsford, Victoria, Australia). The MUFA-rich
breakfast consisted of 96 g muesli baked with 20 g extra
virgin olive oil (Bertolli; Preston, Victoria, Australia) and
served with 285 g skimmed milk. Both breakfast meals,
which have been used previously (Piers et al. 2002), pro-
vided 2·5 MJ energy: 15 % as protein, 43 % as fat and
42 % as carbohydrate. The fibre content of the SFA-rich
breakfast was 12·0 g, while that of the MUFA-rich break-
fast was 11·5 g. The SFA-rich breakfast contained 4·1 g
PUFA, 8·8 g MUFA and 16·1 g SFA, while the MUFA-
rich breakfast contained 5·6 g PUFA, 18·6 g MUFA and
4·9 g SFA, as determined from Australian food compo-
sition tables (NUTTAB95; English & Lewis, 1991).
Diet assessment questionnaire
At the end of each diet, subjects were given a questionnaire
regarding their assessment of diet quality. For each ques-
tion, they were asked to indicate their response by marking
a cross on an unmarked 100 mm line extending between
two extreme ratings (0, 100) and the length to the mark
was then measured with a ruler. The questions were:
(1) How do you rate this diet overall? (2) How did this
diet satisfy your hunger? (3) How do you describe the
taste of this diet? (4) How energetic did you feel while
on this diet?
Anthropometry
Standing height was measured using a wall-fixed stadi-
ometer and recorded to the nearest 1 mm. Body weight
was measured immediately after voiding and after an over-
night fast. Subjects wore light indoor clothing and no
shoes. The measurement was taken on a beam balance
and was recorded to the nearest 100 g. Waist and hip
circumferences were measured as described by Callaway
et al. (1988).
Body composition
Dual-energy X-ray absorptiometry whole-body scans were
performed as described by Piers et al. (2002). Total and
regional body composition was determined with Lunar
software (Lunar software version 1.3; Madison, WI,
USA) used in the extended research mode to provide
data on whole-body and regional (limbs and trunk) lean
tissue mass and FM (g).
Resting and postprandial metabolic rate
Resting and postprandial metabolic rate was measured by
indirect calorimetry using a Deltatrac II metabolic monitor
(Datex Instrumentarium Corp., Helsinki, Finland), an open-
circuit ventilated canopy measurement system. The
measurement was conducted under standardised conditions
using the same measurement protocol as employed in our
previous study (Piers et al. 2002).
Substrate oxidation rates
Whole-body substrate oxidation rates were calculated
using measures of O
2
consumption, CO
2
production, total
urinary N excretion and the equations of Ben-Porat et al.
(1983), with the assumption that N excretion was steady
over the duration of urine collection (Elia & Livesey,
1988; Livesey & Elia, 1988).
Blood pressure and pulse rate
Systolic and diastolic blood pressure and pulse rate were
measured before and after each diet period under standar-
dised conditions (after an overnight fast, in the post-
absorptive state, after having rested in the supine position
for at least 1 h) using a Dinamap portable adult vital
signs monitor (model 100; Critikon, Tampa, FL, USA).
Table 1. Examples of modules provided in the saturated fatty acid-rich and monounsaturated fatty acid-rich test diets
Module SFA-rich modules MUFA-rich modules
1 Natural muesli with creamy milk Toasted muesli with skimmed milk
2 Tomatoes on buttered toast Tomatoes fried in olive oil, toast
4 Poached egg, toast and butter, orange juice Egg fried in olive oil, toast, skimmed milk, orange juice
5 Cornflakes and creamy milk Cornflakes, cashews and skimmed milk
14 Muffins, butter and cottage cheese Muffins, high monounsaturated fat margarine, cottage cheese
15 Vegetable soup and toast with butter Soup made with vegetables fried in olive oil, toast
22 Rump steak stir-fried with celery and
butter, boiled rice
Rump steak stir-fried with celery, almonds
and olive oil, boiled rice
24 Fish cooked in butter, peas, carrots,
potato, oranges
Fish fried in olive oil, peas,
carrots, potato, oranges
27 Roast chicken with carrots and beans,
baked potato with butter and soured
cream, canned apricots with cream
Roast chicken with carrots and beans,
baked potato with high-monounsaturated fat margarine,
canned apricots
31 Cheesecake and ice cream, a glass
of creamy milk and a banana
Fruit cake, ice cream, almonds, and
a glass of skimmed milk
33 Chocolate biscuit with glass of creamy milk Ginger biscuit, almonds and a glass of skimmed milk
37 One glass of white wine, cheese and sultanas One glass of white wine, almonds and sultanas
SFA, saturated fatty acid; MUFA, monounsaturated fatty acid.
Type of dietary fat influences body composition 719
Physical activity assessment
All subjects were asked to maintain a daily physical
activity diary. The diary consisted of four 15 min blocks
for each hour of the day from 06.00 to 23.00 hours. It
was assumed that subjects slept between 23.00 and 06.00
hours, but they were asked to indicate their actual
waking and sleeping times when there was any deviation
from this pattern. Subjects were asked to write down the
nature of the activity predominantly performed during
each 15 min block. These activities were then coded
depending upon the type and intensity of activity. The
total number of 15 min blocks at each activity level was
determined. Energy expenditure (EE) at each level of
activity was obtained by multiplying the measured resting
metabolic rate (kJ per 15 min) by an activity factor
obtained from the literature (Food and Agriculture Organ-
ization/World Health Organization/United Nations Univer-
sity, 1985), appropriate for the type of activity being
performed, and by the number of 15 min blocks for
which the activity was performed during the day. EE
during sleep was assumed to be equal to resting metabolic
rate measured at the end of each diet period. The sum of
the EE associated with the levels of activity over 24 h
gave total EE (kJ/d). Physical activity levels were calcu-
lated by dividing the total EE (kJ/d) obtained from the
self-reported activity diaries by measured resting metabolic
rate (kJ/d).
Blood samples
Fasting and 2 h postprandial (following the standard break-
fast meal) blood samples (10 ml) were collected from all
subjects before and at the end of each diet period. The
samples were centrifuged at 2000 g for 15 min before
plasma was separated and stored at 2 708C. Plasma glu-
cose, insulin concentrations and the lipid profile were
measured in the fasting sample as described by Piers
et al. (2002).
