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Dietary Exchange of an Olive Oil and Sunflower Oil Blend for Extra Virgin Olive Oil Decreases the Estimate Cardiovascular Risk and LDL and Apolipoprotein AII Concentrations in Postmenopausal Women

Sección Departamental de Química Analítica. Departamento de Nutrición y Bromatología I (Nutrición). Facultad de Farmacia. Universidad Complutense, Madrid, SPAIN

Address reprint requests to: Profesor Francisco J. Sánchez-Muniz, Departamento de Nutrición y Bromatología I (Nutrición), Facultad de Farmacia, Universidad Complutense de Madrid 28040-Madrid, SPAIN. E-mail: frasan{at}farm.ucm.es

	ABSTRACT

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Background: Dietary supplementation with Virgin olive oil is considered cardioprotective. Decreasing LDL and apolipoprotein (apo) AII-lipoproteins is also appropriate for CHD protection and treatment.

Aim: To study the effects of an 8%En dietary exchange of linoleic acid for oleic acid on serum and lipoprotein levels and serum and LDL-TBARS in postmenopausal women consuming a diet rich in fat (46%En; saturated/monounsaturated/polyunsaturated profile: 1.1/1.9/1).

Experimental Design: 14 postmenopausal women (63 ± 11 years) were assigned to exchange during 28-day dietary period the culinary oil used for years consisting in a blend of olive oil plus sunflower oil (SO) for extra virgin olive oil (EVOO). SO and EVOO represented 62% of the total lipid intake.

Determinations: Dietary intakes, serum Lp(a), and cholesterol, triglycerides, phospholipids, protein, apolipoproteins AI, AII, B were determined in serum and lipoproteins.

Results: The dietary intervention decreased serum total cholesterol (TC), phospholipids, apo AII (all, p < 0.001) and apo B (p < 0.01). Except for triglycerides, all components of the LDL fraction decreased (at least, p < 0.05). HDL-cholesterol was not affected but HDL-phospholipids and HDL-lipids decreased (at least, p < 0.01). VLDL-apo B and VLDL-proteins decreased (all, p < 0.001). Serum Lp(a), TBARS and LDL-TBARS were not affected by the dietary exchange. The estimate of 10-year cardiovascular risk decreased (p < 0.05). Apo AII (p = 0.061) and LDL-cholesterol (p < 0.05) underwent greater modifications in normocholesterolemics, while LDL-phospholipids (p = 0.094), experienced greater alterations in hypercholesterolemics. No significant interaction was observed between dietary exchange and age (> or <65 yrs).

Conclusions: These findings suggest that the dietary exchange of an olive oil and sunflower oil blend for extra virgin olive decreases LDL and apo AII levels, and the estimate of 10-year cardiovascular risk.

Key words: CHD risk, cholesterol, lipoproteins, postmenopausal women, olive oil, sunflower oil, peroxidation

	INTRODUCTION

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Coronary heart disease (CHD) incidence markedly increases after menopause, becoming the main cause of death in females [1]. The dietary pattern has deeply changed in Spain throughout the last decades rising the fat contribution to total energy to about 50% [2]. Moreover, although olive oil is the representative Mediterranean oil, the use of sunflower oil and olive oil blend (SO) has become popular in Spanish homes, small restaurants, and institutions [3]. This change not only affects the fatty acid composition of the diet but also its minor compound content [4].

At present much is known about the effect on lipid metabolism on the principle fatty acids in the human diet [5,6]. At high consumption levels polyunsaturated fatty acids (PUFA) decrease HDL levels [7] and increase lipoprotein peroxidation risk [8]. CHD patients have significantly lower levels of certain HDL subpopulations that contain only apolipoprotein (apo) AI, and significantly higher levels of other HDL subpopulations containing both apo AI and apo AII [9]. Apo AII increases in hypercholesterolemic women after SFA consumption [10]. Apo AI-enriched HDL appear to play a central role in facilitating reverse cholesterol transport; thus, these HDL protect against the development of [11]. Conversely, HDL rich in apo AII have been related to high cardiovascular risk through mechanisms that may involve inhibition of lecithin cholesterol acyl transferase (LCAT) activity or impaired receptor binding [11,12]. Lipoprotein (a) [Lp(a)] is known to be an independent CHD risk factor [13]. However, with the exception of trans fatty acid, diet seems to have little or no effect on Lp(a) levels [14]. Hypercholesterolemic patients are at greater CHD risk due to their higher LDL and apo B levels [15], increased susceptibility to LDL oxidation [16], and higher Lp(a) levels [13].

