Why is it called virgin olive oil

4.3 Natural Juice of the Olive, Why Extra-Virgin?

The olive tree Olea europea L. is one of the oldest agricultural tree crops and source of olive oil and olives. Agronomic and technological aspects of the olive oil production such as the processing system, ripeness of the olives at harvesting, climate, or cultivar characteristics like use of irrigation have a direct impact in the concentration of minor components of olive oil. Only oils obtained by mechanical extraction and that have not undergone any treatment other than washing, decantation, centrifugation, or filtration are called virgin olive oils. Extra-virgin oil would have even further quality assessment. Oils differ in bioactive composition depending on refining process. Specifically, phenolic compounds and to lesser degree squalene are lost during refining process and only are present in virgin and extra-virgin olive oil.

So, not all olive oils that are in the market are equal. Depending on the manufacturing process, we can found different types of oil:

Virgin olive oil: obtained directly from the ripe fruit by mechanical procedures. It is the only consumed raw without the use of any solvents, so it keeps all its properties intact. Olive oil has excellent antioxidants such as polyphenols and vitamin E, which are lost if the oil is subjected to refining processes. “Extra-Virgin” olive oils are those that have no taste defects and have a very low acidity rate (<0.8%). They are the most expensive ones. Those labeled as “Virgin” olive oils have modest taste defects and a slightly higher acidity level (<2%).

Pure olive oil: which is a blend of refined olive oil and virgin olive oil. In the market, there are varieties of intense flavor and mild taste depending on whether more or less virgin oil olive is added, respectively.

Olive pomace oil: which is obtained from the pulp and seeds of olives after extraction of virgin olive oil using chemical solvents. It must pass a refining process and virgin olive oil is added after to make it suitable for consumption.

Abstract

Virgin olive oil is considered a key component of the Mediterranean diet, being the main source of dietary lipids. Squalene is a terpenoid hydrocarbon found at high concentration in virgin olive oils; it represents their main minor component. Thus squalene is a naturally occurring lipid component consumed by humans as an integral part of a healthy diet. It is recognized as a functional compound of high importance because of its beneficial effects on human health. It could be partially responsible to the health benefits attributed to virgin olive oil. Squalene has several beneficial properties: it is a natural antioxidant, it decreases serum cholesterol concentrations, and it possesses photoprotective, tumor-protective, and cardioprotective properties. Consequently, adequate intake of virgin olive oil provides a continuous supply of squalene, which is considered a remarkable bioactive substance with several interesting biological activities, and it might be sufficient to achieve the health benefits described above.

Olive Oil

Virgin olive oil is a cornerstone of MeD. Although it is a fat, olive oil contains a unique pattern of MUFAs and PUFAs united to a variety of polyphenols (mainly oleuropein aglycone and oleocanthal) that have shown promising results in experimental AD models (Rigacci, 2015). It seems that the polyphenols associated with this plant-derived product could also ameliorate patient lipid profile by reducing LDL and increasing HDL cholesterol and preventing atherosclerosis, maybe due to their capacity to contain lipoprotein oxidation (Hernáez et al., 2014, 2015). Few randomized controlled trials correlate virgin olive oil intake with improved cognitive function (Martínez-Lapiscina et al., 2013; Valls-Pedret et al., 2015), but evidence is still insufficient to determine the real impact of virgin olive oil supplementation.

4.10.1 Antibacterial properties

VOO has shown broad spectrum bactericidal activity against a large number of Gram positive and Gram negative, aerobic and anaerobic, and intracellular and extracellular bacteria (Table 1) [126,208,209]. Bactericidal activity was correlated with VOO biophenol content. Refined olive oil, stripped from biophenols, showed no antibacterial activity. VOO was more potent bactericidal than any of its individual biophenols [208]. The antibacterial activity of VOO depends on its biophenol composition. Synergistic actions have been also noticed. Hence, not all VOO's are expected to have similar antibacterial effects. The major contributors to antibacterial activity of VOO were found to be the dialdehydic form of decarboxymethyl ligstroside aglycone and cinnamic acid [208,209]. The antibacterial activity of VOO depends not only on biophenol composition but also on the pH and time of exposure [221]. In atopic dermatitis, VOO eliminated Staphylococcus aureus infection in 6 of 12 patients (50%) [210]. OFX, OMW, and table olives extracts possess broad spectrum in vitro antibacterial activity (Table 1). HT and OL have been extensively investigated for their antibacterial activities (Table 1). HT shows potent broad spectrum antibacterial activities (minimum inhibitory concentration MIC = 0.03–31 μg/mL). OL is less potent than HT and shows a narrower spectrum of antibacterial activity and TY and VB demonstrated intermediate in vitro antibacterial activity in few studies [217,222–224]. Generally, olive extracts were more effective antibacterial than individual biophenols. Synergistic activities have been reported for biophenol combinations and with other antibiotics [208,213,222]. No clinical or in vivo reports were found on OBP antibacterial activity. The antibacterial mechanism of action of OBP has not been thoroughly investigated though they are known to penetrate cell membranes of both Gram negative and Gram positive bacteria causing damage to the peptidoglycans and cell membrane structure [217,225].