Serum fatty acid analysis
Fatty acid analysis was carried out at the Child Nutrition
Research Centre, Flinders Medical Centre, South Australia,
Australia. Lipids were extracted from serum samples with
chloroform–methanol (Bligh & Dyer, 1959). Serum phos-
pholipids and cholesteryl esters (CE) were separated by
TLC and evaporated to dryness under N
2
. The samples
were methylated in H
2
SO
4
(10 ml/l methanol) at 708C for
3 h. When cooled, methyl esters were extracted into
n-heptane and transferred to vials containing anhydrous
Na
2
SO
4
as the dehydrating agent. Fatty acid methyl
esters were separated and quantified using a Hewlett-Pack-
ard 6890 GC (Hewlett-Packard, Palo Alto, CA, USA)
equipped with a 50 mm capillary column (internal diameter
0·33 mm) coated with BPX-70 (0·25 mm film thickness;
SGE Pty Ltd, Victoria, Australia). The injector temperature
was set at 2508C while the detector (flame ionisation) tem-
perature was 3008C. The oven temperature commenced at
1408C and was programmed to rise at 58C per min to
2208C. The carrier gas He was used at a velocity of
350 mm/s. Fatty acid methyl esters were identified based
on retention time relative to authentic lipid standards
(Nuchek Prep Inc., Elysian, MN, USA). Between-run vari-
ations of the same sample for major fatty acid peaks
(. 2 %) were , 1%.
Ethics
All subjects gave written informed consent to participate in
the study. The Standing Committee on Ethics in Research
on Humans, Monash University, approved the experimental
protocol.
Statistical analysis
Data were analysed using the STATA Statistical Software
(Release 7, College Station, TX, USA) statistical software
package. All results are presented as mean values and stan-
dard deviations unless otherwise stated. The outcome vari-
ables of interest were body weight and FM. The covariates
included energy intake, total fat intake, total EE associated
with physical activity and physical activity level. The
change in a variable of interest associated with a particular
diet and the difference between the changes in a variable of
interest between the two diet periods, in the same subject,
were obtained as follows:
change in variable ¼ measure after diet
2 measure before diet
and
difference in change ¼ change on SFA-rich diet
2 change on MUFA-rich diet:
Where no pre-intervention measures were made, measures
made at the end of each diet period were compared. Pear-
son correlation coefficients were computed to examine
relationships between variables of interest. The difference
between the changes in the variables of interest, or the
difference in variables at the end of each diet period,
were analysed using ANOVA for the 2 £ 2 crossover
study design. This is similar to repeated measures, except
that the treatment factor (effects of the two diets in ques-
tion) was assigned across the time periods. Each subject
received both treatments in a particular sequence (sequence
in which the diets were administered: SF-rich diet !
MUFA-rich diet ¼ 1, MUFA-rich diet ! SFA-rich
diet ¼ 2). Within each subject, a period effect (the tem-
poral order in which the diets were administered to each
individual in each sequence) was also assessed. It was
not possible to separate the sequence effect from any
carry-over effect, as only two time periods were considered
(Yandell, 1997). A significant (P# 0·05) sequence effect
indicates that caution is required in interpreting treatment
effects. When this occurred, we went on to compare the
effects by treatment differences between diets in the first
study period only, using an unpaired t test as has been rec-
ommended (Yandell, 1997). A paired t test was used to
L. S. Piers et al.720
compare paired data within individuals. Regression analy-
sis with robust variance estimates (Stata Reference
Manual: Version 7, 2001; STATA Corporation) was used
to test for any treatment, sequence and period effects,
after adjusting for confounding factors.
Results
Dietary intake
Dietary intake data for the two diet periods are presented in
Table 2. On the SFA-rich diet, men consumed 24 % energy
as SFA, 3 % energy as PUFA and 13 % energy as MUFA,
whereas on the MUFA-rich diet the men consumed 11 %
energy as SFA, 6 % energy as PUFA and 23 % energy as
MUFA. Proportionately, MUFA accounted for approxi-
mately 80 % of the unsaturated fatty acids consumed on
both diets. Although subjects had been asked to eat the
dietary modules ad libitum, results indicated no significant
differences between the SFA- and MUFA-rich diets in total
energy (P¼ 0·16), fat (P¼ 0·17) or carbohydrate (P¼ 0·37)
intake (ANOVA). However, in the case of total energy
and total fat intake, a significant sequence effect was
apparent (P¼ 0·05 and P¼ 0·04 respectively). Conse-
quently, differences in these variables were examined for
the first diet period alone, a procedure recommended
when a significant sequence effect is detected (Yandell,
1997). This analysis (using an unpaired t test) showed
that during the first diet period, those individuals following
an SFA-rich diet had consumed significantly more (14·3
(
SD 2·3) MJ/d, n 4) energy than those individuals following
the MUFA-rich diet (10·6 (
SD 0·5) MJ/d, n 4; P, 0·05). The
best explanation for this difference would appear to be the
greater amount of heavy physical activity by the four indi-
viduals receiving the SFA-rich diet in the first diet period
(214 (
SD 250) kJ/d) compared with those on the MUFA-
rich diet (20 (
SD 40) kJ/d; P¼ 0·22, trend only), a
‘between-subject’ rather than ‘within-subject’ difference.
A significant correlation was also evident between physical
activity level and total energy intake in those on the SFA-
rich diet (n 4, r 0·99, P¼ 0·002), but not in those on the
MUFA-rich diet (P¼ 0·10).
In accordance with the study design, there were statisti-
cally significant differences in the consumption of different
types of fat, intakes of SFA were substantially greater
(P, 0·00005), and MUFA (P, 0·00005) and PUFA
(P¼ 0·0002) intakes substantially less, on the SFA-rich
diet. However, once again a significant sequence
effect (P¼ 0·04) was evident in the ANOVA of SFA
intake. Subsequent regression analysis of SFA intakes,
with physical activity level as a covariate, showed a differ-
ence in SFA intakes between diets (P, 0·0005); however,
the sequence effect was no longer significant (P¼ 0·07).