In contrast to previous documents, the National Cholesterol Education Program now recommends a higher intake of monounsaturated fatty acids (MUFA), in accordance with the experience of the Mediterranean diet [17]. Moreover, many observational epidemiological studies suggest that a high intake of MUFA is associated with reduced coronary risk [18–20]. Although the dietary exchange of MUFA for PUFA has been tested in different populations [21–24], some results are still controversial and the effect of this exchange on Lp(a), lipoprotein composition and HDL-apo AII is not yet well known. Cardiovascular protection decreases with age after menopause [1] and it is thus possible that the dietary exchange of PUFA for MUFA induces different effects on women under and over 65 years of age.

The aims of the current study were to check, in a well-controlled postmenopausal population consuming for years SO oil, the effect of substituting that oil by extra virgin olive oil: (i) on serum lipids and lipoprotein levels and composition; (ii) on serum and LDL peroxides. Furthermore, we studied whether the effects of the dietary intervention depend on serum cholesterol levels and age.

	METHODS

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Subjects
Nuns from an enclosed convent were studied. Subjects were chosen because of their regular lifestyle, age and dietary habits. Fifteen women were initially enrolled in the study, but one was later excluded because she was premenopausal (not a full year had gone by since her last menstruation). The mean age of the 14 volunteers who finished the study was 63 (SD 11). Mean body weight of the subjects was 54.3 (SD 9.3) kg and the mean body mass index was 23.2 (SD 3.4) kg/m². None of the subjects presented previous cardiovascular, metabolic or systemic disease or was taking any medication that might affect lipid metabolism or platelet aggregation. All the women consented to participate in the study. Study protocol was approved by the Spanish Comisión Interministerial de Ciencia y Tecnología and performed in accordance with the Helsinki Declaration.

Experimental Design
Volunteers participate in an intervention study of 28-day length that consisting in exchange the culinary oil used for years (a blend of sunflower and olive oils, both from Koipe, Andújar, Jaén, Spain) for extra virgin olive oil (EVOO) (Comunal Olivarera Mora, Toledo, Spain). A cross-over design was not performed because in a preliminary study we found that the cook preparation at the community kitchen was two difficult and time-consuming because the same food was cooked with two oils. Thus, the logistics involved in food preparation and consumption in the community prevented us from using a cross-over design in the current study. Moreover, the well-controlled postmenopausal population has been consuming the SO oil for years, and the aim of the study was to check the effect of substituting that blend oil by EVOO.

Diets
The diet of the community was assessed using the [precise weighing method.] All ingredients used in the preparation of dishes, as well as the inedible waste, were weighed. The cooked weight of individual portions and table waste was also recorded. Energy and nutrient intakes were calculated using food composition tables for the foodstuff raw weights [25]. A 14-day menu cycle was used. During the intervention period same culinary habits, same foods and same food-ratios was used with respect to the preintervention period. This allows us to prevent collateral effects on lipoproteins related to dietary change behavior. Thus, the single distinguishing feature of the experimental diets involved the culinary oil used. A high proportion of the oils (45%) was consumed raw in salad dressing, while the rest was used for sautéing, frying, post-roasting and in preparing fish, eggs, vegetables and stews.

Laboratory Analyses
Fatty acid composition of the oil was analyzed using a Hewlett-Packard 5890 Series II gas chromatograph (Palo Alto, California, USA) as indicated in [26]. Reverse-phase high-performance liquid chromatography [27] was used for -tocopherol determination, and total polyphenols were determined using the method of Folin-Ciocalteau [28]. Other minor compounds were determined in the non-saponifiable fraction of the oils by gas chromatography [29].

After overnight fasting (12 hours), blood samples were collected by venipuncture. Blood was gently collected after the anthropometric evaluation, thereby avoiding any stress on the part of the volunteers. Total cholesterol (TC), phospholipids and triglycerides in serum and lipoproteins were determined using a Technicon RA-500 autoanalyzer (Tarrytown, New York) and the standard enzymatic methods of Boehringer Mannheim (Mannheim Germany). Apo A-I and apo B were determined by turbidimetry (Behring Turbitimer, Barcelona, Spain) using Dade Behring reactives and protocols. Apo B in VLDL fractions and apo A-II were determined by rocket immunoelectrophoresis [30]. Lp(a) was determined by RIA assay following method and indications of Pharmacia (Mercodia, Uppsala, Sweden). The Lowry et al. method [31] was employed for total protein content determination in VLDL, LDL, and HDL. Reference quality controls (Precinorm, reference 225053 and Precilip reference 781827, Boehringer Mannheim) were included in all assays. External quality control was performed by Welcome Diagnóstico (Spain) in the case of lipid and serum apo A-I and apo B determinations. Inter and intra-assay variation coefficients were 5.5. Analysis for VLDL-apo B and serum apo II and Lp(a) was validated by internal quality control charts using a pool of VLDL fractions and serum pool from healthy people. Intra-assay variation coefficients of pools (n = 50) were 5%. The multi-rule Shewhart procedure were taking into account as decision criteria for acceptation of rejection assay.