Table 1. Antibacterial activity of olive products and OBP

Resistance to Thermal Oxidation of Olive Oil During Frying or at Frying Temperatures

VOO displays great stability when used for frying and other culinary purposes [3,6,7]. Dobarganes and Márquez-Ruiz [6] reported that frying olive oil displays fewer alterations than frying seed oils. Unpublished data from our group suggest that this Rancimat induction period was high but clearly distinct in three Picual olive oils differing in their polyphenol and tocopherol concentrations. Our group found that heating olive oil at 180 °C, despite whether in presence of extracts that were very rich in nonextractable tannins, produced lower thermal oxidation after 48 h than sunflower oil or a homogeneous mix of olive oil plus sunflower oil [30].

Compared with other vegetable oils such as sunflower, cotton, corn, and soybean oils, olive oil presents a lower degree of alteration, as demonstrated by measuring viscosity, polar material, and tocopherol losses (for a review see Sánchez-Muniz et al. [3,7]). A comparative study of the frying behavior of extra VOO, sunflower oil containing a large amount of oleic acid, and “conventional” sunflower oil used repeatedly to fry potatoes is presented in Figure 12. A plausible explanation for the resistance to rapid deterioration of extra VOO at high temperatures may be its fatty acid composition. The production of hydroperoxides and the generation of potentially toxic thermal oxidation compounds in the frying oil is lower with oleic acid than with linoleic acid. That, in turn, implies less uptake of such compounds by the food during frying and thus lower toxicity and healthier foods.

As already mentioned, VOO contains a large amount of minor compounds (α-tocopherol, squalene, and phenolic compounds such as diphenols, phenolic acid, and hydroxytyrosol) with powerful antioxidant capacity. VOO is rich in phytosterols, such as Δ5-avenasterol, a potent antipolymerizing agent [7,27]. Tocopherols undergo gradual degradation during frying or storage. Therefore, supplementation with phenolic compounds has been recommended to preserve the original level of tocopherols in the oil [3,7,25,27,30]. Our group has demonstrated that frequent additions of fresh oil or antioxidants lengthen the frying life of oil, helping to maintain the original quality of the oil because it dilutes the altered compounds and adds minor compounds with antioxidant and antipolymerizing properties. Nonetheless, current legislation in Spain and other countries permits only the addition of antioxidants (heading with VOO) to refined olive oil, not to VOO or extra-VOO.

Olive oil and VOO are more stable than other oils, implying that they can be used more often for frying than other extensively used oils before reaching the 22–25% polar material or the 10–12% polymers cutoff points [31] (Figure 13). Figure 12 shows less polymer formation in olive oil than in other oils during frying and therefore suggests the potentially lower toxicity of products fried in olive oil. Data in Figure 12 and Table 4 suggest that the shelf-life of frying oil depends on how frequently the oil is replenished. The alteration of polymer and cyclic monomer contents of different oils used to fry fresh potatoes and frozen prefried foods is summarized in Table 5. Frying fresh potatoes produces less alteration of the oil. Moreover, oils replenished frequently displayed less alteration than oils to which fresh oil was not added. In conclusion, the use of extra VOO for frying and the practice of frequent oil replenishment reduce oil and food alteration and therefore produce quality foods.

Table 4. Cyclic Monomer and Oligomer Contents of Oils Before and After Frying in Different Conditions Various Types of Foods

Modified from Sánchez-Muniz FJ. Oils and fats: changes due to culinary and industrial processes. Int J Vitam Nutr Res 2006;76:230–37. With permission, Verlag Hans Huber.

Table 5. Oil Addition and Alterations in the Frying Oil and in the Fat Extracted from Fried Foods

Modified from Sánchez-Muniz FJ. Oils and fats: changes due to culinary and industrial processes. Int J Vitam Nutr Res 2006;76:230–37. With permission, Verlag Hans Huber.

