Discussion
Results of this meta-analysis showed an inconclusive association between deteriorated vegetable oils and adverse health effects. Other plant oils such as PO, CNO, CO, EVOO, and SBO did not display any form of health complications except for SFO which was found to have a positive association with obesity and oxidative stress biomarkers. One of the studies in Figure 2; Famuwera et al. (2017) displayed a considerable change in the plasma lipid profile of rats especially in the serum LDL-C level followed by chronic consumption of a 15 %-oxidized palm oil diet that was prepared through continuously heating for 5 days at 180 ℃, 10 min every day. The mean difference of -0.80 between the intervention and control group proved that heated PO was concordant with the elevated levels of serum LDL-C. Changes in lipid serums TC, TG, LDL-C, and VLDL-C in rats have been related to the increase in the risk of cardiovascular diseases including atherosclerosis, hypertension, and neurodegeneration for decades. Nkanu et al. (2017) had the second-largest weight (11.7 %) also reported a 104 % increase in serum LDL-c when thermally HPO was incorporated into the diet. However, its point estimate of effect was situated on the right, which favoured the control group. It was important to note that the latter study has a longer intervention duration of 16 weeks as opposed to the former study with only 28 days. Furthermore, Nkanu et al. (2017) had a larger weight as it offers more vital information therefore being closer to the underlying true effect. Other studies that were not mentioned were either situated on the line of null effect hence being statistically insignificant or contribute 0 % weight to the pooled effect estimate. Based on the test of the overall effect, this comparison was statistically significant as atherosclerosis, obesity, and hypertension were not interrelated with consumption of HPO. There was insufficient evidence to prove the impact of HPO on obesity and weight gain. Odia et al. (2015) recently has proven that fresh palm oil consumption can prevent the heart and blood vessels from the plague, ischemic injuries, and a reduced risk for cardiovascular diseases. However, this suggestion was in opposition to a meta-analysis relating palm oil consumption with heightened LDL-cholesterol (Sun et al., 2015). The rationale of functional alteration in blood vessels can be due to the depletion of antioxidants in oxidized oil.
The was one study that managed to fulfill all inclusion criteria by using CNO as the sample. According to Bautista et al. (2014), CNO was heated for one frying cycle and ten frying cycles at 190 ℃. After 10 weeks of follow-up, Wistar rats were found to have a noticeable increase in adipose tissue as well as early signs of endothelial dysfunction induced by toxic compounds such as peroxynitrite the consumption of repeatedly heated oil (1 and 10 frying cycles). Dyslipidemia including hypertriglyceridemia and hypoalphalipoproteinemia are often related to the increase in abdominal adipose tissue due to the appearance of an abnormal amount of lipids in the blood (Eringa et al., 2013). Interestingly, the caloric consumption of repeatedly heated CNO was higher than fresh CNO because raw oil was less desirable than HCNO due to the absence of organoleptic characteristics. Despite that, the point effect of estimate and overall effect estimate (5.50[95% CI:4.12, 6.87]) favours the control group and suggested that consumption of HCNO in the diet had no deleterious effect on weight (P < 0.00001). A recent reported SR-MA revealed that body fat markers or related anthropometric measures were not significantly affected (P > 0.05) by consumption of CNO. The findings suggested that a modest decrease in body weight indeed as the PUFAs present in CO can regulate proliferation, differentiation, and apoptosis of adipocytes, causing an alteration in genes that increases fat oxidation and reduces fat deposition (Buckley and Howe, 2010).
Data of vasodilation response were taken from (Das et al., 2017) to investigate the adverse effects of corn oil in one, five, and ten frying cycles. Vasodilation is the widening of blood vessels as a result of the relaxation of the blood vessel muscular walls. Vasodilation is a relaxation mechanism in smooth muscle cells of arteries that increases blood flow. Vasodilation is proportional to blood pressure; as the arteries and arterioles dilate, an immediate decrease in blood pressure will be imposed (Wieling et al., 2016). The percentage of vasodilation was significantly lower in the aortic rings of 1 frying cycle of HCO (88.49%±7.91), 5 frying cycles of HCO (68.15%±3.70), and 10 frying cycles of HCO (63.44%±6.91) when compared to the control (105.54% ±9.76) and fresh CO (101.54%±3.72) groups (P < 0.05). In addition to that, the percentage of vasodilation was significantly lower in 5 and 10 frying cycles of HCO compared to 1 frying cycles of HCO (P < 0.05). Based on previous studies, oxidative stress and vascular inflammation which was involved in cardiovascular diseases including hypertension was observed in HCO (Korkmaz et al., 2013). A reported study postulated that atherosclerotic lesion scores for fatty plaques, fatty streaks, and fibrous plaque scores were significantly higher in rabbits that were treated with HCO. Rabbits were also found negative in terms of weight gain as HCO had higher unsaturation (Deen et al., 2021), therefore, more likely to be oxidized and less palatable, causing a reduction in feeding efficiency (Idris et al., 2018). However, Figure 4 shows none of the studies were statistically significant as the point effect of the estimate were on the line of no effect and could be confirmed by the test of overall effect (P = 0.82). We observed a lack of clinical trials that incorporates corn oil into diets which indicates a need for more research papers in order to truly establish the effects of CO on human health. The physicochemical properties of CO are superior in terms of bioactive compounds and oxidative stability, it is highly refined and high in inflammatory n -6 fatty acids which outweighs its beneficial effects.
