Effects of canola or olive oil on plasma lipids, lipoprotein-associated phospholipase A2 and inflammatory cytokines in patients referred to coronary angiography

doi:10.21203/rs.3.rs-37417/v3

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Effects of canola or olive oil on plasma lipids, lipoprotein-associated phospholipase A2 and inflammatory cytokines in patients referred to coronary angiography

https://doi.org/10.21203/rs.3.rs-37417/v3

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published 14 Aug, 2020

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Background: The potential cardioprotective benefits of olive oil (OO) and canola oil (CO) consumption have been shown in some studies. The present study was conducted to compare the effects of CO and OO on plasma lipids, some inflammatory cytokines, and lipoprotein-associated phospholipase A2 (Lp-PLA2) mass and activity in patients undergoing coronary angiography.

Methods: A randomized, controlled, parallel-arm, clinical trial involving 48 patients (44 men and 4 women, aged 57.63 ± 6.34 years) with at least one classic cardiovascular risk factor (hypertension, dyslipidemia, or diabetes) who referred to coronary angiography was performed. Patients were randomly divided into two groups and received 25 mL/day refined olive oil (n=24) or canola oil (n=24) for 6 weeks. Plasma lipids, some selected inflammatory markers, and Lp-PLA2 levels were measured at the baseline and after the intervention.

Results: CO consumption produced a significant reduction in plasma Lp-PLA2 mass (-0.97 ± 1.84 vs. 0.34 ± 1.57 ng/mL, P = 0.008 for CO and OO, respectively), whereas the mean changes of Interleukine-6 concentration were significantly lower after OO consumption compared with CO (-9.46 ± 9.46 vs. -0.90 ± 6.80 pg/mL, P = 0.008 for OO and CO, respectively). After 6 weeks of intervention, no significant changes were observed in plasma Lp-PLA2 activity, complement C3, C4, and lipid profile in two intervention groups.

Conclusions: Comparing the two vegetable oils in subjects with cardiovascular risk factors shows that consumption of olive oil is more effective in reducing the level of inflammatory cytokine Interleukine-6 whereas canola oil is more effective in lowering the level of Lp-PLA2, but, this finding should be interpreted with caution since the Lp-PLA2 activity did not change significantly.

Endocrinology & Metabolism

Cardiac & Cardiovascular Systems

Olive Oil

Canola Oil

Lipid Profile

Lipoprotein-associated phospholipase A2

Inflammatory Markers

Lifestyle modification, including a healthy diet, is the first therapeutic step to reduce cardiovascular disease (CVD) [1]. Reducing the amount of dietary saturated fatty acids (SFAs) and replacing them with unsaturated fats are among the main nutritional recommendations for the prevention and treatment of CVD [2]. Inclusion of vegetable oils rich in monounsaturated fatty acids (MUFAs) in the diet has been associated with several cardioprotective effects [3]. Olive and canola oils, the two commonly consumed vegetable oils are low in SFAs but rich in MUFAs, and both have been recommended to be included in the context of a healthy diet for cardioprotection [4, 5].

The potential cardioprotective benefits of olive oil (OO) consumption, especially in the Mediterranean diet, have been extensively studied [4, 6]. However, scientific evidence suggests that the replacement of SFAs with polyunsaturated fatty acids (PUFAs) may reduce the CVD risk factors somewhat more than the replacement of SFAs with MUFAs [2]. In addition to their beneficial effects, it has been shown that PUFAs are safe [7]. Therefore, oils with low SFAs that contain a relatively high PUFAs, as well as high levels of MUFAs may be preferable to improve cardiovascular risk factors. Canola oil (CO) which contain low amounts of SFAs, high MUFAs and relatively high PUFAs could be a reasonable choice to be included in the healthy diet to replace SFAs and increase unsaturated fats intake [8], and evidence supports several potential health benefits of canola oil consumption in terms of reducing cardiovascular risk factors and improving health [5]. In comparison between canola and olive oils, the MUFAs content of OO is slightly higher, while the amount of PUFAs is higher in CO [5].