Although subjects consumed less dietary fibre on the
SFA-rich diet (P¼ 0·02), once again there was a significant
sequence effect (P¼ 0·003). An independent t test of the
fibre intake during the first dietary period showed that sub-
jects (n 4) on the SFA-rich diet consumed a significantly
greater amount of fibre (42·3 (
SD 1·8) g/d) compared with
subjects (n 4) on the MUFA-rich diet (34·5 (
SD 1·6) g/d;
P¼ 0·02). There was no significant difference between
diets in alcohol intake (P¼ 0·55).
Table 2. Dietary intakes during the two diet periods*
(Mean values and standard deviations for eight subjects)
SFA-rich diet MUFA-rich diet Difference between diets
Statistical significance of effect: P
Variables Mean
SD % Energy Mean SD % Energy SFA2 MUFA 95 % CI
Energy (kJ/d) 12565 2475 11897 2319 668 2 325, 1660 0·16
Total fat (g/d) 137 27 40 130 26 40 7 2 4, 18 0·17
Saturated fat (g/d) 83 16 24 36 7 11 48 2 41, 54 , 0·00005†
Monounsaturated fat (g/d) 43 9 13 73 14 23 2 30 2 36, 2 23 , 0·00005†
Polyunsaturated fat (g/d) 11 3 3 21 6 6 2 10 2 13, 2 7 0·0002†
Carbohydrate (g/d) 318 53 306 53 12 218, 43 0·37
Fibre (g/d) 36 8 40 8 2 5 2 8, 2 1 0·016†
Alcohol (g/d) 11 12 12 15 2 1 2 6, 4 0·55
SFA, saturated fatty acid; MUFA, monounsaturated fatty acid.
* For details of subjects, diets and procedures, see Table 1 and p. 718.
† Values were significantly different using an ANOVA for a 2 £ 2 crossover study design, from intake during SFA-rich diet period.
Type of dietary fat influences body composition 721
Diet ratings
Subjects indicated (scale 0 – 100) that they felt more physi-
cally energetic on the MUFA-rich diet (81 (
SD 18)) than on
the SFA-rich diet (55 (
SD 24)), a difference that was stat-
istically significant (ANOVA, P¼ 0·01). They also tended
to prefer the MUFA-rich diet (78 (
SD 12)) to the SFA-
rich diet (60 (
SD 29)), although this difference fell short
of statistical significance (P¼ 0·09). Otherwise, subjects
found the two diets comparable in terms of satiety (SFA-
rich diet 80 (
SD 21) v. MUFA-rich diet 89 (SD 15);
P¼ 0·32) and taste (SFA-rich diet 66 (
SD 23) v. MUFA-
rich diet 69 (
SD 17); P¼ 0·80).
Anthropometry and body composition
All subjects had a BMI . 25 kg/m
2
. Six of the eight sub-
jects had waist circumferences . 0·99 m. Although there
was no significant difference in the change in waist circum-
ference (P¼ 0·15) or change in hip circumference
(P¼ 0·73) during the two diet periods, the difference in
the change in waist:hip ratio (0·03) was of borderline stat-
istical significance (P¼ 0·05, Table 3).
Body weight and composition, and the absolute change
on the two diets, are presented in Table 3. ANOVA
showed significantly higher body weight after the SFA-
than the MUFA-rich diet (P¼ 0·0015). FM (P¼ 0·0037),
% body fat (P¼ 0·03), trunk FM (P¼ 0·01) and limb FM
(P¼ 0·03) (Fig. 1) were also significantly greater after the
SFA-rich diet. However, a significant sequence effect
(P¼ 0·03) was evident in the ANOVA of the change in
limb FM. Once again, an unpaired t test of the difference
in the change in limb FM in the first dietary period only
was carried out (Yandell, 1997). The change was signifi-
cantly greater in the subjects on the SFA-rich diet (0·7
(
SD 0·6) kg, n 4) compared with those on the MUFA-rich
diet (2 0·9 (
SD 0·5) kg, n 4; P¼ 0·005). No significant
difference was found in the change in lean tissue mass
(P¼ 0·20) (Fig. 1). FM measured at the end of the SFA-rich
diet was found to remain significantly greater than that
measured at the end of the MUFA-rich diet after adjusting
for energy intake (2·7 (robust
SE 0·7) kg, P¼ 0·007), total
fat intake (2·7 (robust
SE 0·7) kg, P¼ 0·007), fibre intake
(2·3 (robust
SE 0·8) kg, P¼ 0·022), self-reported total EE
(2·7 (robust
SE 0·6) kg, P¼ 0·004) or physical activity
level (2·7 (robust
SE 0·6) kg, P¼ 0·004).
Energy expenditure
No significant differences (ANOVA, P. 0·05) between
diets were evident in the change in resting metabolic rate
(P¼ 0·93) or change in diet-induced thermogenesis
expressed in absolute terms (P¼ 0·54), as % energy content
in the meal (P¼ 0·55) or as change in post-meal total
energy output (P¼ 0·44).
Total urinary nitrogen excretion and substrate oxidation
rates
There were no significant differences on ANOVA of the
change in total urinary N excretion (P¼ 0·80), protein
oxidation rate (P¼ 0·80), fasting fat oxidation rate
(P¼ 0·98), postprandial fat oxidation rate (P¼ 0·98), fasting
carbohydrate oxidation rate (P¼ 0·97) or postprandial
carbohydrate oxidation rate (P¼ 0·57) between the two
diet periods (Fig. 2). The change in FM was not signifi-
cantly correlated with postprandial fat oxidation rates on
either the MUFA-rich (r 2 0·25, P¼ 0·56) or SFA-rich
(r 0·17, P¼ 0·70) diets. However, it tended to be inversely
correlated with postprandial carbohydrate oxidation rates
on the MUFA-rich (r 2 0·65, P¼ 0·08), but not on the
SFA-rich (r 0·20, P¼ 0·64) diet.
