Applied nutritional investigation
Effects of olive oil and tomato lycopene combination on serum
lycopene, lipid profile, and lipid oxidation
Kiran D. K. Ahuja, M. BiomedSc., Jane K. Pittaway, B. BiomedSc.,
and Madeleine J. Ball, M.D.*
School of Human Life Sciences, University of Tasmania, Launceston, Tasmania, Australia
Manuscript received March 1, 2005; accepted July 20, 2005.
Abstract Objective: We compared the effect of two diets (a diet high in olive oil and a diet high in
carbohydrate and low in olive oil) with high lycopene content and other controlled carotenoids on
serum lycopene, lipids, and in vitro oxidation.
Methods: This was a randomized crossover dietary intervention study carried out in Launceston,
Tasmania, Australia in healthy free-living individuals. Twenty-one healthy subjects who were 22 to
70 y old were recruited by advertisements in newspapers and a university newsletter. A randomized
dietary intervention was done with two diets of 10 d each. One diet was high in olive oil and the
other was high in carbohydrate and low in olive oil; the two diets contained the same basic foods
and a controlled carotenoid content high in lycopene.
Results: Significant increases (P ? 0.001) in serum lycopene concentration on both diets were to
similar final concentrations. Higher serum high-density lipoprotein cholesterol (P ? 0.01), lower
ratio of total cholesterol to high-density lipoprotein (P ? 0.01), and lower triacylglycerols (P ?
0.05) occurred after the olive oil diet compared with the high-carbohydrate, low-fat diet. There was
no difference in total antioxidant status and susceptibility of serum lipids to oxidation.
Conclusions: Serum lycopene level changes with dietary lycopene intake irrespective of the
amount of fat intake. However, a diet high in olive oil and rich in lycopene may decrease the risk
of coronary heart disease by improving the serum lipid profile compared with a high-carbohydrate,
low-fat, lycopene-rich diet. © 2006 Elsevier Inc. All rights reserved.
Olive oil; Lycopene; Intervention diet; Carotenoids
Mediterranean diets are thought to protect against car-
diovascular disease and this effect has been credited to a
variety of foods such as fruits and vegetables, olive oil, and
red wine . The beneficial dietary components of some of
these foods include carotenoids in fruits and vegetables,
monounsaturated fat and polyphenolic compounds in olive
oil, and flavanoids in red wine [2,3]. Among the carot-
enoids, lycopene, present in tomatoes and tomato products,
probably has the highest antioxidant capacity .
Epidemiologic and case-control studies have suggested a
possible beneficial effect of high dietary intake and/or high
serum or tissue levels of lycopene because of a decreased
risk of cardiovascular diseases [5–9]. Population studies
have shown a positive association between reported intake
of lycopene-rich foods and plasma levels [10,11]. Interven-
tion studies have observed increased serum lycopene levels
with increased intake of tomatoes and tomato products, the
richest source of lycopene [12–14].
Lycopene availability from food may depend on several
factors. Season, heating, and processing of tomato products
may change the amount of bioavailable lycopene. Pro-
longed heat treatment (?2 h at 100°C) of tomatoes de-
creases the total carotenoid content and more so in peeled
than in unpeeled tomatoes . Single-meal studies have
This study was funded by the Clifford Craig Medical Research Trust,
Launceston, Tasmania, Australia.
Part of the data from this study was presented at the 27th Annual
Scientific Meeting of the Nutrition Society of Australia; Hobart, Australia;
* Corresponding author. Tel.: ?61-3-6324-5480; fax: ?61-3-6324-3658.
E-mail address: email@example.com (M.J. Ball).
