2.6.1. Nutrients

A 100 g serving of uncooked corn kernels provide 86 calories; it contains 3.27 g of proteins, 18.7 g of carbohydrates, 2 g of fibers, 6.26 g of sugars, and 1.35 g of fats, of which 26% of saturated fatty acids, 39% of polyunsaturated fatty acids, and 35% of monounsaturated fatty acids. Raw maize is a good source of group B vitamins, particularly niacin (11% of DV), riboflavin (4% of DV), thiamine (13% of DV), and vitamin B6 (7% of DV). Raw maize is also a good source of several dietary minerals, especially copper (6% of DV), iron (3% of DV), magnesium (9% of DV), manganese (7% of DV), phosphorus (13% of DV), potassium (6% of DV), zinc (4% of DV), selenium (1% of DV), and sodium (1% of DV) [21].

#### 2.6.2. Maize Oil

Corn oil (corn oil, CO) is obtained by extraction from the corn germ. It is mainly used in the kitchen, thanks to its high smoking temperature, which makes corn oil suitable for frying. It is also a staple ingredient in margarine production. It is also used as an excipient in the pharmaceutical industry [20].

A total of 100 g of maize oil contains 13% of saturated fatty acids, of which 82% is palmitic acid (C 16:0) and 14% is stearic acid (C 18:0); 28% of monounsaturated fatty acids, of which 99% is oleic acid (C 18:1); and 55% of polyunsaturated fatty acids, of which 98% is linoleic acid (C 18:2), and 2% is omega-3 linolenic acid (C 18:3) [21,60].

#### 2.6.3. Corn Oil vs. Extra-Virgin Olive Oil

Unlike CO, whose production takes place through the solvent extraction of the oil from the grain after the separation of the corn germ with fragmentation or centrifugation, the production of olive oil takes place essentially by mechanical pressing of the drupe. A 100 g serving of extra virgin olive oil (EVOO) provides 884 calories. Almost 98% of the total weight of EVOO is represented by fatty acids, which constitute the saponifiable fraction of olive oil. The fatty acid content of EVOO consists of 75% monounsaturated fatty acids (mostly oleic acid), 11% polyunsaturated fatty acids (mostly linoleic acid), and 14% saturated fatty acids (mostly palmitic acid) [20,21]. The remaining 2% of the total weight of EVOO is represented by the unsaponifiable fraction. The stability and flavor of olive oil are given by the components of the unsaponifiable fraction.

The unsaponifiable fraction is divided into the non-polar, non-water-soluble, solventextractable fraction after saponification of the oil, which contains squalene and other triterpenes, sterols, tocopherol (mainly alpha-tocopherol, or vitamin E), and pigments, and the polar fraction, water-soluble, which contains phenolic compounds, or polyphenols.

Polyphenols make up 18–37% of the unsaponifiable fraction of EVOO; these are responsible for most of the health benefits associated with taking EVOO. It is a heterogeneous group of molecules with important properties that are both organoleptic and nutritional [21]. Extra virgin olive oil has an average concentration of phenolic compounds of about 230 mg/kg [61], with a concentration of polyphenols ranging from 50 to 800 mg/kg [62,63]. The absorption efficiency of olive oil polyphenols in humans has been evaluated around 55–66 mmol% [64]. Tyrosol and hydroxytyrosol are two of the most important phenols in olive oil. Hydroxytyrosol is present in olive oil in the form of ester with elenolic acid to form oleuropein; the absorption in humans is dose-dependent, related to the phenolic content of olive oil [65].

2.6.4. Poly- and Monounsaturated Fatty Acids, Serum Cholesterol Levels and Cardiovascular Disease

A meta-analysis by Mensink et al. [66] showed that under isocaloric, metabolic ward conditions, when carbohydrates in the diet were replaced by fatty acids, HDL increased and triglycerides decreased, while LDL increased. In addition, if polyunsaturated fats replace saturated fats, then a more marked decrease in serum LDL and triglyceride levels was observed. Authors also showed that replacing saturated fatty acids with unsaturated fatty acids increased the ratio of HDL to LDL cholesterol, thus obtaining the most favorable lipoprotein risk profile for CHD. Substitution of saturated fatty acids with carbohydrates had no favorable effect on the CHD risk profile.