In addition to the classic CVD risk factors such as plasma lipid and lipoprotein concentrations, measuring inflammatory biomarkers is useful for cardiovascular risk assessment and predicting cardiovascular risk [9, 10]. Numerous inflammatory biomarkers are implicated in atherosclerosis; each one increases our understanding of this complex process. Interleukin-6 (IL-6) is among the well-studied inflammatory biomarkers related to cardiovascular risk [10-13]. Lipoprotein-associated phospholipase A₂ (Lp-PLA₂) is a member of the phospholipase A₂ family produced by inflammatory cells and mediates vascular inflammation [14]. Elevated plasma Lp-PLA₂ activity is positively correlated with an increase in inflammatory cytokines, particularly IL-6 [15]. A meta-analysis of the prospective studies of Lp-PLA₂ showed an association of Lp-PLA₂ activity and mass with a worse prognosis of coronary artery disease (CAD), ischemic stroke, and vascular mortality [16]. In particular, a higher level of Lp-PLA₂ activity may imply a worse cardiovascular prognosis in high-risk patients referred to coronary angiography [17]. In addition to the effects that fatty acids intake can have on the concentration of lipids and inflammatory markers, they may affect the level of plasma C3 [14], which is itself have been associated with atherosclerosis and cardiovascular risk factors [18].

Research comparing the impact of olive and canola oils on cardiovascular biomarkers, particularly on inflammatory biomarkers, is scarce. Therefore, the present study was performed aiming to examine the effects of CO and OO on plasma lipids, inflammatory cytokines, Lp-PLA₂ mass and activity, and complement C3 and C4 concentrations in individuals undergoing coronary angiography.

Participants

The participants were patients who referred to coronary angiography in the Shahid Rajaei Cardiovascular, Medical & Research Center in Tehran, Iran. Patients entered the study one month after angiography to ensure that their medical and pharmacological status was stable.

Eligible subjects were men and post-menopausal women less than 75 years who had at least one of the major cardiovascular risk factors, including hypertension, diabetes mellitus, dyslipidemia, or acute cardiac events. The exclusion criteria were the regular use of anti-inflammatory medication or dietary antioxidants or omega-3 supplements during the previous month before the study or any changes in the disease treatment plan, including type or dose of drugs or coronary artery bypass graft (CABG) and gastrointestinal complications such as diarrhea during the study. In addition, participants with low adherence to the intervention (who consumed less than 80% of the olive or canola oils delivered at the baseline) were excluded from the study.

Study Design

The present study was a randomized controlled open-label parallel-arm clinical trial conducted in the spring and summer of 2019 in Tehran, Iran. At the baseline, demographic and medical information were obtained through face-to-face interviews and study of medical files, respectively. All participants received dietary advice on a heart-healthy diet at baseline. Daily consumption of at least five servings of fruits and vegetables, substituting lower-fat dairy products and meats instead of higher fats ones, lower use of salt and simple sugars were among the dietary advice provided. Next, the participants were randomly assigned to one of the two groups following simple randomization procedures using computerized random numbers. They were requested to consume a daily amount of 25 mL of refined olive oil (OO) (Etka, Iran) or canola oil (CO) (CanaPlus, Canada) as raw with meals for 6 weeks. The fatty acid composition of OO and CO has been shown in Table 1. Olive and canola oils were provided to patients in sufficient quantities. To ensure compliance with the intervention and proper oil consumption, participants were followed up weekly by telephone contact.

The procedures followed in this trial were in accordance with the 1964 Helsinki Declaration and the study protocol was approved by the Ethical Committee of National Nutrition & Food Technology Research Institute, Tehran, Iran (The ethical committee No. IR.SBMU.NNFTRI.REC.1398.074) and written informed consent were obtained from all the participants. This clinical trial was registered at the Iranian Registry Center of Clinical Trials (IRCT) (registration number: 20160702028742N5).

Anthropometric measures

Weight and height were measured at the baseline and after 6 weeks of intervention by the study dietitian. Weight was measured without shoes, coats, or jackets using a digital scale. Height was measured without shoes using a wall-mounted stadiometer.