Olive oil consists of 85 % of the types of fats consumed in the Mediterranean diet whose consumption is related to a lowered risk of cardiovascular diseases, cancer, and Alzheimer’s disease. An in vivo study by (Ghorbel et al., 2015) suggested the protective effects of EVOO on hepatoxicity due to the decrease in liver damage induced by aluminum and acrylamide. Furthermore, a 40 % (P < 0.05) relative risk reduction and nonsignificant 18 % risk reduction in Type 2 Diabetes was discovered through the intervention group that consumed a Mediterranean diet that was supplemented with EVOO compared to the control diet group. The forest plot in Figure 4 (P = 0.003) was in agreement with both studies above. The susceptibility of cells is influenced by the composition of fatty acids as it is able to alter the cell membrane’s fatty acids. Cells enriched with MUFAs present in EVOO have been shown to be less vulnerable to damage caused by oxidation. Furthermore, MUFAs in EVOO is associated with a lowered risk of coronary heart disease and thereby inducing a desirable effect on health. In investigating the relationship between consumption of foods fried by olive oil and incidence of weight change and obesity in a Mediterranean prospective cohort study, subjects who used olive oil for frying purposes gained slightly lesser weight and showed the lesser risk of obesity compared to other oil types. However, the effects were minor, as explained by the mean difference of 0.50[95% CI: 0.31, 0.69]. As food items are being fried in high heat, it absorbs a large amount of oil and becoming a major nutritional critical point by increasing the fat content and calories. However, it is an additive, leading to people consuming them in large amount at one sitting unknowingly. EVOO has reported to only suffered from a loss of tocopherol and phenolic compound from a sixty minutes frying procedure but not a fatty acid pattern change. One of the statistically significant studies which its point estimate of effect favours the control group suggested that TBARS increased, not from the fatty acid composition change but through the loss of antioxidants and a heightened number of toxic compounds. Even so, a stable source of oil like EVOO is also susceptible to crucial oxidative modifications that will impose health effects on both structure and function of organs. Despite the accessibility of an array of epidemiological and experimental evidence tying the benefits of consumption of EVOO in limiting certain pathologies, the toxicological hazards related to thermally oxidized EVOO is still severely lacking.
The composition of SFO consists of approximately 86 % of polyunsaturated and monosaturated fatty acids causing a significantly lower thermal stability. It is especially susceptible to heat, air, and light which accelerates SFO oxidation. SFO was reported to lose up to 76 % of tocopherols and reached > 25 % of total polar compounds (TPC) during a frying process (Wiege et al., 2020; Juarez et al., 2011). Thermal alterations were prevalent in HSFO including more than 10 % increase of polymeric and dimerized triacylglycerols. Among the listed vegetable oils, only HSFO proved to cause obesity and oxidative stress (P < 0.0001). Food efficiency ratio was lower in diets with fresh SFO than HSFO, as the palatability was acceptable when the TPC was between 25 – 30 %. Not only that, polyaromatic hydrocarbons (PAHs) are known as one of the carcinogenic compounds with mutagenic properties that are formed and accumulated during thermal deterioration. Other toxic components formed during the heating of oil such as MDA and TBARS are reliable lipid peroxidation markers in rats. GSH is known as one of the scavengers of reactive oxygen species (ROS) and the GSH/GSSG ratio is included as one of the oxidative stress markers in this comparison as it is directly proportional to biological redox status (Zitka et al., 2012; Pawelczyk et al., 2017). A consumption of a meal rich in lipids or carbohydrates that increases the susceptibility of oxidative damage that is caused by the imbalance of ROS and antioxidant system is known as the postprandial oxidative state. A randomized crossover human study that has the second largest weight on this comparison table (17.4%) explained that the increased ingestion of ROS from deep-fried breakfast causes a significant damage to molecules in the organism, leading to inflammation process and initiation of atherosclerosis through the oxidation of LDL, vasoconstriction and thrombogenicity. Unfortunately, this was the only study that has its horizontal line of 95 % CI crossing the line of no effect, suggesting the difference between the control and intervention group was not statistically significant. Due to the small number of studies included in this meta-regression, this interpretation was still tentative, yet it further insinuates that HSFO can cause overweight and oxidative stress.