Phenolic Compounds

Virgin olive oil contains phenolic substances that affect its stability and flavor. Tyrosol (4-hydroxyphenethyl alcohol) and hydroxytyrosol (3,4-dihydroxyphenethyl alcohol) are usually mentioned as the major constituents. Other phenolic compounds are caffeic acid, o-coumaric acid, p-coumaric acid, ferulic acid, gallic acid, homovanillic acid, p-hydroxybenzoic acid, p-hydroxyphenylacetic acid, protocatechuic acid, sinapic acid, syringic acid, tyrosol glucoside, and vanillic acid. Aglycons of oleuropein and ligstroside, the esters of hydroxytyrosol and tyrosol with elenolic acid, diacetoxy and dialdehydic forms of these aglycons, elenolic acid, and flavonoids have been also reported to be present in the polar fraction of virgin olive oil (Figure 9).

The content in phenolic compounds differs from oil to oil (a few to more than 400 mg per kilogram of oil, expressed as caffeic acid). When the level exceeds 300 mg kg−1, the oil may have a bitter taste. However, a high polyphenol content appears to be beneficial for the shelf-life of the oil, and there is a good correlation of stability and total phenol or o-diphenol content. Among the various phenolic compounds tested for their contribution to the stability, hydroxytyrosol and caffeic acid were found to be the most potent antioxidants.

Dietary antioxidants present in exra virgin olive oil were found to increase the resistance of low-density lipoproteins to in-vitro or in-vivo oxidation experiments. According to a large number of reports, hydroxytyrosol is the most important biophenol of olive oil similar to the phenolic compounds encountered in green tea and in red wine. Oleuropein also presents valuable functional properties, but it occurs in olive oil only in trace amounts. It is found in abundance in olives and olive leaves. (See PHENOLIC COMPOUNDS.)

Nutrition

Dietary constituents were linked to PUD long before the discovery of H. pylori, with subsequent research demonstrating certain foods to be protective against H. pylori infection. Accordingly, nutrition is considered a key component of ulcer prevention and symptom management.

Meal timing influences PUD, with skipping breakfast11 and consuming large meals shortly before bedtime shown to increase the risk of PUD.12

Fruit and vegetable intake reduces the risk of developing ulcers, with epidemiological studies demonstrating that a diet high in plant-based fiber and vitamin A (e.g., carrots, spinach, mango, sweet potatoes, and apricots) helps protect against PUD.13 Flavonoids, compounds found throughout the plant world, have been found to be protective against H. pylori infection and are present in concentrated amounts in citrus, berries, onions, parsley, green tea, red wine, and dark chocolate.14 Sulforaphanes, which are phytochemicals found in vegetables such as Brussels sprouts, broccoli, cabbage, cauliflower, bok choy, turnips, and radishes, are also protective against H. pylori infection.15

Studies have specifically shown that virgin olive oil (30 g daily for 2 weeks) or broccoli sprouts (70 g a day for 8 weeks) have the ability to decrease and potentially eliminate H. pylori.15,16 Foods containing capsaicin (chili) have been shown to be protective against ulcers.17 Capsules of chilies (fruit of the plant genus capsicum) are reviewed in the botanical section of this chapter for acute symptom relief. Other common foods demonstrating protective effects against H. pylori include banana, honey, garlic, ginger, okra, pomegranate, and apple.18-24 There is likely synergy in ingesting combinations of these beneficial foods, a good example of “nutrition is medicine.”

Foods found to be associated with a reduced risk of Helicobacter pylori infection include fruits and vegetables rich in carotenoids (yellow, orange), flavonoids (purple and blue vegetables, red wine, and green tea), sulforaphanes (cruciferous vegetables, including cabbage and broccoli), olive oil, garlic, honey, apple, capsaicin (chili), and fermented foods rich in probiotics (yogurt, miso, aged cheese, and sauerkraut).

Milk increases PUD risk, likely due to increased stimulation of acid production.25 Nonetheless, fermented dairy products and other food with probiotics, such as yogurt, aged cheeses, and sauerkraut, have been shown to be protective against H. pylori.26,27

Evidence regarding coffee and caffeine, long thought to be risk factors for PUD, is lacking; however, they are known risk factors for reflux disease.