Lipoproteins were isolated by 22 hours of density-gradient ultracentrifugation using the salt gradient composition suggested by Terpstra et al. [32] and then desalted. However, ultracentrifugation was performed at 8°C instead of 20°C to ensure less lipoprotein thermal damage [26].

Thiobarbituric acid-reactive substances in serum (serum-TBARS) and LDL (LDL-TBARS) was determined according to Yagi [33]. Estimates of 10 years were calculated in accordance with ATP III report after considering the subjects’ age, tobacco consumption, blood pressure, TC and HDL-cholesterol [17].

Statistical Analyses
The paired t-test was employed to study the dietary exchange effect on lipids and lipoproteins. Data with a non-parametric distribution were normalized by logarithmic transformation. The effects on lipoprotein percent composition were checked by the Wilcoxon and U-Mann Whitney tests. Repeated measures ANOVA was used to assess the effects of the oil exchange on normo (TC <6.21 mM) and hypercholesterolemic women (TC 6.21 mM) and in women aged or <65.

	RESULTS

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Dietary Assessment
Food intake was determined to be exactly the same through both dietary periods (Table 1). Fats and oils contributed two-thirds of the total lipid consumption in both experimental periods. The study oils provided 62% of the total fat intake in both periods. The energy contribution of oleic acid was 19.6% in the SO diet and 27.5% in the EVOO diet. However, linoleic acid was higher in the SO diet (10.0%) and lower in the EVOO one (2.2%). Palmitic acid, other SFA and other PUFA (e.g. -3 PUFA) contributions were similar in both diets (Table 1). Polyphenols and squalene were higher in the EVOO diet, while all sterols and -tocopherol were higher in the SO one (Table 2). Body weight did not significantly change throughout the study (data not shown).

View this table: [in this window] [in a new window]   Table 4. Changes in Lipids and Apolipoproteins and in Serum TBARS and LDL-TBARS by the Dietary Intervention in Normo (Total Cholesterol, TC <6.21 mmol/L) and Hypercholesterolemics (TC 6.21 mmol/L)

View this table: [in this window] [in a new window]   Table 5. Effects of the Dietary Intervention in VLDL and LDL of Normocholesterolemics (TC <6.21 mmol/L) and Hypercholesterolemics (TC 6.21 mmol/L)

View this table: [in this window] [in a new window]   Table 6. Changes in Some CDH Risk Ratios and CHD Risk by the Dietary Intervention in the Whole Population and in Normo (Total Cholesterol, TC <6.21 mmol/L) and Hypercholesterolemics (TC 6.21 mmol/L)

	DISCUSSION

 
Dietary Assessment
Fat energy contribution of basal diet was very high. This is in agreement with the current diet of most population groups in Spain [2] and far from recommended [2,17–20]. As both diets presented the same energy profile and cholesterol content, results obtained will be discussed taking into account fatty acid and dietary minor compound changes.

Serum and Lipoprotein Lipid Change
The most interesting consequence of the dietary exchange involves a decrease in serum TC, LDL-cholesterol, LDL-apo B, and apo AII levels suggesting a net anti-atherogenic effect [17–20]. This effect was confirmed taking into account the reduction in the estimates of 10-years CHD risk score in this already low 10-years CHD-risk group [17]. Moreover, VLDL-apo B levels also decreased. These results agree with those of others [5,24] although other studies did not found significant differences [34] or describe that PUFA diets have a higher effect on decreasing TC and LDL-cholesterol than MUFA diets [5,6]. Nevertheless, most studies differ with regard to experimental design, population age, basal cholesterol and lipoprotein levels, energy contribution of fat, SFA, MUFA, and PUFA and cholesterol [21,23,24,35]. In this respect, during the EVOO dietary period PUFA %En was lower while MUFA %En was higher than the corresponding values in any other related study consulted. Baudet & Jacotot [36] have suggested that the decrease of LDL during MUFA and PUFA diets is related to a modification of LDL receptor (LDL-R) activity. MUFA and PUFA decrease LDL levels to a greater extent than SFA by increasing the cholesterol ester pool size, stimulating the mRNA genesis of LDL-R [37,38]. This regulatory effect increases when dietary cholesterol level is high [38,39]. Dietschy [39] has demonstrated that oleic acid stimulates LDL-R activity twice as much as linoleic acid in hamsters. This effect can be explained because oleic acid is a better and more efficient substrate than linoleic acid for the acyl CoA cholesterol acyl transferase (ACAT) enzyme, thus increasing cholesterol esterification in the liver. Patients on MUFA diets tend to display a greater lymphocyte LDL-R activity than those of on PUFA diets [40].