Nutrition 22 (2006) 259–265
0899-9007/06/$ – see front matter © 2006 Elsevier Inc. All rights reserved.
shown higher serum levels of lycopene when tomatoes have
been consumed cooked rather than raw [16–18] and when
the tomatoes have been cooked with fat than without
[18,19], possibly because cooking or heating weakens the
bond between lycopene and the tissue matrix and facilitates
the passage of lycopene into a lipophilic phase, making it
more bioavailable . Cooking or processing has been
reported to transform all-trans-lycopene to cis-lycopene
[20,21], which is better absorbed, probably because cis-
isomers are more soluble in bile acid micelles, although
studies have suggested that lycopene is resistant to heat-
induced all-trans to cis conversion under conditions regu-
larly employed in the food industry or during food prepa-
Similarly, 3- and 5-d meal studies have suggested that
dietary fat influences plasma levels of lycopene when to-
matoes are consumed with olive oil rather than without oil
[23,24]. However, our previous 14-d study of a lycopene-
rich diet showed that a high monounsaturated fat-enriched
sunflower oil diet (36% of energy as total fat and 23.6% of
energy as monounsaturated fat) induced similar effects on
serum lycopene levels as a high-carbohydrate, low-fat diet
(15% of energy as total fat and 4.1% of energy as mono-
unsaturated fat) .
Studies have also compared the effect of carotenoid-
controlled fruit and vegetable intakes with high monounsat-
urated fat versus those with high-carbohydrate, low-fat in-
take on oxidation of isolated low-density lipoprotein (LDL)
cholesterol [26,27], a risk factor for coronary heart disease
(CHD) [28,29]. In one study the dietary carotenoid intake
was controlled and serum carotenoid levels were measured
to confirm similarity ; however, in another study ,
intakes of fruit and vegetables were controlled but serum
levels of carotenoids were not measured to ascertain
whether the lower susceptibility of LDL to oxidation on the
monounsaturated fat diet was due to differences in fat intake
or a combination of differences in fat intake and serum
carotenoid levels. Another study compared the effect of 7-d
consumption of tomato products with extra virgin olive oil
versus sunflower oil on antioxidant activity as measured by
ferric-reducing ability of plasma and found an increased
activity with olive oil .
Although extra virgin olive oil is the type most studied
with respect to CHD, this oil may not be the cooking oil
preferred by Australians because of its strong flavor and
cost. Extra virgin and virgin oils are ideal for Mediterranean
cooking and for salads; for other cooking styles and for
people without a Mediterranean background, refined or light
olive oil may be more palatable because of its milder flavor,
light texture, and lower cost. Refined olive oil constituted
73% of olive oil imports in 2000 to 2001 . However, it
will have fewer antioxidants because some of these com-
pounds are removed in refining.
To our knowledge, no study has examined the effect of
short-term intake (10 d) of a carotenoid-controlled lycopene-
enriched diet with high or low amounts of refined olive oil
on serum lycopene levels.
Materials and methods
Healthy non-smoking men and women who were 22 to
70 y old and had no history of heart disease were invited to
take part in the study by newspaper advertisements and a
university newsletter. Exclusion criteria included the use of
any medication that affects blood lipids or blood pressure,
use of vitamin and/or mineral supplements, pregnancy, or
The scientific ethics committee of the Launceston Gen-
eral Hospital (Tasmania, Australia) approved the study pro-
tocol, and informed written consent was obtained from each
Study and dietary design
Before starting the dietary interventions, participants
were asked to record 4-d (2 d of the week and 2 d of the
weekend) weighed food diet diaries, which were used to
calculate usual dietary intake using Food Works 2.10 with
Nuttab 95 and AusNut database (Xyris, Brisbane, Austra-
lia). The crossover study consisted of two 10-d treatment
periods in random order (assigned by number allocation).
Before starting the intervention diets, each participant was
assigned a number. A randomization sheet was obtained
(GraphPad Quickcal software, available at http://www.
graphpad.com) and participants were allotted to start on one
of the two diets: one high in olive oil (OO) and the other
high in carbohydrate and low in olive oil (LO). On com-
pletion of the first diet, participants were given a “washout”
period of 16 d and then they started the second diet. The
washout period of 16 d on the usual diet was given between
diets to ascertain that premenopausal women were in the
same phase of their menstrual cycles at the start of the two
dietary periods. For 2 d before starting each diet, partici-
pants were asked to take a low carotenoid, especially low
lycopene diet, to decrease the effects of acute intake of
carotenoids on blood tests .