4.2.3 Coronary Heart Disease

Different randomized controlled trials have shown that virgin olive oil intake is associated with beneficial effects on cardiovascular risk factors, such as the lipid profile, blood pressure, inflammation, and thrombosis.1,32 Another study indicated that a daily intake of nuts (between 12.5% and 25% of total energy) increases the OA and MUFA serum phospholipid fraction in patients with T2DM39; this fact contributes to a decrease in coronary heart disease (CHD), lipid risk factors, and overall 10-year CHD risk.39 Moreover, a case-control study in Greece has reported a 47% lower risk of CHD, while 82% protection has been shown in a Spanish study in patients with a previous event.92,93 The results of a cross-sectional study suggested that the consumption of PUFA and MUFA may be associated with a lower coronary risk profile in a healthy population.94 Additionally, the European Prospective Investigation into Cancer and Nutrition in Italy (EPICOR) found a strong reduction in CHD risk among participants with a high intake of olive oil (approximately 30 g/day).95 The EPIC study also found a 22% lower risk and a 7% lower incidence of CHD for every 10 g/day of olive oil intake in the Spanish cohort9; moreover, they found a 25% lower CHD risk for every 10 g/day of olive oil intake in never alcohol drinkers.

On the other hand, a meta-analysis of clinical trials and prospective studies reported no association between circulating plasma concentrations of OA with coronary outcomes.96 However, in this meta-analysis, the authors did not include the different potential studies with positive results regarding the intake of MUFA, PUFA, and CHD risk.

Olive Oil

MUFA-rich olive oil is the main source of fat in the MedDiet. Virgin olive oil, produced by mechanically pressing ripe olives, contains multiple bioactive compound beyond MUFA, such as polyphenols, phytosterols and vitamin E [59]. Epidemiologic evidence suggests that olive oil consumption is inversely associated with CVD risk and all-cause and CVD mortality [60]. Recently, the PREDIMED trial revealed that a MedDiet enriched with EVOO decreased CVD risk by 30% [22]. Similarly, a beneficial effect has been demonstrated for intermediate phenotypes such as blood lipids, insulin sensitivity, glycemic control, and blood pressure [24,25]; use of an EVOO-enriched MedDiet was also inversely associated with new-onset T2D [26]. In a PREDIMED substudy, baseline total olive oil consumption, especially the EVOO variety, was associated with a significantly lower risk of CVD events (39%) and CVD mortality (48%), and for each increase of 10 g/day (two teaspoons) in EVOO intake, CVD and mortality risk decreased by 10% and 7%, respectively [61]. A recent meta-analysis concluded that epidemiologic studies consistently found an inverse association between olive oil consumption and stroke, but there were inconsistencies among studies regarding olive oil intake and CHD as the end-point [60].

Several studies have examined the antiinflammatory and vasculoprotective effects of olive oil compounds. In vitro studies have shown that oleic acid prevents endothelial activation by inhibiting the expression of leukocyte adhesion molecules [62], scavenging intracellular reactive oxygen species [63], or interfering with the activation of NF-κB, a key modulator of the inflammatory response [64]. In in vitro studies, Carluccio et al. showed that incubation of endothelial cells with oleic acid increased the proportion of oleate in total cell lipids while diminishing the relative proportions of SFA in association with endothelial antiinflammatory actions [62]. Oleic acid was able to reduce the inflammatory effects of SFA on human aortic endothelial cells by suppressing the incorporation of stearic acid into phospholipids [65]. Human LDL enriched in oleic acid lowered monocyte chemotaxis by 52% and reduced monocyte adhesion by 77%, compared with linoleic acid-enriched LDL, which increased oxidative stress [65]. Isolated LDL from healthy subjects who had consumed an oleic acid-rich diet for 8 weeks promoted a decrease in the expression of ICAM-1 [66]. Inflammatory markers, such as CRP, IL-6 and ICAM-1, were lower after both short-term (3 months) and long-term (2 years) consumption of olive oil-rich diets [67,68]. After consumption of EVOO (containing 1125 mg polyphenols/kg and 350 mg tocopherols/kg), as compared with refined olive oil (containing no polyphenols or tocopherols), there was a postprandial reduction in inflammatory mediators derived from arachidonic acid, such as thromboxane B2 and 6-keto-prostaglandin F1α [69], with a decrease in serum levels of ICAM-1 and VCAM-1 [70]. In patients with stable CHD, the daily consumption of 50 mL of refined olive oil with different doses of phenolic compounds for 3 weeks improved other inflammatory markers, such as CRP or IL-6 [71]. Several PREDIMED reports confirm the antiinflammatory effect of the MedDiet supplemented with EVOO in comparison with the control diet [24,28–30].