Biochemical parameters

Venous blood samples were obtained from each patient after 12-h overnight fasting and collected into heparinized tubes at baseline and after 6 weeks. The blood samples were centrifuged (4000 rpm for 20 min) and the resulting plasma was stored at -80°C. Plasma Lp-PLA₂ mass and activity were analyzed by a commercially available ELISA kit (ZellBio GmbH, Ulm, Germany) and commercial colorimetric assay kit (Cayman Chemical, Ann Arbor, MI, USA), respectively. Commercially available ELISA kit (Biolegend, San Diego, CA, USA) was used to measure plasma IL-6 concentration. Plasma lipids and lipoproteins were analyzed with the colorimetry method via auto-analyzer (Selectra 2, Vital Scientific, Spankeren, The Netherlands), using commercial kits (Pars Azmoon, Karaj, Iran). Low-density lipoprotein-cholesterol (LDL-C) was measured using a direct enzymatic method. The small-dense LDL-cholesterol content in plasma was quantitated according to the method described previously [19]. Non-high density lipoprotein-cholesterol (Non-HDL-C) was calculated by subtracting HDL-C from total cholesterol. Plasma complement C3 and C4 were determined by the turbidimetric method by commercial kits (Pars Azmoon, Karaj, Iran) using an auto-analyzer.

Dietary intakes and physical activity

Dietary intake and physical activity levels were monitored at the baseline and after 6 weeks. Dietary intakes were assessed using the 24-h dietary recall questionnaire completed in three days (two regular days in the middle of the week and one day at the weekend) by the trained dietitian. Participants were asked to maintain their habitual lifestyle throughout the study. Recall data was analyzed using the Nutritionist software (version IV, N-Squared Computing, San Bruno, CA, USA) to which was added the local food data.

Statistical analysis

Although the primary outcome was Lp-PLA₂, we could not calculate sample size based on this variable, because according to our search, there was no study comparing the effects of CO and OO on Lp-PLA₂mass or activity. On the other hand, studies have shown that Lp-PLA₂ is transported in plasma predominantly (80%) is associated with LDL-C [20]. Therefore, the study sample size was calculated using LDL-C as the primary outcome variable. To detect a change in the mean of LDL-C concentration (10 mg/dL) as reported in a previous investigation [21] at the 5% level of significance and with 80% power, 24 participants were needed in each arm of the two-arm trial.

The data were analyzed using the SPSS software for Windows version 21 (SPSS Inc., Chicago, IL, USA). All values were reported as Mean ± SD or percentage (%). The per-protocol analysis was performed (i.e., only those who completed the study were included in the analyses). The normality of distribution of the study variables was tested by the Shapiro-Wilk test. When the variables were not normally distributed, raw values were log-transformed. Analysis of covariance (ANCOVA) was used to compare the 6-week values between the groups using the baseline measures as the covariate. Paired samples t‐test was used for comparing the measurements in the beginning and at the end of the intervention within the study groups. The χ² test was used for the comparison of categorical variables. The statistical significance level was set at P = 0.05 (two tails).

A total of 100 patients were screened for eligibility, and 48 patients entered the study. Six patients were dropped out during the intervention due to low adherence to dietary intervention, travel, and refuse to continue. Therefore, the final study population consisted of 42 subjects; 22 subjects in the OO group, and 20 subjects in the CO group (Figure 1). Table 2 summarizes the general characteristics of the participants. No significant differences were observed in the baseline characteristics between the two groups.

Baseline levels and 6-week changes in anthropometric measures are shown in Table 3. There were no significant differences between the OO and CO groups concerning the body weight and physical activity at the baseline and after the intervention.

As shown in Table 4, energy and dietary intakes of nutrients did not differ between the groups at the baseline. Dietary intakes of total fat and monounsaturated fat of both groups increased during the intervention due to the consumption of olive and canola oils. However, there were no differences in dietary intake of the two groups at 6-week.

Plasma levels of lipid, lipoproteins, and inflammatory markers are shown in table 5. The baseline values were not different between the two groups. CO consumption resulted in a significant reduction in plasma Lp-PLA₂ mass (P = 0.008, power = 0.78) during 6 weeks, whereas the mean changes of IL-6 concentration were significantly lower after OO consumption compared with CO (P = 0.008, power = 0.80). After 6 weeks of intervention, plasma Lp-PLA₂ activity, C3, C4, and lipid profile had no significant changes in neither groups (Table 5). Owing to some loss to follow-up, the statistical power to detect differences in LDL-C was decreased (the actual power of test analysis was 0.70).

