In the current study, we investigated the effects of canola and olive oils for 10 weeks on lipid profile and NAFLD severity among women with PCOS. We found canola oil has beneficial effects on some lipid profile parameters and fatty liver severity. Also, olive oil consumption led to significant improvement in the fatty liver severity while had no effects on the lipid profile. Previous studies have reported that changes in dietary fatty acid composition, especially replacement of SFA with PUFA and MUFA improve blood lipid levels even in those participants with low initial concentrations (1, 2). In our study, participants in the canola oil group showed a significant decrease in serum TG and Non-HDL concentrations and TC/HDL, LDL/HDL, and TG/HDL ratios. Also, we showed a marginally significant effect regarding TC and LDL concentration in the canola oil. Similar to our findings, Ghobadi et al. in a meta-analysis study showed that canola oil decreased LDL and TC compared to sunflower oil and saturated fat(3). Also, Sarkkinen et al. Performed a 6-month dietary intervention trial in hypercholesterolemic patients and found that LDL-C levels in the canola oil group were lowered (3.7%) from baseline levels (4). The effects of canola oil on TC and LDL may be dependent on the types of fatty acids that are replaced by the oil, study duration, and baseline levels of TC and LDL (5).
According to the previous findings, the influence of various oils on blood lipids is controversial. Some researchers reported that TG and very-low-density lipoproteins (VLDL) levels were increased after consuming olive oil compared with canola and sunflower oils (6, 7), while others have found different results (8, 9). Both olive oil and canola oil contain high amounts of MUFA (10). A higher intake of MUFA can improve the entry of TG into the blood circulation that could speed up its clearance (11).In our trial, it could be the reason for the significant decrease in TG concentrations after consuming canola oil, however, this mechanism is not true about the effect of olive oil as it led to a slight increase in TG levels but it is not statistically significant. Canola oil is a good source of oleic acid, ALA, and phytochemicals (12). It is not well known the exact mechanisms of Canola oil on serum lipids, however, it is probably related to its fatty acid composition, which is high in MUFAs and PUFAs, particularly ALA (13). It has been shown that a higher amount of ALA intake can increase insulin secretion, improve insulin sensitivity, and lipoprotein lipase activity, leading to serum TG reduction (14). Moreover, the PUFA content of canola oil can down-regulate the VLDL-c and apolipoprotein-B100 synthesis, which can lower serum TG concentrations (12, 15). Previous studies have reported that a dietary pattern with a higher amount of PUFA can decrease serum LDL-c and TC, but not TG and HDL-c (16, 17). In the present study, canola oil supplementation caused a marginally significant reduction in the LDL-c and TC concentrations (Table4). In line with our findings, Salar et al. in a clinical trial showed that canola oil at the dose of 30 g/day decreased serum LDL-c more than sunflower oil, a poor source of ALA (18). Furthermore, in the Sacks et al.'s trial, they found a significant decrement in serum levels of LDL-c and TC/HDL ratio following the replacement of SFA by canola oil (19). We found that canola oil consumption led to a significant reduction in TC/HDL, LDL/HDL, and TG/HDL ratios, which are known as the main predictors of CVD (20). It has been reported that a higher intake of canola oil can reduce the risk of coronary heart disease and all-cause and cardiovascular mortality due to its PUFA content (13).
We were unable to find any significant reduction in lipid profile regarding the olive oil consumption. The results of some previous studies are in contradiction with our findings. Jamal et al. in an RCT evaluated the effect of olive oil on lipid profiles and blood glucose levels in type 2 diabetic patients. They found that olive oil in a dosage of 30 mL/day caused a significant decrease in serum levels of TG, TC, and LDL- c (21). Venturini et al. in their clinical trial found that extra virgin olive oil (20 mL/day) in combination with fish oil (3 g/day) could decrease serum levels of TC and TC/HDL-c and LDL-c/HDL-c indexes (22). Also, it has been reported that extra virgin olive oil in a dosage of 4 g/day in mildly hypocholesterolemic participants was associated with favorable changes in plasma lipid profile (23). In a recent meta-analysis, researchers reported that olive oil cause a significant reduction in serum levels of TC, LDL-c, and TG (24). The mechanisms by which olive oil can exert its beneficial antioxidative effect can be clarified by polyphenol activity or through the cumulative protective effect of both its polyphenols and MUFA content (25).