The role of dietary fat in insulin resistance and T2D has been of clinical interest for decades. In general, intake of MUFA or enrichment of membrane lipids with these fatty acids has been found to be neutral regarding either diabetes risk in epidemiological studies [72] or glycemic control in diabetic patients in RCTs comparing MUFA to carbohydrate-rich diets [73]. However, recent data from subjects of a Mediterranean country with high-dietary MUFA intake in the form of olive oil show a significant inverse association between the serum phospholipid proportions of oleic acid, the main MUFA, and insulin resistance assessed by the HOMA method [74]. The KANWU study was a parallel-arm feeding trial in 162 healthy subjects who were given diets with 37% energy from fat, either a high-SFA diet (17% SFA, 14% MUFA) or a high-MUFA diet (8% SFA, 23% MUFA) [75]. The main finding was that substitution of MUFA for SFA improved insulin sensitivity, which was impaired on the SFA diet (− 10%) but did not change on the MUFA diet. Another important finding was that subjects with total fat intake > 37% of energy obtained no benefit from MUFA. While this is consistent with results from a controlled lifestyle intervention trial where changes in estimated desaturase activities (derived from plasma fatty acid composition) were related to changes in insulin sensitivity only in subjects with a total fat intake below 35.5% of energy intake [76], it does not concur with findings from the PREDIMED study, whereby the MedDiet with EVOO reduced T2D risk in spite of having a total fat intake of 42% of daily energy [26]. In line with the KANWU study, a controlled short-term trial in 59 healthy subjects reported impaired insulin sensitivity in those who consumed a SFA-enriched diet compared with those who consumed a MUFA-rich diet, both diets having a total fat content of 38% of energy [77].

Results from the EUROLIVE study have confirmed the in vivo antioxidant properties of olive oil polyphenols in humans [78]. The EUROLIVE was a large, crossover, multicenter clinical trial performed in 200 individuals from five European countries. Participants were randomly assigned to receive 25 mL/day of three similar olive oils, but with different phenolic content, in intervention periods of 3 weeks. The results showed that all olive oils increased HDL-cholesterol and the ratio between reduced and oxidized forms of glutathione and decreased triglycerides, total cholesterol: HDL-cholesterol ratios, and DNA oxidative damage [78,79]. Consumption of medium- and high-phenolic content olive oil also reduced circulating oxidized LDL and other biomarkers of oxidation. In another RCT conducted in 25 healthy men, consumption of olive oil with a modestly elevated (but real life) polyphenol content versus a low-polyphenol one induced a significant decrease in apolipoprotein B levels, total LDL particle number, and small dense LDL particles [80]. Thus, beyond oleic acid, the polyphenols in virgin varieties of olive oil are presumably responsible for many of its beneficial cardiometabolic effects, including preservation of endothelial function.

Some RCTs have tested the effects of consumption of different types of olive oil on endothelial function in either chronic or acute studies. Concerning chronic studies, a small nonrandomized study in 11 diabetic patients showed that an olive oil-enriched diet attenuated the FMD-determined endothelial dysfunction present during consumption of a baseline diet high in PUFA, while at the same time reducing insulin resistance; no details on the type of olive oil used were provided [81]. In another chronic study, a crossover RCT of dietary supplementation with 30 mL of polyphenol-enriched olive oil versus a polyphenol-depleted olive oil during 4 months in 24 women with mild hypertension, the polyphenol-rich oil improved endothelial function as measured by PAT, together with a decrease in blood pressure and reduction in levels of CRP and oxidized LDL [82].

Several acute studies have examined the effects of olive oil meals on endothelial function measured in the postprandial state. High-fat meals impair postprandial endothelial function, which is a relevant outcome in dietary studies. The first postprandial FMD study using olive oil was carried out by Vogel et al. in 10 healthy volunteers who were given five different meals containing 50 g fat each [83]. FMD was measured at baseline and 3 h postprandially. A meal with 50 mL EVOO and bread impaired postprandial FMD, while similar meals with canola oil and bread, salmon with cereals, EVOO with bread and vitamins, and EVOO with bread, vinegar and vegetables did not, implying that vascular reactivity was preserved due to antioxidants in vegetables. That antioxidants (polyphenols) are important to preserve postprandial endothelial function was demonstrated by Ruano et al. in postprandial studies performed in 21 hypercholesterolemic subjects who were given test meals containing bread and 40 mL virgin olive oil either enriched or depleted in polyphenols [84]. Improvement of the RHI (measured with PAT) via reduced oxidative stress and increased NO metabolites was reported after the intake of the phenol-rich olive oil in comparison with the low-phenol one. Another acute study showing improved postprandial FMD in healthy subjects after acute consumption of both 250 mL red wine and 50 mL “green” (virgin) olive oil, two main components of the MedDiet, supports the importance of polyphenols for improved vascular reactivity [85]. However, not all studies are consistent in showing a beneficial effect of EVOO. For instance, in another acute study, 37 healthy volunteers were randomized to receive 50 mL of maize oil, cod liver oil, soya oil, EVOO or water as an isolated meal and endothelial function was measured by VOP at baseline and 3 h postprandially [86]. No changes of postischemic forearm blood flow, serum VCAM-1 or total lipid peroxidation were observed after EVOO. Nevertheless, the consumption of a sizeable amount of oil without any other food is far from a customary meal, which may explain the discrepancy with other studies. Also, not all olive oils labeled as “extra-virgin” contain comparable amounts of polyphenols.