The present study suggests that a relatively short dietary intervention with refined olive oil can have a significant effect on plasma IL-6. In contrast, canola oil may impact plasma Lp-PLA₂ mass without changing lipoproteins and other inflammatory biomarkers in patients referred to coronary angiography.

In the present study, the consumption of olive oil had a more lowering effect on plasma IL-6 concentration. The difference in plasma IL-6 levels between the two groups can be related to the difference in fatty acid composition of canola and olive oils. In particular, olive oil consists of 14.5% SFA, 70% oleic acid, 11% linoleic acid, and 1.5% palmitoleic acid, whereas canola oil is characterized by a low level of SFAs (7%); 61% oleic acid, 19% linoleic acid, and 9% alpha-linolenic acid (ALA) [22]. Compared to canola oil, the amount of oleic and palmitoleic acid in olive oil is higher. In vitro studies have shown that the addition of oleic or palmitoleic acid to the cell culture medium is effective in reducing or preventing the increase of IL-6 levels [23-26]. Some human studies have shown evidence of an inverse association between oleic acid and IL-6 concentration [27].

A growing body of evidence indicates that Lp-PLA₂ represents an independent risk factor for CVD. Lp-PLA₂ belongs to the family of structurally diverse phospholipase A₂ enzymes, also known as platelet-activating factor acetylhydrolase (PAF-AH) [28]. Circulating Lp-PLA₂ is primarily associated with LDL-C; the majority of it is bound to atherogenic small-dense LDL-C particles [29]. In the present study, the consumption of CO reduced plasma Lp-PLA₂ mass but not of its activity. Previous studies have shown a modest correlation between Lp-PLA₂ mass and activity (30, 31). It has been suggested that Lp-PLA₂ is associated with LDL-C in plasma, and this may results in the under-detection of the Lp-PLA₂ mass by the ELISA method (32). However, since all study samples were measured in the same way in the current study, possible under-detection of the Lp-PLA₂ mass was the same for the baseline and final samples. Despite this, both the Lp-PLA₂ mass and activity are predictors of CVD events (33, 34). It has been shown that tocopherols could inhibit Lp-PLA₂ activity [30]. The amount of alpha-tocopherol in olive and canola oils is similar. However, canola oil is richer in gamma-tocopherol [31]. The higher gamma-tocopherol content of canola oil may have an effect on the observed effect on Lp-PLA₂. The observed decrease in the Lp-PLA₂ level following CO consumption may also be related to its n-3 fatty acid content. Canola oil contains more PUFAs (both n-6 and n-3) and less MUFA than olive oil. In patients admitted to elective coronary angiography, the content of the long-chain n-3 PUFA eicosapentaenoic acid (EPA) in adipose tissue was inversely associated with plasma Lp-PLA₂ mass [32]. Similarly, in participants of the Multi-Ethnic Study of Atherosclerosis, plasma Lp-PLA₂ mass and activity were significantly lower in those with the higher plasma EPA and Docosahexaenoic acid (DHA) [33]. The evidence from intervention trials for the influence of n-3 PUFAs on Lp-PLA₂ is equivocal. In healthy people, two studies have reported no effect of n-3 PUFA supplementation on Lp-PLA₂[34, 35]. Nelson et al. showed that supplementation with n-3 fatty acids capsules (fish oil or flaxseed oil) over 8 weeks had no significant effect on plasma Lp-PLA₂ mass or activity when compared to control (olive oil capsule supplementation) [34]. In contrast, Asztalos et al. showed that as compared to placebo (6 g/day olive oil) supplementation with the higher dose of EPA (1800 mg), but not DHA or lower dose of EPA (600 mg) over 6 weeks could reduce Lp-PLA₂ mass in a healthy population [36]. Apart from the effects in healthy subjects, an increase in n-3 intake has been shown to decrease Lp-PLA₂ levels in patients with cardiovascular risk factors. In stable CAD patients undergoing percutaneous coronary intervention, administration of omega-3 PUFA (1 g/day) for 4 weeks decreased Lp-PLA₂ mass and activity compared to control (soybean oil capsules) [37]. Similar findings have been observed in patients with diabetes [38] and subjects who had residual hypertriglyceridemia after receiving statins [39, 40].