Blood pressure and pulse rates
Table 3 shows the effect of diet on blood pressure and
pulse rate. The difference in change in diastolic blood
pressure (P¼ 0·08) and mean arterial pressure (7·1 (95 %
CI 2 0·1, 14·4) mmHg; P¼ 0·05) were of borderline signifi-
cance (ANOVA). No significant difference was found in
the change in systolic blood pressure (P¼ 0·13) or in
pulse rate (P¼ 0·92).
Lipid profile, glucose and insulin concentrations
Lipid profile, glucose and insulin concentrations, fatty acid
composition of serum CE are presented in Table 4.
There was a significantly greater change in total cholesterol
concentration on the SFA-rich as compared with the
MUFA-rich (P¼ 0·004) diet. However, the difference in
the change in LDL-cholesterol was just short of statistical
significance (1·1 mmol/l, P¼ 0·07). No significant differ-
ences were observed in the change in other lipid fractions,
or in fasting glucose or insulin concentrations.
Fatty acid profile in cholesteryl esters
The absolute changes in all classes of fat found in plasma
CE are presented in Table 4. Total SFA in CE (g/100 g
total fatty acids) was significantly greater on the SFA-rich
as compared with the MUFA-rich (P¼ 0·0003) diet. How-
ever, as a significant sequence effect was observed, an
unpaired t test was performed to compare the subjects on
the SFA-rich diet v. those on the MUFA-rich diet in the
first diet period only (Yandell, 1997). This indicated a sig-
nificantly (P¼ 0·02) greater change in percentage SFA in
CE had occurred in the four subjects on the SFA-rich diet
(2·5 (
SD 1·1) g/100 g total fatty acids) as compared with
the four subjects on the MUFA-rich diet (2 0·8 (
SD 0·8)
g/100 g total fatty acids). Total MUFA in CE (P¼ 0·04),
but not oleic acid (18 : 1n-9) content in CE (P¼ 0·61), was
greater on the SFA-rich diet. Total n-6 PUFA in CE was
lower on the SFA-rich diet (P¼ 0·0001), while total n-3
PUFA (P¼ 0·0008) was higher. However, ANOVA indi-
cated a significant (P, 0·05) sequence effect occurring
with both n-6 and n-3 PUFA content. Analysis of the
change in n-6 PUFA in CE on the two diets, with an inde-
pendent t test in the first study period, showed a decrease
in the subjects on the SFA-rich diet (2 6·1 (
SD 2·2) g/
100 g total fatty acids, n 4) and an increase in subjects on
the MUFA-rich diet (0·9 (
SD 1·1) g/100 g total fatty
acids, n 4). The change in total n-6 PUFA in CE was
L. S. Piers et al.722
Table 3. Changes in anthropometry, body composition as measured by dual energy X-ray absorptiometry, blood pressure and pulse rate on the two diets‡
(Mean values and standard deviations for eight subjects)
SFA-rich diet MUFA-rich diet
Before After Change Before After Change
Variable Mean
SD Mean SD Mean SD Mean SD Mean SD Mean SD
Waist circumference (m) 0·995 0·085 0·996 0·084 0·0001 0·024 1·022 0·068 0·992 0·075 2 0·030 0·045
Hip circumference (m) 1·036 0·062 1·020 0·066 2 0·015 0·019 1·045 0·053 1·035 0·063 2 0·010 0·039
Waist:hip ratio 0·97 0·06 0·98 0·07 0·01 0·03 0·98 0·05 0·96 0·04 2 0·02* 0·02
Weight (kg) 91·2 12·1 91·7 12·1 0·5 0·9 92·7 11·6 91·1 12·3 21·6* 1·1
FM (kg) 24·9 5·6 25·9 5·9 1·0 1·6 26·6 5·3 25·0 5·9 2 1·7* 0·8
Trunk FM (kg) 14·4 3·4 15·1 3·5 0·7 1·1 15·2 3·2 14·4 3·4 2 0·8* 0·4
Limb FM (kg) 9·3 2·5 9·6 2·6 0·3 0·8 10·2 2·4 9·5 2·8 2 0·7* 0·5
Body fat (%) 27·2 3·3 28·0 3·6 0·9 1·7 28·4 3·0 27·3 3·3 21·1* 0·7
Lean tissue mass (kg) 62·9 7·1 62·1 6·7 20·8 1·5 62·6 6·8 62·5 6·9 2 0·1 0·7
Systolic blood pressure (mmHg) 116·6 11·8 117·4 13·2 0·8 6·7 122·4 10·9 114·4 8·9 2 8·0 7·1
Diastolic blood pressure (mmHg) 69·5 9·3 70·8 8·8 1·3 5·0 73·9 7·4 69·3 6·9 2 4·6† 6·1
Mean arterial pressure (mmHg) 85·9 10·3 87·4 9·4 1·5 4·6 89·8 7·2 84·1 7·7 2 5·6* 5·6
Pulse rate (beats per min) 57·3 4·6 56·1 6·3 2 1·1 8·5 57·0 6·0 56·4 3·6 2 0·6 4·0
SFA, saturated fatty acid; MUFA, monounsaturated fatty acid; FM, fat mass.
Mean values were significantly different from those of the SFA-rich diet (2 £ 2 crossover study design, ANOVA; *P# 0·05).
Mean value had a trend towards a significant difference from that of the SFA-rich diet (2 £ 2 crossover study design, ANOVA; †P, 0·05).
‡ For details of subjects, diets and procedures, see p. 718.
Type of dietary fat influences body composition 723
predominantly due to a change in linoleic acid (18 : 2n-6)
(P¼ 0·001).
Physical activity
ANOVA of self-reported physical activity diaries indicated
no significant difference in total EE between diets (SFA-
rich diet 10·1 (95 % CI 9·2, 11·0) v. MUFA-rich diet 9·7
(95 % CI 8·9, 10·6) MJ/d; P¼ 0·40). There were no signifi-
cant differences in self-reported EE associated with sleep
(P¼ 0·71), sitting (P¼ 0·42) and light (P¼ 0·36), moderate
(P¼ 0·11) or heavy physical activity (P¼ 0·99)
(ANOVA). There was also no significant difference in
physical activity level between the two diet periods
(P¼ 0·80).