Both diets were isocaloric to the usual diets of the
participants. All participants received precise food rec-
ommendations and individual dietary plan with the quan-
tities of foods to be consumed. The two diets (OO and
LO) contained the same basic foods. The OO diet was
designed to provide 35% to 37% of energy from fat and
about 42% to 44% of energy from carbohydrates. The LO
diet was designed to provide 15% to 17% of energy from
fat and 65% of energy from carbohydrates. The protein
content of the two diets was designed to be 15% to 18%
of energy. Diets were designed to provide similar
amounts of fiber, vitamin C, and alcohol. Both diets were
high in lycopene (19.5 mg/d, as analyzed by high-pres-
sure liquid chromatography), which was achieved by
K.D.K. Ahuja et al. / Nutrition 22 (2006) 259–265
consuming tomato soup (Heinz Ready to Serve, 300
g/can; H. J. Heinz, Melbourne, Australia) and tomato
paste (50 g). Other carotenoid intakes were low but
controlled. Because there is no Australian database avail-
able for calculation of individual carotenoids in food, the
U.S. Department of Agriculture (USDA) carotenoid da-
tabase was used. Average daily intakes of cryptoxanthin,
?-carotene, ?-carotene, and lutein plus zeaxanthin in the
OO and LO dietary periods were 60, 18, 1204, and 970
?g, respectively . Hence, lycopene contributed about
90% to the total carotenoid content in the two diets.
Because the lycopene content of food may change with
the season and processing, participants were provided
with a single batch of tomato soup and tomato paste
(donated by H. J. Heinz). For the same reason recipes and
instructions for cooking and heating of these products
were given. Participants were instructed to use the same
utensils and microwave or stove for heating the soup for
the same period in both dietary periods. Participants were
instructed to add tomato paste to the food at the last
stages of cooking, mix it well, cook on high for 2 min,
and simmer for 4 min. Recipes for curries and pasta sauce
with 5 g of olive oil (for the LO diet) and 30 g of olive
oil (for the OO diet) using these instructions were pro-
vided to participants. Fruit intake was restricted to two
pieces a day (apple, banana, or pear). Vegetable intake
was restricted to 100 g of frozen green peas and corn mix,
mushrooms, white onion, radish, or iceberg lettuce. In-
dividually packed breakfast cereal (natural muesli for the
LO diet and toasted muesli with light olive oil for the OO
diet) and Bertolli extra light olive oil (donated by IGA,
Moonah, Tasmania, Australia) was provided to partici-
pants. To provide the equivalent energy on the LO diet,
poly joule, a glucose polymer (Nutricia Australasia,
NSW, Australia), was provided to the participants. Due
to differences in the amount of oil intake, the vitamin E
content between the two diets was different, with the OO
diet providing more vitamin E than the LO diet. No effort
was made to equalize vitamin E content between diets
because foods rich in vitamin E are usually high in fat
and supplements would have changed the emphasis of the
study, which was to compare diets containing the same
basic foods with different amounts of oils and not food
While on the intervention diets, participants were asked
to record 4-d weighed food diaries. These were analyzed
using Food Works software (Xyris) to calculate and com-
pare nutrient intake between diets and to check dietary
compliance. Participants were also contacted regularly to
discuss any problems related to the diets and to provide
encouragement and support.
Body weight was measured regularly and participants
were asked to keep their physical activity similar while
on the two diets. Fasting blood samples were collected at
the start and end of the two dietary periods. For serum
separation, blood was allowed to coagulate for 1 h (pro-
tected from natural light) and then centrifuged at 800g at
4°C for 20 min. Serum was aliquotted and stored at
?70°C for later analysis. All biochemical analyses were
subsequently performed in the same run to decrease in-
Serum lycopene concentrations were analyzed by using a
high-pressure liquid chromatographic method modified
from Talwar et al.  and Su et al. . Standard stock
solution was prepared under red light by dissolution of
lycopene (Sigma Aldrich, Sydney, Australia) in tetrahydro-
furan and stored under nitrogen at ?80°C. An internal
standard of ?-tocopherol acetate in 95% ethanol solution
was added to the standard solution and to serum samples.
Hexane was added to separate the phase containing carote-
noids, which was then dried under nitrogen. The sample
was reconstituted with tetrahydrofuran. Mobile phase of
methanol-acetonitrile-tetrahydrofuran (75:20:5, v/v) con-
taining 0.01% (w/v) ascorbic acid was used. The sample
was analyzed by using a Shimadzu SCL-10A with a diode
array detector (GenTech Scientific, Arcade, NY, USA) and
a flow rate of 1.8 mL/min at a 450-nm wavelength. Coef-
ficient of variation for lycopene was 13.8%.