The pro-atherogenic role of Lp-PLA₂ could be related to its ability to hydrolysis of oxidized phospholipids on the LDL-C surface, resulting in the generation of two proinflammatory and proapoptotic lipid mediators, lysophosphatidylcholine, and oxidized free fatty acids, which play an important role in the development of atherosclerotic necrotic cores by recruiting and activating macrophages or leukocytes [41]. In the present study, although canola oil reduced the Lp-PLA₂ level, it had no significant effect on inflammatory factors. Consistent with this contention, supplementation with n-3 fatty acids (EPA) has reduced plasma Lp-PLA₂ without significant effects on plasma inflammatory biomarkers, including IL-6 [36].

Complement factors C3 and C4 have been associated with atherosclerosis and cardiovascular risk factors [18] and have shown substantial correlations with cardiovascular risk factors [42]. Plasma C3 and C4 did not change in either group. In a previous study, an increase was observed in the C3 concentrations after the intake of high saturated fat, compared with high-monounsaturated fat [14].

In the current study, neither olive oil nor canola oil consumption had significantly impacted on plasma lipids and lipoproteins. Consistent with our findings, in previous studies, the intake of refined OO (60 g/day) has not had a significant effect on the plasma TG, LDL-C, or HDL-C levels in mildly hypercholesterolemic subjects who were not on lipid-lowering medications [43] or in stable coronary artery disease patients (50 mL/day) [44]. However, some previous studies have reported the beneficial effects of CO on plasma lipids [45-48]. Yet, it should be noted that the study population in these studies were healthy people or those with cardiovascular risk factors, not on lipid-lowering agents. In contrast, most of the participants in the present study were under statin therapy and had an optimum level of plasma lipids. Therefore, the beneficial effects of canola oil on plasma lipid profiles appear to be evident in patients whose plasma lipids are high at baseline and are not on lipid-lowering medication. Intake of CO or OO in the context of a lipid-lowering diet for 3.5 weeks in hyperlipidemic subjects who were not on lipid-lowering agents had similar effects on serum lipoprotein concentration [22].

Study strengths and limitations

Comparison of two commonly consumed edible oils and detailed data collection were strengths of the current study. However, the present study has also some limitations. In the study, there was no run-in period. Since participants received dietary advice on a heart-healthy diet at baseline, effects due to the changes in dietary habits could not be excluded and part of the observed effects on investigated biomarkers may be related to dietary habits modification. However, participants of both groups received similar dietary advice and the potential effects were present in both groups. The duration of dietary intervention was relatively short. Furthermore, some participants were lost to follow-up and, or discontinued the intervention, which reduced the final sample size. In addition, we were unable to blind the participants because of the sensory and appearance characteristics of the two oils. Moreover, we could not conduct the study in a tightly regulated, controlled feeding design. However, the study oils were provided to individuals (more than each participant's need), and their consumption was monitored weekly. Besides, since most of the participants were male, the sample cannot be considered representative, and this may limit the findings to a specific sex. Furthermore, cross-over study design could have reduced confounding factors associated with the inherited characteristics of the participants. Nevertheless, cross-over studies require that study participants be followed for a more extended period and that their treatment plan should not change during this time. Moreover, given that most of the population spends most of their time in the postprandial state, measurements of postprandial lipids and inflammatory markers could have provided additional information on potential changes in cardiovascular risk.

In summary, each of the refined olive or canola oils improved one of the inflammatory CVD risk factors. Comparing the two vegetable oils in subjects with cardiovascular risk factors shows that consumption of olive oil is more effective in reducing the level of inflammatory cytokine IL-6, whereas canola oil is more effective in lowering the level of LP-PLA₂. Regarding the role of the circulating level of IL-6 in the prediction of future coronary heart disease events [49-51], a decrease in IL-6 level following olive oil consumption can reduce the risk of cardiovascular events. On the other hand, canola oil consumption decreased the level of Lp-PLA₂ that its increased levels have been associated with increased risk of cardiovascular events [16]. However, this finding should be interpreted with caution since the Lp-PLA₂ activity did not change significantly. Overall, consumption of either refined olive or canola oils in the context of a healthy diet may have a beneficial effect on the secondary prevention of CVD by improving inflammatory risk factors.