Discussion
Overall, subjects gained FM (1·0 (
SD 1·6) kg) during the
SFA-rich diet and lost FM (2 1·7 (
SD 0·8) kg) during the
MUFA-rich diet (Table 3). These changes in body compo-
sition were observed despite the absence of statistically
significant differences in total energy or fat intake during
the two diet periods (Table 2). The changes in lean tissue
mass in both diet periods were small and did not signifi-
cantly affect the resting metabolic rate. Men on the SFA-
rich diet gained FM predominantly on the trunk (0·7 (
SD
1·1) kg) rather than on the limbs (0·3 (SD 0·8) kg). In con-
trast, on the MUFA-rich diet, similar amounts of body fat
were lost both from the trunk (2 0·8 (
SD 0·4) kg) and from
the limbs (2 0·7 (
SD 0·5) kg) (Fig. 1), a finding that is in
accordance with our previous study (Walker et al. 1996).
The higher FM (þ 2·64 kg) at the end of the SFA-rich
diet as compared with the MUFA-rich diet, when
expressed as energy amounted to 82·8 MJ over 4 weeks,
calculated at 31·4 kJ/g fat (Berrino et al. 2001). Differences
in energy intake and physical activity data on the two diets
explain only part of this difference. We can attribute
46·5 MJ of this difference to a greater energy intake on
the SFA-rich diet (the upper limit of the 95 % CI in the
mean difference in energy intake: 1660 kJ/d for 4 weeks).
A further 14 MJ can be attributed to a subtle increase in
physical activity on the MUFA-rich diet (the difference
between upper limit of the 95 % CI of total EE reported
for the MUFA-rich diet and the mean total EE reported
for the SFA-rich diet: 10·6 v. 10·1 MJ/d for 4 weeks
respectively). There is some subjective evidence for this,
as questionnaires given to the subjects at the end of each
diet period indicated that subjects felt ‘more energetic’
on the MUFA-rich diet (P¼ 0·01), which is consistent
with one of our earlier studies (Walker et al. 1995). The
remaining difference can be explained on the basis of our
previous results (Piers et al. 2002), relating to differences
in fat oxidation rates between SFA-rich and MUFA-rich
meals. In that study, we proposed that an individual
whose energy intake was 10·0 MJ/d might oxidise an
extra 670 kJ/d by consuming MUFA rather than SFA.
In the current study, the observed mean energy intake on
the MUFA-rich diet was 11·9 MJ/d. Extrapolating, an
extra 797 kJ/d might be burnt on the MUFA-rich diet, or
22·3 MJ over 4 weeks, which is the energy difference
otherwise unaccounted for.
The observed changes in body weight and body fat were
accompanied by trends towards reduced waist:hip ratio and
blood pressure (diastolic and mean arterial pressure) on the
MUFA-rich diet (Table 4), indicative of physiological sig-
nificance. It is well established that weight gain or loss,
over as short a period as 1–2 months, is accompanied by
an associated change in blood pressure (McCarron &
Reusser, 1996). In addition, the waist:hip ratio is positively
and independently correlated with systolic arterial pressure
in male hypertensive patients (Raison et al. 1992).
Fig. 1. Effect of saturated fatty acid-rich (B) and monunsaturated
fatty acid-rich (A) diets on changes in body weight, fat mass (FM),
trunk FM, limb FM and lean tissue mass. Values are means with
standard deviations shown by vertical bars (n 8). For details of sub-
jects, diets and procedures, see Tables 1 and 2 and p. 718.
Fig. 2. Fat (A) and carbohydrate oxidation rates (B) measured in
the basal state and following breakfast meals that differed only in
the type of fat, one containing predominantly saturated fat and the
other monounsaturated fat. The measurements were made prior to
and at the end of two diet periods during which the macronutrient
composition of the diet was held constant, but the type of fat was
varied so that it was rich in saturated fatty acids (SFA) in one
diet period and monounsaturated fatty acids (MUFA) during the
other.–W –, Before SFA-rich diet; –D–, before the MUFA-rich diet;
–X – , after the SFA-rich diet; –O –, after the MUFA-rich diet.
Values are means with standard deviations shown by vertical bars
(n 8). For details of subjects, diets and procedures, see Tables 1
and 2 and p. 718.
L. S. Piers et al.724
Observed resting and postprandial substrate oxidation
rates at the end of the two diets did not differ from those
observed with the same test meal before the diets (Fig. 2).
The observed difference between SFA- and MFA-rich test
meals given at the end of the diets, however, appeared
smaller than observed previously (Piers et al. 2002). This
was not unexpected, as the enlarged fat store at the end
of the SFA-rich diet possibly promoted a chronic increase
in fat oxidation unrelated to the meal consumed (Flatt,
1995). This chronic increase in fat oxidation rate, in
response to a high fat intake, eventually permits a new pla-
teau of fat balance and energy balance to be achieved at a
higher body weight and FM; this is why body weight and
FM do not keep increasing linearly (Flatt, 1995). While
there is now considerable evidence in human subjects
that dietary fat type can influence fat oxidation rates
(Jones et al. 1985, 1992; Jones & Schoeller, 1988;
DeLany et al. 2000; Piers et al. 2002), until the present
study there has been no information on the impact this
may have on body weight and body composition. However,
animal studies indicate the potential differential impact of
different dietary fats on body composition in the longer
term (Matsuo et al. 1995; Takeuchi et al. 1995; Bell et al.
1997). Bell et al. (1997) compared MUFA-rich (rapeseed
oil) and SFA-rich (beef fat) diets (40·8 % energy from
fat) in mice. Animals fed the MUFA-rich diet deposited
significantly less body fat than mice fed the high-SFA
diet: entirely consistent with our present results in human
subjects.
Throughout our present study, foods and beverages were
supplied as modules of fixed macronutrient composition,
but differing energy content, as described by Stubbs et al.
(1995). This procedure was adopted to determine if subjects
would then consume more food on the SFA-rich diet. In fact,
taste and satiety responses to the two diets did not differ and
they allowed very similar total energy and total fat intake
(Table 2). Hence, change in the type of fat per se did not
appear to affect total fat consumption. The observed signifi-
cant sequence effect on fibre intake cannot be explained.
Although all modules were designed to have similar fibre
content, subject selection of individual modules resulted in
a difference of 5 g/d between diets in fibre intake (Table 2).