Lipid measurements were performed in complete runs
for each participant by using an RA 1000 auto analyzer
(Technicon, Cranesville, PA, USA) and enzymatic choles-
terol reagent (ThermoTrace, Sydney, Australia). Serum
level of high-density lipoprotein (HDL) cholesterol was
measured with the same reagent after precipitating other
serum lipoproteins with polyethylene glycol (QChem HDL
cholesterol kit, Special Diagnostics, Sydney, Australia). Se-
rum triacylglycerols were measured with the G.P.O Trinder
Triglycerides Reagent (ThermoTrace). LDL cholesterol was
calculated using Friedewald’s equation .
Copper-induced serum oxidation was performed in du-
plicate according to the method of Schnizter et al.  by
using a multiposition spectroscope (Varian 1E; Varian Inc.,
Palo Alto, CA, USA) with Cary WinUV 1.00(6). The sam-
ple constituted of a 50-fold dilution of serum in phosphate
buffered saline containing sodium citrate. The reaction was
initiated at 37°C with 100 ?M copper and absorbance was
read at a 245-nm wavelength every 10 min for 400 min. Lag
phase before oxidation, maximal rate of oxidation, and time
to achieve maximal rate of oxidation were calculated from
the data obtained.
Total antioxidant status (TAS) was measured by using a
calorimetric method on a RA 1000 autoanalyzer (Techni-
con) at a 600-nm wavelength according to the method
described by Miller et al. . The protocol included mix-
ing ABTS®/metmyoglobin reagent with serum and initiat-
ing the reaction with hydrogen peroxide. 6-Hydroxy-
2,5,7,8-tetramethylchroman-2-carboylic acid was used as
the standard for the assay.
K.D.K. Ahuja et al. / Nutrition 22 (2006) 259–265
Statistical analysis was performed with SPSS 11 (SPSS,
Chicago, IL, USA) and STATA 8.2 (STATA Corp., College
Station, TX, USA). Repeated measures analysis of variance
using general linear modeling with robust standard error
estimation, which was adjusted for order and period effects,
was used to compare the effect of the study diets on mea-
surements of carotenoids, lipids, and lipoproteins. In addi-
tion, 95% confidence intervals were calculated by using
asymmetrical bootstrap estimation. Post hoc testing for het-
eroscedasticity and missing variables demonstrated that the
assumptions of the regression model were not violated.
Twenty-four subjects participated in the study. Three
subjects withdrew within the first 4 d of the first dietary
period for personal reasons. Twenty-one subjects (15
women and 6 men; 44.4 ? 12.3 y old, mean ? standard
deviation) completed the study (Table 1). Nine participants
commenced the OO diet first and 12 the LO diet.
Nutrient intake data, calculated from the 4-d diet records
on the two dietary periods, are presented in Table 2. Intakes
of carbohydrates and fat were in the target range. The OO
diet provided more than three times the energy from mono-
unsaturated fatty acid compared with the LO diet. Protein
intake was slightly (statistically significant) higher on the
LO diet than on the OO diet. However, this small difference
of 1.5% is not expected to have an effect on the serum
parameters measured. Total energy, ratio of polyunsaturated
to saturated fat, and intakes of fiber, vitamin C, dietary
cholesterol, and alcohol were similar on the two diets. The
reported intake of carotenoid-rich foods (estimated with the
USDA database) was also similar between the two diets.
Concentrations of serum lycopene, total cholesterol,
LDL cholesterol, HDL cholesterol, and triacylglycerols on
day 1 were similar on the two diets. After 10 d of lycopene-
rich diets, there was a similar increase in serum lycopene
levels. Figure 1 presents the changes (mean difference and
95% confidence intervals) in serum lycopene, lipid, and
lipoprotein levels on the OO diet compared with the LO
diet. There was no significant difference in serum levels of
Oxidizability of serum and antioxidant status at the end of the OO and
Lag phase (min)†
Maximal rate of oxidation (?abs/
?time) ? 100†
Highest optical density (abs)†
Time at maximal rate of oxidation
Total antioxidant status (mmol/L)‡
102.63 ? 17.54103.25 ? 25.17
0.21 ? 0.06
0.64 ? 0.06
0.20 ? 0.06
0.65 ? 0.07
148.89 ? 24.47
1.17 ? 0.13
148.33 ? 24.79
1.23 ? 0.35
abs, absorbance; ?, change; LO, diet low in olive oil; OO, diet high in
* Mean ? standard deviation.