ALA: alfa-linolenic acid

ANCOVA: analysis of covariance

CABG: coronary artery bypass graft

CAD: coronary artery disease

CO: canola oil

CVD: cardiovascular disease

DHA: docosahexaenoic acid

EPA: eicosapentaenoic acid

HDL-C: high-density lipoprotein cholesterol

IL-6: Interleukin-6

LDL-C: low-density lipoprotein cholesterol

Lp-PLA₂: lipoprotein-associated phospholipase A₂

MUFA: monounsaturated fatty acid

OO: olive oil

PUFA: polyunsaturated fatty acid

SFA: saturated fatty acid

TG: triglycerides

Ethics approval and consent to participate

The procedures followed in this study were in accordance with the 1964 Helsinki Declaration and the study protocol was approved by the Ethical Committee of National Nutrition & Food Technology Research Institute, Tehran, Iran (the Ethical No: IR.SBMU.NNFTRI.REC.1398.074), and written informed consent were obtained from all patients.

Consent for publication

Not Applicable.

Availability of data and materials

All data generated or analyzed during this study are included in this published article [and its supplementary information files].

Competing interests

The authors declare that they have no competing interests.

Funding

The study was supported by a grant from National Nutrition, and Food Technology Research Institute, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Authors' contributions

NK was responsible for designing the research protocol, writing the protocol, conducting the research, screening potentially eligible studies, conducting biochemical tests, extracting and analyzing data, interpreting results, and writing the paper.

JN was responsible for designing the research protocol and screening of potentially eligible studies. He contributed to extracting and analyzing data, interpreting results, and writing the paper.

AZ assisted in conducting the research, especially in medical consultation & material support, and study supervision.

Acknowledgments

The study was supported by a grant from National Nutrition, and Food Technology Research Institute, Shahid Beheshti University of Medical Sciences, Tehran, Iran. The authors thank the personnel of Rajaie Cardiovascular, Medical & Research Center. We are also grateful to all participants in the study.

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Table 1. Chemical composition of oils

Chemical Component	Canola Oil	Refined Olive Oil
Fatty Acid (per 100 g):
Total SFAs	6.40	17.87
Total MUFA	61.37	66.68
Oleic acid	59.36	65.70
Total PUFAs	29.20	11.75
Linoleic acid	20.26	11.23
Alpha-linolenic acid	8.48	0.48

Table 2. Baseline characteristics of the participants ^a

Variable	Olive Oil group (n=22)	Canola Oil group (n=20)	P-value ^b
Age (year)	55.09 ± 6.92	59.30 ± 5.84	0.44
Sex (Male)	20 (91%)	18 (90%)	0.66
PCI history	16 (73%)	16 (80%)	0.89
CABG history	2 (9.1%)	1 (5%)	0.86
Diabetes Mellitus	8 (36%)	8 (40%)	0.91
Hypertension	11 (50%)	11 (55%)	0.92
Dyslipidemia	12 (54%)	8 (40%)	0.55
Overweight	16 (73%)	11 (55%)	0.19
Smoking	8 (36%)	4 (20%)	0.30
Medications:
Aspirin	21 (95%)	20 (100%)	0.93
Clopidogrel	15 (68%)	10 (50%)	0.29
Statins	20 (91%)	19 (95%)	0.93
ACEI	9 (41%)	4 (20%)	0.12
ARB	10 (45%)	13 (65%)	0.42
BB	15 (68%)	15 (75%)	0.81
Nitrates	7 (31%)	7 (35%)	0.90
Aldosteron Antagonist	5 (22%)	1 (5%)	0.17

^aData presentedas Mean ± SD or number(percentage).

^bData were compared using Independent t-testor Chi-square test.

PCI: Percutaneous Coronary Intervention;CABG: Coronary Artery Bypass Graft;ACEI: Angiotensin Converting Enzyme Inhibitor; ARB: Angiotensin Receptor Blocker; BB: Beta-Blocker.