This difference, however, does not account for the differ-
ences in the change in FM, as this difference persisted
after statistical adjustment for fibre intake. There were
large differences between diets in the type of fat consumed.
The difference in SFA intake between diets was 48 g/d
(Table 2). These differences in fat intake were associated
with blood lipid changes that provide objective evidence
of dietary adherence (Table 4). On the SFA-rich diet, the
plasma SFA fraction of plasma CE was 4·9 % higher
(P¼ 0·001), while total n-6 PUFA was 10·3 % lower
(P¼ 0·0001). In particular, the proportion of linoleic acid
(18 : 2n-6), an essential fatty acid, fell markedly on the
SFA-rich diet and rose on the MUFA-rich diet, a difference
of 2 9·0 % (P¼ 0·001). The concentration of linoleic acid in
plasma CE is well known to be reflective of dietary linoleic
acid intake (Sinclair et al. 1987; Sanders et al. 1994;
Sarkkinen et al. 1994). The difference in the change in
oleic acid (18 : 1n-9) was not significant (P¼ 0·61), but
oleic acid is a non-essential fatty acid that can be synthesised
from carbohydrate and is a poor indicator of dietary oleic
acid intake (Sanders et al. 1994). Changes in the lipid profile
(Table 4) were also consistent with dietary change (Table 2),
with total and LDL-cholesterol rising on the SFA-rich diet
and falling on the MUFA-rich diet, in accordance with the
well established effects of SFA and MUFA (Hegsted et al.
1993). We did not include a washout period between the
two diet periods, because previous studies have indicated
that this is unnecessary when the dietary intervention
period is . 3 weeks (Bonanome & Grundy, 1988; Fuentes
et al. 2001).
There are several limitations in the present study. The
first is the small number of subjects who participated.
Table 4. Changes in serum lipids, fatty acid profile of cholesteryl esters and plasma glucose and insulin concentrations on the two diets
(Mean values and standard deviations for eight subjects)
SFA-rich diet MUFA-rich diet
Before After Change Before After Change
Mean
SD Mean SD Mean SD Mean SD Mean SD Mean SD
Serum lipids
Total cholesterol (mmol/l) 4·8 0·5 5·4 0·6 0·60 0·70 5·3 0·6 4·6 0·5 20·76* 0·56
Triacylglycerol (mmol/l) 1·6 1·2 1·8 1·4 20·18 1·13 1·4 0·5 1·6 0·7 0·19 0·65
LDL-cholesterol (mmol/l) 3·0 0·4 3·5 0·6 0·44 0·82 3·4 0·5 2·8 0·4 2 0·56† 0·43
HDL-cholesterol (mmol/) 1·0 0·3 1·0 0·1 0·01 0·22 1·1 0·1 1·0 0·2 2 0·09 0·17
Fasting glucose (mmol/l) 5·4 0·6 5·4 0·5 2 0·04 0·60 5·5 0·5 5·4 0·5 2 0·15 0·52
Fasting insulin (mU/ml) 7·7 3·3 7·9 4·0 0·20 3·68 8·6 3·9 7·9 3·8 2 0·66 2·44
Fatty acids in cholesteryl esters (g/100 g total fatty acids)
Total SFA 11·6 1·2 14·5 1·2 2·9 1·1 13·2 1·9 11·2 0·9 2 2·0* 1·9
Total MUFA 27·1 2·1 29·4 3·1 2·3 2·3 28·1 3·1 27·5 2·0 2 0·6* 2·2
Oleic acid (18 : 1 n-9) 22·8 1·9 23·3 1·5 0·5 2·1 22·5 1·8 23·6 1·6 1·1 1·9
Total n-6 PUFA 58·7 3·5 52·4 3·4 2 6·3 2·3 55·2 4·7 58·9 3·1 3·7* 3·6
Linoleic acid (18 : 2 n-6) 49·0 4·4 43·1 4·0 2 5·9 2·4 45·5 4·3 48·5 4·3 3·1* 3·2
Total n-3 PUFA 2·2 0·8 3·1 0·6 0·9 0·4 3·0 0·6 2·1 0·8 2 0·9* 0·4
SFA, saturated fatty acid; MUFA, monounsaturated fatty acid; PUFA, polyunsaturated fatty acid.
Mean values were significantly different from those of the SFA-rich diet (2 £ 2 crossover study design, ANOVA; *P# 0·05).
Mean value had a trend towards a significant difference from that of the SFA-rich diet (2 £ 2 crossover study design, ANOVA; †P¼ 0·07).
Type of dietary fat influences body composition 725
The results need confirmation in larger studies of a similar
design. Second, it is possible that subjects consciously
restricted their intake on the MUFA-rich diet, as they
were free-living and their meals were not supervised.
Subjects had no reason to do this, however, as they were
never told that the purpose of the study concerned changes
in body weight. Throughout the study, they were constantly
encouraged to eat to appetite and extra food modules were
always made available. From their expressed preference
for the MUFA-rich diet, we would possibly have expected
more overeating in this phase, rather than the SFA-rich
phase of the study. Third, it is possible that subjects were
more physically active during the MUFA-rich diet. There
was some subjective evidence for this from the question-
naire. Whether increased physical activity was the cause,
or consequence, of the loss of FM on the MUFA-rich
diet cannot be determined from the present study. Although
it remains possible theoretically that the observed differ-
ences are the result of a pure coincidence, this seems unli-
kely given that all subjects systematically gained weight
and FM on the SFA-rich diet and all subjects systemati-
cally lost weight and FM on the MUFA-rich diet.
The results of our current study are consistent with some
recent findings in other dietary studies. An ad libitum diet
low in animal fat and refined carbohydrates and rich in
low-glycaemic-index foods, MUFA, n-3 PUFA and
phyto-oestrogens favourably modified the hormonal profile
of postmenopausal women when compared with a high-
SFA control diet (Berrino et al. 2001). That MUFA-rich
diet also significantly decreased body weight (4·06 v.