The UC Riverside Research team postulated that SBO was related to obesity, diabetes, and impose adverse effects on neurological conditions such as autism, Alzheimer’s diseases, and depression. Both of the modified and non-modified SBO had a similar effect on the brain pronounced on the hypothalamus. With the research on male rats, the oxytocin levels were found to be reduced after the ingestion of SBO (Deol et al., 2020). Besides, the intervention group of mice fed with HSBO was found a significantly lower liver α-tocopherol, but the liver TBARS levels were significantly higher than the groups consuming fresh SBO. This finding was following several reported studies suggesting oxidized frying oil to compromise antioxidant status in tissues (Liao et al., 2005). Peroxisome proliferator-activated receptor (PPAR)-α is a type of nuclear receptor that is activated by ligand transcriptional factor. PPAR-α oversees regulating the expression of genes in organisms taking part in fatty acid β-oxidation and plays a vital role in energy homeostasis. PPAR-α agonists have demonstrated their anti-inflammatory and anti-thrombotic actions in previous research that prevents atherosclerosis events to worsen through altering its metabolic risk factors, reducing atherosclerotic plaque formation and the probability of coronary heart disease (CHD), especially in metabolic syndrome (Van Ruth et al., 2010). The study with a mean difference of 5.30[95% CI: 2.77, 7.83] showed that ingestion of HSBO by maternal mice not only affects hepatic PPAR-α activity but carries on to its offspring in adulthood as well. In addition, a significant and steady increase (P < 0.05) in blood pressure was observed since from the first month until the end of intervention duration in rats fed with 5 and 10 frying cycles of HSBO samples by 20 % and 33 %, respectively, compared to the control group. In contrast, this increment was not observed in the control group and fresh SBO group. This result was in agreement with a study by (Leong et al., 2008) suggesting an increase in blood pressure was in conjunction with prolonged consumption of heated vegetable oil.
Deep frying induces flavours which is described as fruity, nutty, buttery, burnt, and grassy. These flavour notes depend on the type of oil and the number of frying times, but it is not affected by the frying temperature. The subtle taste of these aromas is due to the oxidation of linoleic acid present. When the oxidation increase, a fishy odor can be generated and desirable notes degraded. This, the oil is deteriorated and not suitable for consumption. A palatable and desirable fried flavour is commonly produced at the optimal concentration of oxygen, as poor and weak flavour is produced when there is low concentration of oxygen and vice versa, off flavours are produced in high levels of oxygen which agrees with studies included in this meta-regression as well as previously reported studies (Burenjargal and Totani, 2008; Totani and Ojiri, 2007). Volatile compounds from linoleic or linolenic acids such as dienal, alkenals, lactones, and hydrocarbons contributes to the fried flavour compounds. Antioxidant mechanisms present in vegetable oils including tocopherol and tocotrienols are retained in refined vegetable oils with a modest loss of 30 % of antioxidants during the deodorization phase. However, these antioxidant contents dissociate rapidly and completely during oil oxidation and become less effective during high temperatures. In addition, carotenes are unable to exhibit protective effects on oils in the absence of other antioxidants. Carotene works synergistically together with tocotrienols as it is able to regenerate carotenes from its radicals. This effect has been observed during the frying of potato slices at 163 ℃. Lignan compounds were found to be much more effective during deep-fat frying (Fan and Eskin, 2015). Free fatty acid (FFA) is another factor that increases the vulnerability of oil to oxidation. The amount of unsaturation in FFA influences the oxidative stability of oil tremendously rather than its chain length. Significant effects have been seen on the thermo-oxidative degeneration in plant oils that concedes with a recent study done by (Sayyad, 2015) that claimed the frying performance of SFO was determined by the content of linoleic acid rather than the composition of tocopherol.