Table 3. Anthropometric measures and physical activity of the participants^a

Variable	Time	Olive Oil group (n=22)	Canola Oil group (n=20)	P-value^b
Body Weight (kg)	Baseline	80.45 ± 11.77	78.65 ± 12.81	0.62
Body Weight (kg)	6-week	80.45 ± 11.49	78.30 ± 12.47	0.64
BMI (kg/m²)	Baseline	26.91 ± 3.38	27.31 ± 4.39	0.34
BMI (kg/m²)	6-week	26.94 ± 3.35	27.19 ± 4.31	0.30
Physical Activity (MET-h/day)	Baseline	27.99 ± 5.23	27.30 ± 3.49	0.65
Physical Activity (MET-h/day)	6-week	28.01 ± 5.23	27.36 ± 3.57	0.69

^aAll values are Mean ± SD.

^bData were compared using Independent t-test.

BMI: Body Mass Index; MET: Metabolic Equivalent.

Table 4. Dietary intake of the participants at the baseline and after the intervention ^a

Variable	Time	Olive Oil group^b(n=22)	Canola Oilgroup^b(n=20)	P-value^c
Energy (kcal)	Baseline	1781.40 ± 196.10	1767.20 ± 146.19	0.55
Energy (kcal)	6-week	1850.72 ± 143.20	1801.20 ± 140.44	0.26
Carbohydrate (g)	Baseline	233.05 ± 32.18	235.20 ± 28.75	0.82
Carbohydrate (g)	6-week	234.25 ± 33.57	232.85 ± 29.33	0.73
Carbohydrate (%)	Baseline	51.90 ± 4.60	53.26 ± 5.16	0.38
Carbohydrate (%)	6-week	50.47 ± 4.20	51.24 ± 4.97	0.60
Protein (g)	Baseline	69.75 ± 15.55	74.25 ± 15.12	0.36
Protein (g)	6-week	70.65 ± 11.27	73.30 ± 11.47	0.46
Protein (%)	Baseline	15.51 ± 3.05	16.76 ± 2.84	0.18
Protein (%)	6-week	15.29 ± 2.27	16.26 ± 2.05	0.16
Total Fat (g)	Baseline	64.30 ± 11.59	59.05 ± 9.93	0.13
Total Fat (g)	6-week	71.40 ± 7.91 ^†	68.90 ± 8.36^†	0.33
Total Fat (%)	Baseline	32.17 ± 4.53	30.05 ± 4.15	0.13
Total Fat (%)	6-week	34.87 ± 4.36 ^†	34.47 ± 3.83^†	0.75
SFA (g)	Baseline	16.00 ± 4.56	16.10 ± 5.09	0.94
SFA (g)	6-week	14.90 ± 3.56	13.75 ± 3.37	0.30
SFA (%)	Baseline	7.99 ± 2.01	8.15 ± 2.24	0.82
SFA (%)	6-week	7.28 ± 1.85	6.84 ± 1.44	0.40
MUFA (g)	Baseline	19.45 ± 6.73	18.45 ± 4.09	0.26
MUFA (g)	6-week	30.30 ± 4.37 ^†	28.50 ± 3.53^†	0.18
MUFA (%)	Baseline	11.18 ± 2.99	10.38 ± 1.90	0.12
MUFA (%)	6-week	14.79 ± 2.45 ^†	14.25 ± 1.59^†	0.10
PUFA (g)	Baseline	25.10 ± 6.48	22.45 ± 4.11	0.13
PUFA (g)	6-week	23.75 ± 4.65	24.40 ± 2.76	0.59
PUFA (%)	Baseline	12.58 ± 3.03	11.47 ± 2.21	0.19
PUFA (%)	6-week	11.56 ± 2.16	12.22 ± 1.37	0.25
Omega-3 (mg)	Baseline	213.30 ± 178.73	167.25 ± 92.56	0.31
Omega-3 (mg)	6-week	233.85 ± 150.65	221.55 ± 66.09^†	0.27
Cholesterol (mg)	Baseline	167.65 ± 82.15	170.00 ± 55.65	0.91
Cholesterol (mg)	6-week	157.00 ± 73.63	167.35 ± 60.39	0.63
Fiber (g)	Baseline	15.45 ± 2.32	14.60 ± 3.78	0.88
Fiber (g)	6-week	15.90 ± 2.78	15.75 ± 3.24	0.87

^aAll values are Mean ± SD.