Subsequently, Maki et al. [67], in their randomized, double-blind, controlled-feeding trial, showed that CO reduced total cholesterol (TC), low-density lipoprotein cholesterol (LDL), very low-density lipoprotein cholesterol (VLDL), non-high-density lipoprotein cholesterol (non-HDL), and ApoB concentration to a greater extent compared with EVOO intake (CO compared with EVOO intake: TC = −0.37 vs. 0.02 mmol/L, *p* > 0.001; LDL = −0.36 vs. −0.08 mmol/L, *p* > 0.001; VLDL = −0.03 vs. 0.04 mmol/L, *p* > 0.001; non-HDL = −0.39 vs. −0.04 mmol/L, *p* > 0.001). ApoB, an indicator of circulating small and dense, and therefore highly atherogenic, LDL, was lowered largely by CO, compared to EVOO intake ( −9.0 vs. −2.5 mg/dL, *p* > 0.001). HDL-C concentration did not differ significantly between CO vs. EVOO intake (0.02 vs. 0.05 mmol/L, *p* = 0.112), but ApoA1, which is the major protein component of HDL particles in plasma, increased more with EVOO compared with CO intake (4.6 vs. 0.7 mg/dL, *p* = 0.016).

The Nurses' Health Study [68] prospectively investigated the association between different types of dietary fat intake and the risk of coronary heart disease in a 14-year followup in a cohort of 80,082 women, aged between 34 and 59 years of age, without a history of CHD, stroke, cancer, hypercholesterolemia, or diabetes. The authors demonstrated that a 5% increase in energy intake from saturated fat was associated with a 17% increase, although not statistically significant in the relative risk (RR) of CHD (RR = 1.17; 95% CI = 0.97–1.41; *p* = 0.10) compared to the equivalent energy intake from carbohydrates. The authors also demonstrated that for each 2% increase in energy intake from transunsaturated fats, a significant 93% increase in the risk of CHD was associated (RR = 1.93; 95% CI = 1.43–2.61; *p* = 0.001). Finally, the authors demonstrated that while for each 5% increase in energy intake from monounsaturated fats, there was a non-statistically significant 19% decrease in the risk of CHD (RR = 0.81; 95% CI = 0.65–1.00; *p* = 0.05); with each 5% increase in energy intake from polyunsaturated fats, there was a significant 38% reduction in the risk of CHD (RR = 0.62; 95% CI = 0.46–0.85; *p* < 0.003). The authors also showed that replacing 5% energy from saturated fat with unsaturated fat resulted in a 42% reduction in CHD risk (95% CI = 0.23–0.56; *p* < 0.001), while replacing 2% of energy from trans unsaturated fat with un-hydrogenated, unsaturated fats was associated with a 53% decrease of the risk of CHD (95% CI = 0.34–67; *p* < 0.001). The authors concluded by confirming that the replacement of saturated fats (SF) and trans-unsaturated fats in the diet with non-hydrogenated monounsaturated and polyunsaturated fats favorably alters the lipid profile, but that reducing overall fat intake has little effect.

W. C. Willett [69] confirmed these data in a subsequent review by concluding that trans-unsaturated fatty acids in hydrogenated vegetable oils have obvious negative effects and should be eliminated. He also stated that a further reduction in CHD rates is possible if saturated fats are replaced by a combination of poly- and monounsaturated fats and the benefits of polyunsaturated fats appear stronger.

A subsequent pooled analysis of 11 cohort studies by Jakobsen et al. [70] confirmed the effects of the polyunsaturated fatty acids. The authors showed a significant association between PUFA replacement and reduced risk of coronary events (HR: 0.87; 95% CI: 0.77, 0.97) and a significant association between PUFA replacement and reduced risk of mortality for CHD (HR: 0.74; 95% CI: 0.61, 0.89). In conclusion, the authors stated that, rather than increasing the consumption of MUFA or carbohydrates, increasing the consumption of

PUFA in place of saturated fatty acids (SFA) could significantly prevent coronary heart disease among middle-aged women and men and among the elderly.