†n ? 16.
‡n ? 19.
Baseline characteristics of study participants (n ? 21)*
Total cholesterol (mmol/L)
LDL cholesterol (mmol/L)
HDL cholesterol (mmol/L)
44.4 ? 12.3
24.3 ? 3.5
5.06 ? 0.78
3.09 ? 0.72
1.43 ? 0.38
2.36 ? 1.00
1.20 ? 0.60
BMI, body mass index; HDL, high-density lipoprotein; LDL, low-
* Mean ? standard deviation (n ? 15 women, 6 men).
Dietary nutrient intakes on the OO and LO diets*
Total fat (%energy)
Monounsaturated fat (%energy)
Polyunsaturated fat:saturated fat
8.49 ? 1.46
16.72 ? 2.52
47.45 ? 4.31
35.16 ? 3.55
19.55 ? 2.05
0.77 ? 0.21
128.29 ? 58.00
240.86 ? 52.67
112.18 ? 23.74
127.32 ? 34.18
30.99 ? 7.48
8.33 ? 1.44
18.10 ? 2.15†
64.70 ? 4.80†
16.84 ? 4.05†
6.39 ? 2.77†
0.86 ? 0.37
124.23 ? 44.71
317.62 ? 52.51†
169.05 ? 33.26†
147.70 ? 37.37†
32.44 ? 7.52
LO, diet low in olive oil; OO, diet high in olive oil.
* Mean ? standard deviation (n ? 18); as analyzed from 4-d records.
†Statistically significant difference from OO diet (P ? 0.05).
Fig. 1. Change in serum lycopene and lipids between a diet high in olive oil
and one low in olive oil. Mean differences and 95% confidence intervals were
tein; LDL, low-density lipoprotein; TC, total cholesterol.
K.D.K. Ahuja et al. / Nutrition 22 (2006) 259–265
lycopene, total cholesterol, and LDL cholesterol at the end
of the two dietary periods. HDL cholesterol was higher and
the ratio of total to HDL cholesterol and triacylglycerol
levels were lower at the end of the OO diet compared with
the LO diet. Body weight did not change over the two
Table 3 presents the results of diluted serum copper-
induced oxidation, and TAS at the end of the two diets. No
statistically significant difference was seen for lag phase of
serum oxidation, maximal change in absorbance, time for
maximal change in absorbance, or TAS.
The study compared the effects of a lycopene-rich diet
high in olive oil and a lycopene-rich diet low in olive oil on
serum lycopene levels, serum lipids, and some measure-
ments of antioxidant status. Unlike many previous studies,
the olive oil used was refined olive oil, which has fewer
polyphenolic compounds, which have a beneficial effect in
decreasing CHD. This present investigation confirmed the
results of other studies by showing an increase in serum
lycopene with an increase in dietary lycopene [30,39,40].
The results were similar to our previous 14-d study with
diets high in lycopene, in which the fat intake at two feasible
extremes (16% and 36% of total energy) did not appear to
influence serum lycopene levels . The main difference
between the two studies was the source of monounsaturated
fat, which was Bertolli extra light olive oil in this study
versus Sunola sunflower oil, which is high in monounsatu-
rated fat, in the previous study. This suggests that, even
though lycopene is a fat-soluble compound and its absorp-
tion might be influenced by the amount of dietary fat intake,
as little as 15% of energy from fat is enough to allow an
increase of serum lycopene levels by at least two-fold,
especially if the diets are also high in dietary lycopene. This
increase appears to occur irrespective of whether the source
of fat is monounsaturated fat is enriched sunflower oil or
olive oil. The increase also occurred irrespective of the age
of the subjects.