0·54 kg in the control group), waist:hip ratio, total choles-
terol, fasting glucose level and area under the insulin
curve after an oral glucose tolerance test. In another
recent study (McManus et al. 2001), a moderate fat
(35 % energy), controlled energy, Mediterranean-style
diet rich in MUFA (15 – 20 % energy) has been shown to
be superior to a low-fat (20 % energy) high-carbohydrate
diet for weight reduction. In that study, there was superior
long-term participation and adherence with the MUFA-rich
diet and greater weight loss. Other studies comparing SFA-
rich to MUFA-rich diets, however, have not reported sig-
nificant differences in the magnitude of weight loss
(Mata et al. 1992; deLorgeril et al. 1999; Williams et al.
1999; Vessby et al. 2001). The mechanisms whereby
SFA become more readily diverted to adipose tissue sto-
rage and the effects this may then have on body metab-
olism and energy balance remain to be elucidated. The
peroxisome proliferator-activated receptors (a, d (or b)
and g), a subfamily of the nuclear receptor gene family,
have emerged recently as important physiological sensors
of lipid levels and may provide a molecular mechanism
whereby dietary fatty acids modulate lipid homeostasis.
In vitro studies show that unsaturated fatty acids (both
MUFA and/or PUFA) are more effective in stimulating
peroxisome proliferator-activated receptor a than SFA
(Kliewer et al. 1997; Halvorsen et al. 2001). Such results
suggest a plausible mechanism, among others, for our
present observations.
In conclusion, the results of our present study suggest
that the previously observed greater fat oxidation rate
following a MUFA-rich test meal, as compared with a
SFA-rich test meal, can result in a small but significant
reduction in body weight and FM in men whose dietary
SFA content is largely replaced with MUFA, within
4 weeks. This effect could possibly have been enhanced
by subtle, unconscious, increases in physical activity
and/or decreases in energy intake; however, there were
no detectable changes in basal or postprandial EE. This
is a novel result and it requires confirmation, perhaps
using a whole-body calorimeter to measure EE and
substrate oxidation rates in a larger number of subjects
over a longer period of time, possibly in conjunction
with the doubly-labelled water technique to measure
free-living EE.
Acknowledgements
This project was supported by a project grant (no.
981019) from the National Health and Medical Research
Council, Australia. We would like to thank the volun-
teers who participated in this study, without whose
cooperation none of this would be possible. We would
also like to thank: Ms Margaret Halley and Ms Cheryl
Greig for help with the preparation of the diets; Mr
David Hamilton-Smith and the Food Service Department,
The Kingston Centre, Cheltenham, Victoria, Australia,
for the donated provisions and food preparation facilities;
Ms Elaine Yeow for logistical support; Ms Connie
Karschimkus for processing the blood and urine samples;
Dr Boyd Strauss for use of the body composition facil-
ity; Mr Mark Neumann for the serum fatty acid ana-
lyses; Dr Zhiqiang Wang and Dr Bircan Erbas for
statistical advice.
References
Bell RR, Spencer MJ & Sherriff JL (1997) Voluntary exercise and
monounsaturated canola oil reduce fat gain in mice fed diets
high in fat. J Nutr 127, 2006– 2010.
Ben-Porat M, Sideman S & Bursztein S (1983) Energy metabolism
rate equation for fasting and postabsorptive subjects. Am J
Physiol 244, R764– R769.
Berrino F, Bellati C, Secreto G, et al. (2001) Reducing
bioavailable sex hormones through a comprehensive change in
diet: the diet and androgens (DIANA) randomized trial. Cancer
Epidemiol Biomarkers Prev 10, 25–33.
Bligh EG & Dyer WJ (1959) A rapid method of total lipid extraction
and purification. Can J Biochem Pharmacol 37, 911–917.
Blundell JE & MacDiarmid JI (1997) Fat as a risk factor for over-
consumption: satiation, satiety, and patterns of eating. JAm
Diet Assoc 97, S63 –S69.
Bonanome A & Grundy SM (1988) Effect of dietary stearic acid
on plasma cholesterol and lipoprotein levels. N Engl J Med
318, 1244 –1248.
Bray GA & Popkin BM (1998) Dietary fat intake does affect
obesity! Am J Clin Nutr 68, 1157– 1173.
Callaway CW, Chumlea WC, Bouchard C, et al. (1988) In Anthro-
pometric Standardisation Reference Manual, pp. 39 –54 [TG
Lohman, AF Roche and R Martorell, editors]. Champaign, IL:
Human Kinetics Books.
DeLany JP, Windhauser MM, Champagne CM & Bray GA
(2000) Differential oxidation of individual dietary fatty acids
in humans. Am J Clin Nutr 72, 905 –911.
L. S. Piers et al.726
deLorgeril M & Salen P (2000) Modified Cretan Mediterranean
diet in the prevention of coronary heart disease and cancer.
World Rev Nutr Diet 87, 1 –23.
deLorgeril M, Salen P, Martin JL, Monjaud I, Delaye J &
Mamelle N (1999) Mediterranean diet traditional risk factors,
and the rate of cardiovascular complications after myocardial
infarction: final report of the Lyon Diet Heart Study.
Circulation 99, 779– 785.
Elia M & Livesey G (1988) Theory and validity of indirect
calorimetry during net lipid synthesis. Am J Clin Nutr 47,
591– 607.
English R & Lewis J (1991) Nutritional Values of Australian
Foods. Canberra: Australian Government Printing Service.
Flatt JP (1995) Use and storage of carbohydrate and fat. Am J
Clin Nutr 61, 952S –959S.
Food and Agriculture Organization/World Health Organization/
United Nations University (1985) Energy and Protein Require-
ments: Report of a Joint FAO/WHO/UNU Expert Consultation.
Technical Report Series no. 724, Geneva: WHO.
Fuentes F, Sanchez E, Sanchez F, et al. (2001) Mediterranean and
low-fat diets improve endothelial function in hypercholestero-
lemic men. Ann Intern Med 134, 1115– 1119.
Garg A (1994) High-monounsaturated fat diet for diabetic
patients. Is it time to change the current dietary recommen-
dations? Diabetes Care 17, 242– 246.
Halvorsen B, Rustan AC, Madsen L, et al. (2001) Effects of long-
chain monounsaturated and n-3 fatty acids on fatty acid oxi-
dation and lipid composition in rats. Ann Nutr Metab 45,
30– 37.