The lack of beneficial effects of olive oil on blood lipids may arise for some reason. Olive oil contains more SFA than canola oil that can impair the lipid profile. Besides, the n-6/n-3 ratio is higher in olive oil than that of canola oil (58). Several studies have illustrated that a higher intake of n-6 PUFA increases the risk of CVD and it is independently associated with elevated serum TC and TG (26).
In the present study, we showed that both olive and canola oils could decrease fatty liver severity, however, no significant difference was observed between them. In agreement with our finding, Nigam et al. in an interventional study including 93 males with NAFLD showed that consumption of olive oil and canola oil at the dose of 20 g/day led to a significant decline in fatty liver grade and other NAFLD risk factors (27). In another study, Kruse et al. compared the efficacy of canola oil and olive oil on hepatic steatosis in obese men. In their study, 27 obese men consumed 50 g/day of either canola or olive oils for 8 weeks and results showed that canola oil compared to olive oil caused a greater reduction in hepatic steatosis (28).
Dietary ingredients, especially the type and amount of fats, are important in the deposition of liver fat and are responsible for 15% of the liver fat content. Dietary fat can exacerbate hepatic steatosis in both direct and indirect pathways via influencing the adipose tissues (29). The positive effects of olive oil on hepatic fat content can be clarified by the faster oxidation of MUFAs than SFA in the postprandial phase (30). For instance, consumption of diets rich in MUFA (28% to total calories) for 8 weeks by patients with type 2 diabetes reduced liver fat by 30%, and this decline was associated with augment of postprandial β oxidation of fatty acids (31). Similarly, Errazuriz et al. in an RCT showed that high MUFA intake (28% Calorie, half as olive oil) in prediabetes patients for 12 weeks lowered hepatic fat and improved hepatic and total insulin sensitivity (32). Additionally, a high-MUFA diet boosts lipoprotein lipase activity more than a diet rich in SFA which leads to enhanced clearance of circulating triglyceride-rich lipoproteins (33). Also, a higher amount of MUFA and ALA in canola oil can exert beneficial effects against fatty liver by the improvement of insulin sensitivity, glucagon-like peptide-1 responses, and up-regulation of glucose transporter-2 expression in the liver of insulin-resistant participants (34). Besides, a higher intake of MUFA and ALA can increases lipid oxidation, inhibits hepatic triacylglycerol synthesis, and decreases insulin resistance (35).
In our study, we included only women. As mentioned, there is a sex difference in the conversion of ALA to EPA and DHA that is higher in women than in men. It has been reported that females had higher erythrocyte phospholipid EPA, lower adipose tissue EPA and higher plasma DHA content. Previous studies showed that there is an inverse relationship between the menopausal status of women and the age of female participants with the change in plasma EPA content after olive oil supplementation (36, 37). A part of the inconsistency in our results compared to other studies could be due to these reasons.
We have not found any significant effect from the sunflower oil on lipid profile and Fatty liver severity. Sunflower oil is a rich source of omega-6 fatty acids. Previous studies have shown that a high intake of foods rich in omega-6 fatty acids can exacerbate inflammation and liver damage. Due to the dietary pattern of the Iranian people and the cheapness of sunflower oil compared to olive or canola oil, most people, especially middle-income or low-income families, use this type of oil in their food preparation.
As a strength of our study, its design as a randomized clinical trial to assess three types of conventional oils from different sources can be mentioned. We encountered some limitations in our investigation. The main limitation of this study was the method of fatty liver evaluation. Ultrasound is not very accurate to detect mild cases of the fatty liver compared to the fibroscan method. Also, we couldn't measure the ALA, EPA, and DHA content of erythrocyte membranes as a good indicator of participants' adherence.