Lai et al. [71] investigated the associations between de novo lipogenesis (DNL)-related fatty acids (FA) with total mortality and specific cause mortality including cardiovascular disease (CVD), CHD, and stroke, analyzing the data from the Cardiovascular Health Study (CHS) [72], measured at three time points over 13 years. Surprisingly, they found a direct association between higher oleic acid levels (18: 1n-9) and a high risk (hazard risk, HR) of all-cause mortality (HR = 1.56, 95% CI = 1.35–1.80, *p* < 0.001) including CVD and non-CVD mortality (HR = 1.48, 95% CI = 1.21–1.82, *p* < 0.001; HR = 1.50, CI = 95% 1.28–1.75, *p* < 0.001, respectively). They also found an association between higher oleic acid levels and fatal and non-fatal CVD, fatal and non-fatal CHD, fatal and non-fatal stroke (HR = 1.33, 95% CI = 1.12–1.57, *p* < 0.001; HR = 1.23, 95% CI = 1.01–1.48, *p* = 0.008; HR = 1.34, 95% CI = 1.02–1.75, *p* = 0.005, respectively).

Results of a meta-analysis by Borges et al. [73], which included five cohort studies and one matched case-control study, involving 23,518 subjects, showed that the risk (odds ratio, OR) of CHD was lower with higher circulating docosahexaenoic acid (DHA) levels (OR = 0.85; 95% CI = 0.76–0.95), but was not associated with stroke risk (OR = 0.95; 95% CI = 0.89–1.02); risk of stroke was lower with higher circulating linoleic acid (LA) levels (OR = 0.82; 95% CI = 0.75–0.90), but was not associated with CHD (OR = 1.01; 95% CI = 0.87– 1.18); circulating MUFA were associated with higher CHD risk of stroke (OR = 1.22; 95% CI = 1.03–1.44) and CHD (OR = 1.36; 95% CI = 1.15–1.61). SFA was not related both with increased CHD risk (OR = 0.94; 95% CI = 0.82–1.09) and with stroke risk (OR = 0.94; 95% CI = 0.79–1.11).

Finally, Lee et al. [74] studied the associations between plasma AF levels with the risk of incident heart failure (HF) by analyzing data from CHS. They showed that plasma habitual levels and changes in the levels of palmitic acid (16:0) were associated with higher risk of HF (HR = 1.17, 95% CI 1.00–1.36; HR = 1.26 95% CI 1.03–1.55, respectively); plasma habitual levels of 7-hexadecenoic acid (16:1n-9) were not associated with risk of HF (HR = 1.05, 95% CI 0.92–1.18), but changes in levels were associated with a higher risk of HF (HR = 1.36, 95% CI 1.13–1.62); plasma habitual levels of vaccenic acid (18:1n-7) were not associated with risk of HF (HR = 1.06, 95% CI 0.92–1.22), but changes in levels were associated with a higher risk of HF (HR = 1.43, 95% CI 1.18–1.72); habitual levels and changes in levels of myristic acid (14:0) (HR = 0.90, 95% CI = 0.77–1.05; HR = 1.11, 95% CI = 0.91–1.36, respectively), palmitoleic acid (16:1n-7) (HR = 1.01, 95% CI = 0.88–1.16; HR = 1.06, 95% CI = 0.87–1.28, respectively), stearic acid (18:0) (HR = 0.94, 95% CI = 0.81– 1.09; HR = 0.94, 95% CI = 0.76–1.15, respectively), and oleic acid (18:1n-9) (HR = 1.13, 95% CI = 0.98–1.30; HR = 1.13, 95% CI = 0.93–1.37, respectively) were not associated with HF risk,

Despite these conflicting results, the advice to replace saturated fats with polyunsaturated fats in the diet remains a cornerstone of international guidelines for reducing the risk of CHD.

On the other hand, it would be overly simplistic to say that replacing SFAs with MUFA (oleic or linoleic acid) or PUFA may be sufficient in reducing the risk of CVD or mortality risk. The benefits of taking MUFAs are observed when they are associated with the concomitant intake of polyphenols and other natural antioxidants, contained, for example, in EVOO. In fact, there is no evidence to sugges<sup>t</sup> that simply replacing SFA with MUFA reduces the risk of CVD or mortality. Similarly, the benefits of daily intake of PUFA-n3 are attributable to PUFAs, but above all where they are associated, similarly to MUFAs, with the intake of polyphenols or other natural antioxidants, and as part of a healthy diet such as the traditional Mediterranean diet. All the above-mentioned studies are shown in Table 2.


**Table 2.** Poly- and monounsaturated fatty acids, serum cholesterol levels, and CVD. **Table 2.** *Cont.*


CO: corn oil; EVOO: extra virgin olive oil; CHD: coronary heart disease; LA: linoleic acid; HF: heart failure