The results differ from those of a 5-d dietary study that
compared the effects of a single daily meal high in lycopene
when taken with extra virgin olive oil with those without oil
. The difference in results may be attributed to the study
design, namely not randomized or crossover, or sample size
(total seven subjects; four subjects had tomato meals with
olive oil and three had no oil with tomato meals) and the
study did not control for any other meals of the day. In
contrast, the present investigation was a randomized, cross-
over study with the same basic foods over 10 d, with a
difference in total fat intake over the two dietary periods. It
is also possible that serum lycopene levels respond differ-
ently to lycopene intake with or without fat for the first
week and that high lycopene intake and 14% of energy from
fat or 35% of energy from fat per day has no differential
effect after a week or 9 d of regular consumption.
Although the diets were of short duration and the con-
centrations of serum lipids and lipoproteins are unlikely to
have reached their final values, the results were in accor-
dance with the meta-analyses by Clarke  and Mensink
and Katan , suggesting that diets enriched in monoun-
saturated fat increase HDL cholesterol, lower the ratio of
LDL to HDL, and lower serum triacylglycerols compared
with high-carbohydrate, low-fat diets.
In vitro susceptibility to oxidation was performed on
serum rather than on isolated LDL cholesterol to take into
account the presence of water-soluble antioxidants and
HDL cholesterol, because oxidation of LDL in the body
would not occur in isolation but in the presence of other
components of serum .
Copper-induced oxidation of serum and TAS analysis
showed no significant difference at the end of the two
dietary periods. This suggests that antioxidant activity and
lycopene concentration were similar on the two diets. Other
short-term studies, with controlled carotenoid intakes, have
indicated lower susceptibility of LDL to oxidation after
high-fat, monounsaturated fat-enriched diets compared with
high-carbohydrate, low-fat diets [26,27]. This has been at-
tributed (in combination or individually) to the difference in
amount of monounsaturated fat and the amount of vitamin E
in the diet. Phenols present in olive oil have also been
suggested to act as antioxidants, and Ramirez-Tortosa et al.
 found an increased effect on LDL oxidation with extra
virgin olive oil compared with refined olive oil in men with
vascular disease. In the present investigation, monounsatu-
rated fat, phenol, and vitamin E intakes were about 30, 3,
and 10 mg higher per day, respectively, on the OO diet
versus the LO diet. There are two possible reasons for the
lack of difference in oxidation in the present study, namely
analytical and/or dietary differences. First, the water-soluble
antioxidants in the serum that are not present in isolated
LDL may exceed and mask any effects of the antioxidant
capacity of monounsaturated fatty acids in serum. Second,
higher levels of compounds with antioxidant properties such
as phenol and/or vitamin E are required than were present in
the OO diet to show a difference in serum oxidation .
However, a study in Greek smokers that compared the
effects of diets with controlled vitamin E, high phenol level,
and low levels of phenol and olive oil showed no difference
in plasma oxidation, with the difference in phenol intake as
high as 19 mg/d . As for the effect of vitamin E on
oxidation, clinical data are conflicting and controversial,
and there is very little evidence that it inhibits lipid peroxi-
dation in healthy humans .
In conclusion, over 10 d, high dietary lycopene intake
increased serum lycopene levels irrespective of the amount
of fat in the diet. However, a diet high in refined olive oil
may decrease the risk of CHD by improving lipid profiles in
comparison with a high-carbohydrate diet, even though the
K.D.K. Ahuja et al. / Nutrition 22 (2006) 259–265
two diets appeared to have a similar effect on bioavailability
H. J. Heinz (Melbourne, Australia) provided the tomato
products and I. G. A. Moonah (Tasmania, Australia) provided
the olive oil for the study. Elaine Whitham (Toxicology/Spe-
cial Biochemistry, Department of Chemical Pathology, Wom-
en’s and Children’s Hospital, Adelaide, Australia) performed
the carotenoid analysis. Dr. Iain Robertson, MMedSci., M.M.,
M.P.H. (School of Human Life Sciences) provided biostatisti-
cal support. Mr. Dale Kunde (School of Human Life Sciences)
and James Sharman (Queensland University of Technology,
Brisbane, Australia) advised in setting up the serum oxidation
assay. Murray Frith and staff from the School of Chemistry,
University of Tasmania, provided the spectroscope.
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