6 Mediterranean style diets, dietary fiber and risk of CVDs

Mediterranean-style diets are characterized by vegetables, whole grains, nuts, fish, poultry, virgin olive oil that are rich sources of dietary fiber, micronutrients, antioxidants and monounsaturated fat, and amino acids in the diets. These diets have a low-GI and have been proven to decrease the risk of CVDs and diabetes in cohort studies, as well as in randomized trials [54–56]. The dietary fiber content can be estimated to vary from 25 g to 35 g/day in Mediterranean-style diets. In a typical Mediterranean diet eating population, the median (percentile 25–75) energy-adjusted intake of fiber was 29.4 g/day (23.9–36.4 g/day) [60]. Major sources of fiber intake were fiber from vegetables (median, 10.1; percentile 25–75, 7.3–13.6 g/day), fiber from fruit (5.0, 3.1–8.5 g/day), fiber from cereals (4.8, 3.6–7.7 g/day), and fiber from legumes (3.7, 2.7–4.7 g/day). The study included 171 cases, with myocardial infarction, whom were less than 80 years of age and sex-matched control subjects showing that three upper quintiles of fiber intake were inversely associated with myocardial infarction [60]. After adjustment for nondietary and dietary confounders, an inverse linear trend was clearly significant, indicating the highest relative reduction of risk (86%) for the fifth quintile (OR = 0.14, 95% CI: 0.03–0.67). An inverse association was also apparent for fruit intake, but not for vegetables or legumes. It seems that a substantial part of the protective effect of the Mediterranean diet on coronary risk might be attributed to a high intake of fiber and fruit. The adverse effects of Western diets are mainly due to refining and high content of sugar, glucose, and fructose [61,62].

Since high-GI of foods have been associated with increased risk of CAD, there is a need to find out if low-GI foods can cause incremental benefits with respect to CAD, among people adhering to the traditional Mediterranean diet [63]. The Greek European Prospective Investigation into Cancer and Nutrition included 20,275 participants free of CVDs, cancer, or diabetes at baseline and without incident diabetes. After a median follow-up of 10.4 years, 417 participants developed CAD, including 162 deaths from the disease. A significant positive association of GI with CAD incidence emerged (HR for the highest vs. the lowest tertile = 1.41, 95% CI: 1.05–1.90). The association with glycemic load was more significant among subjects with higher BMI. A greater adherence to Mediterranean diet with low/moderate glycemic load was associated with lower risk of CAD incidence (HR = 0.61, CI: 0.39–0.95) and mortality (HR = 0.47, 95% CI: 0.23–96). It is possible that a high dietary glycemic load increases the risk of CAD and a high glycemic load diet with suboptimal adherence to the traditional Mediterranean pattern. A low/moderate glycemic load diet could lead to a 40% reduced risk for CAD, and over 50% reduced risk for death from CAD [63]. In a further study involving 1658 individuals, the baseline CV risk was estimated with the Framingham risk score [64]. Participants were divided into two groups: individuals at low risk (CV < 10) and individuals with CV risk ≥10. After a 12-year mean follow-up, 220 deaths, 84 due to CV diseases, and 125 incident CV events occurred [64]. The adherence to the Mediterranean diet was low in 768 (score 0–2), medium in 685 (score 4–5), and high in 205 (score >6) individuals. Interestingly the values of BMI, waist circumference, fasting glucose, and insulin significantly decreased from low to high diet adherence only in participants with CV risk ≥10. Greater adherence to the Mediterranean diet was associated with reduced fatal and nonfatal CV events, especially in individuals at low CV risk, thus suggesting the usefulness of promoting this nutritional pattern in particular in healthier individuals [64].