Hegsted DM, Ausman LM, Johnson JA & Dallal GE (1993)
Dietary fat and serum lipids: an evaluation of the experimental
data. Am J Clin Nutr 57, 875– 883.
Jones PJ, Pencharz PB & Clandinin MT (1985) Whole body
oxidation of dietary fatty acids: implications for energy utiliz-
ation. Am J Clin Nutr 42, 769– 777.
Jones PJ, Ridgen JE, Phang PT & Birmingham CL (1992)
Influence of dietary fat polyunsaturated to saturated ratio on
energy substrate utilization in obesity. Metab Clin Exp 41,
396– 401.
Jones PJ & Schoeller DA (1988) Polyunsaturated:saturated ratio
of diet fat influences energy substrate utilization in the
human. Metab Clin Exp 37, 145 –151.
Kliewer SA, Sundseth SS, Jones SA, et al. (1997) Fatty
acids and eicosanoids regulate gene expression through direct
interactions with peroxisome proliferator-activated receptors
alpha and gamma. Proc Natl Acad Sci USA 94, 4318 –4323.
Lissner L & Heitmann BL (1995) Dietary fat and obesity:
evidence from epidemiology. Eur J Clin Nutr 49, 79– 90.
Livesey G & Elia M (1988) Estimation of energy expenditure, net
carbohydrate utilization, and net fat oxidation and synthesis by
indirect calorimetry: evaluation of errors with special reference
to the detailed composition of fuels. Am J Clin Nutr 47,
608– 628.
McCarron DA & Reusser ME (1996) Body weight and blood
pressure regulation. Am J Clin Nutr 63, 423S –425S.
McManus K, Antinoro L & Sacks F (2001) A randomized
controlled trial of a moderate-fat, low-energy diet compared
with a low fat, low-energy diet for weight loss in overweight
adults. Int J Obes Relat Metab Disord 25, 1503– 1511.
Mata P, Garrido JA, Ordovas JM, et al. (1992) Effect of dietary
monounsaturated fatty acids on plasma lipoproteins and
apolipoproteins in women. Am J Clin Nutr 56, 77– 83.
Matsuo T, Shimomura Y, Saitoh S, Tokuyama K, Takeuchi H &
Suzuki M (1995) Sympathetic activity is lower in rats fed a
beef tallow diet than in rats fed a safflower oil diet. Metab
Clin Exp 44, 934 –939.
Piers LS, Walker KZ, Stoney RM, Soares MJ & O’Dea K (2002)
The influence of the type of dietary fat on postprandial fat
oxidation rates: monounsaturated (olive oil) versus saturated
fat (cream). Int J Obes Relat Metab Disord 26, 814 –821.
Raison JM, Achimastos AM & Safar ME (1992) Sex-dependence
of body fat distribution in patients with obesity and hyperten-
sion. Clin Exper Hypertens 14A, 505 –525.
Sanders K, Johnson L, O’Dea K & Sinclair AJ (1994) The effect
of dietary fat level and quality on plasma lipoprotein lipids and
plasma fatty acids in normocholesterolemic subjects. Lipids 29,
129– 138.
Sarkkinen ES, Agren JJ, Ahola I, Ovaskainen ML & Uusitupa
MI (1994) Fatty acid composition of serum cholesterol
esters, and erythrocyte and platelet membranes as indicators
of long-term adherence to fat-modified diets. Am J Clin Nutr
59, 364 –370.
Sinclair AJ, O’Dea K, Dunstan G, Ireland PD & Niall M (1987)
Effects on plasma lipids and fatty acid composition of very low
fat diets enriched with fish or kangaroo meat. Lipids 22, 523 –529.
Storlien LH, Hulbert AJ & Else PL (1998) Polyunsaturated fatty
acids membrane function and metabolic diseases such as
diabetes and obesity. Curr Opin Clin Nutr Metab Care 1,
559– 563.
Storlien LH, Tapsell LC, Fraser A, et al. (2001) Insulin resistance.
Influence of diet and physical activity. World Review Nutr Diet
90, 26 –43.
Stubbs RJ (1998) Nutrition Society Medal Lecture. Appetite,
feeding behaviour and energy balance in human subjects.
Proc Nutr Soc 57, 341– 356.
Stubbs RJ, Harbron CG, Murgatroyd PR & Prentice AM (1995)
Covert manipulation of dietary fat and energy density: effect
on substrate flux and food intake in men eating ad libitum.
Am J Clin Nutr 62, 316 –329.
Takeuchi H, Matsuo T, Tokuyama K, Shimomura Y & Suzuki M
(1995) Diet-induced thermogenesis is lower in rats fed a lard
diet than in those fed a high oleic acid safflower oil diet, a
safflower oil diet or a linseed oil diet. J Nutr 125, 920 –925.
Vessby B, Unsitupa M, Hermansen K, et al. (2001) Substituting
dietary saturated for monounsaturated fat impairs insulin
sensitivity in healthy men and women: The KANWU Study.
Diabetologia 44, 312– 319.
Walker KZ, O’Dea K, Johnson L, et al. (1996) Body fat
distribution and non-insulin-dependent diabetes: comparison
of a fiber-rich, high-carbohydrate, low-fat (23 %) diet and a
35 % fat diet high in monounsaturated fat. Am J Clin Nutr 63,
254– 260.
Walker KZ, O’Dea K, Nicholson GC & Muir JG (1995) Dietary
composition, body weight, and NIDDM. Comparison of high-
fiber, high-carbohydrate, and modified-fat diets. Diabetes
Care 18, 401– 403.
Willet WC (2002) Dietary fat plays a major role in obesity: no.
Obes Rev 3, 59 –68.
Williams CM, Francis-Knapper JA, Webb D, et al. (1999)
Cholesterol reduction using manufactured foods high in mono-
unsaturated fatty acids: a randomized crossover study. Br J
Nutr 81, 439– 446.
Yandell BS (1997) Practical Data Analysis for Designed Exper-
iments. Boca Raton, FL: CRC Press.
Type of dietary fat influences body composition 727
