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.