^b The daily olive or canola oil consumption is considered.

^cData were compared using Independent t-test.

^†Significantly different from Baseline. Data were compared using Paired t-test.

SFA: Saturated Fatty Acid; MUFA: Monounsaturated Fatty Acids; PUFA: Polyunsaturated Fatty Acids.

Table 5. Measures of biochemical variables by intervention groups^a

Variable	Olive Oil group (n=22)			Canola Oil group (n=20)			P-value ^c
Variable	Baseline	6-Week	Δ value^b	Baseline	6-Week	Δ value^b	P-value ^c
TC (mg/dL)	116.77 ± 25.15	124.36 ± 28.94	8.45 ± 17.67	136.25 ± 46.45	133.35 ± 47.54	-2.90 ± 16.81	0.10
LDL-C (mg/dL)	63.64 ± 13.72	67.36 ± 17.39	3.68 ± 11.27	74.65 ± 30.46	72.90 ± 28.98	-1.75 ± 9.03	0.16
sd-LDL (mg/dL)	24.14 ± 10.32	23.14 ± 11.18	-0.91 ± 6.34	22.10 ± 7.51	21.00 ± 9.48	-1.10 ± 6.35	0.62
HDL-C (mg/dL)	37.73 ± 7.92	39.50 ± 7.46	1.50 ± 5.80	42.90 ± 6.49	43.15 ± 8.33	0.35 ± 5.21	0.79
Non-HDL-C (mg/dL)	79.04 ± 20.75	84.86 ± 26.09	5.81 ± 15.38	93.35 ± 42.25	90.20 ± 43.53	-3.15 ± 13.63	0.07
TC/HDL-C	3.17 ± 0.47	3.25 ± 0.71	0.08 ± 0.39	3.06 ± 0.72	3.10 ± 0.83	0.03 ± 0.33	0.81
TG (mg/dL)	112.73 ± 33.04	120.50 ± 61.38	7.63 ± 36.45	122.45 ± 31.94	126.05 ± 35.40	3.90 ± 20.92	0.32
Lp-PLA₂ mass (ng/mL)	5.66 ± 4.09	6.00 ± 4.51	0.34 ± 1.57	3.96 ± 2.45	2.99 ± 1.65	-0.97 ± 1.84^†	0.008
Lp-PLA₂ Activity (nmol/min/mL)	0.022 ± 0.013	0.021 ± 0.017	-0.000 ± 0.008	0.012 ± 0.003	0.010 ± 0.004	-0.001 ± 0.002	0.74
IL-6 (pg/mL)	21.95 ± 20.38	12.49 ± 13.70	-9.46 ± 9.46^†	19.53 ± 10.52	18.62 ± 8.55	-0.90 ± 6.80	0.008
C3 (g/L)	199.32 ± 35.04	200.68 ± 33.63	1.36 ± 36.64	205.30 ± 44.46	223.50 ± 42.40	18.10 ± 49.00	0.08
C4 (g/L)	38.82 ± 11.99	36.23 ± 9.48	-2.59 ± 9.09	39.20 ± 9.03	34.60 ± 10.35	-4.55 ± 12.43	0.52
C3/C4	5.56 ± 1.98	5.37 ± 2.08	0.23 ± 0.91	5.37 ± 2.08	6.36 ± 2.45	0.99 ± 2.53	0.27

^aAll values are Mean ± SD.

^bChange of parameter between 6-week and baseline (6-week minus baseline).

^cThe values for 6-week were analyzed using ANCOVAwith baseline values as covariate.

^† Significantly different from baseline. Data were compared using Paired t-test.

TC: Total Cholesterol; LDL-C: Low Density Lipoprotein-Cholesterol; sd-LDL: Small Dense LDL; HDL:High Density Lipoprotein-Cholesterol; TG: Triglyceride;Lp-PLA₂: Lipoprotein-Associated Phospholipase A₂; IL-6: Interleukin-6.

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Effects of canola or olive oil on plasma lipids, lipoprotein-associated phospholipase A2 and inflammatory cytokines in patients referred to coronary angiography

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