The absence of any change in HDL-cholesterol levels concurs with the findings of several studies, excepting that of Mata et al. [22]. PUFA %En was higher than 14% in almost two-thirds of the studies reviewed, and HDL-cholesterol decreased more than 2.5 mg/dL in only two of the studies. According to Matson & Grundy [7], PUFA-enriched diets decrease HDL-cholesterol levels more than oleic acid-enriched diets only when linoleic intake is above 28%En.

After the dietary intervention, apo AII decreased much more than apo AI suggesting the presence apo AII-impoverished HDL and thus the improvement of the antiatherogenic properties of HDL via the reverse cholesterol transport [10–12]. Moreover, the presence of lower apo AII in HDL may also be a determinant in receptor interaction and this could be of physiopathological relevance [11,12]. The decrease found in apo AII differs from results of others [22] and may be explained by the different MUFA, PUFA and cholesterol contents of both study diets.

Our data concur with bibliography where Lp(a) is thought to be rather insensitive to dietary modifications [14]. The decrease in serum phospholipids contrasts with the increase observed by Valsta et al. [24]. The reduction of phospholipids could be related to the low PUFA availability for phospholipid synthesis caused by the low linoleic content of the EVOO diet. The decrease in LDL-apo B was remarkable. As each LDL contains only one apo B molecule, this decrease implies that there were fewer LDL particles after the dietary intervention. The reduction in total apo B was the result of a decrease of apo B in VLDL and LDL. McNamara [41] postulated that the hypocholesterolemic effect of MUFA intake relates to changes in LDL apo B production rates. Changes observed in apo B differ from those described by others [22,42] and suggest that the dietary intervention lowers CHD risk.

Serum and LDL-TBARS were similar following both dietary periods. Moreover, the relative LDL-TBARS transport (% of serum TBARS in LDL) was 33% in the SO diet and 32% in the EVOO diet. These results coincide with those of others [16], who showed that neither MUFA nor PUFA intake led to changes in the peroxidation lag-phase, but differ from others that indicate that MUFA intake diminished LDL-oxidation susceptibility [8,43]. These results appear to be a consequence of the equilibrium between pro- and anti-oxidant factors. Thus, (i) dietary intervention decreases the PUFA content of lipoproteins, making them less susceptible to peroxidation [19,44]; (ii) MUFA n-6 increase the PUFA n-3 content of platelet and membrane phospholipids more than PUFA n-6 [45], which in turn increases susceptibility of lipoprotein peroxidation during the EVOO diet; (iii) Phenolic compounds and squalene were higher in the EVOO diet while tocopherols and some sterols were higher in the SO diet. Thus, their respective antioxidant properties would be counterbalanced [4,19].

According to our data, a large percentage of peroxides is carried by lipoproteins other than LDL [e.g. very low density lipoproteins and high density lipoproteins (HDL)] (67% in SO and 68% in EVOO). This coincides with the results of others [46] and suggests that HDL play an important role in antioxidant protection [47].

Normocholesterolemics vs. Hypercholesterolemics
Although hypercholesterolemic women differed greatly from normocholesterolemics with regard to lipids and lipoproteins, the dietary intervention affected both groups similarly, except in LDL values. Thus, as a result of the dietary exchange, LDL-cholesterol levels dropped almost 5 times more in normo than in hypercholesterolemics, suggesting that MUFA increase LDL-R activity more than PUFA in that group of women. However, the effect on LDL-phospholipids was 5 times greater in hyper than in normocholesterolemics. We far from know the physiological and pathological consequences of the decrease of LDL-phospholipids but it may be related to the previously mentioned lower availability for phospholipids and the higher availability for liver cholesterol esterification of oleic acid. Taking into account the predictive value of TC/LDL-cholesterol and LDL-cholesterol/HDL-cholesterol ratios on CHD risk [48], the changes observed also suggest higher benefits among normocholesterolemics.

Higher serum and LDL-TBARS levels were found in hypercholesterolemic women following both diets, suggesting their greater susceptibility to LDL oxidation. According to Holvoet & Collen [16], the higher susceptibility to LDL oxidation observed in CHD patients is partly a result of the fatty acid composition of the LDL particles and partly due to the reduction of endogenous antioxidants such as vitamin E. In normocholesterolemics, the relative transport of peroxides by LDL was 44% and 41.1% in the SO and EVOO periods, respectively, while it was 30% and 28.6% in hypercholesterolemics during the same periods.

In concordance with Garrido et al. [49], women over 65 tended to display more altered lipid and lipoprotein values than those under 65 in both periods. However, dietary intervention did not affect any lipid or lipoprotein parameter of the younger or older postmenopausal women differently.

Lipoprotein Composition Changes
After the dietary intervention, the relative composition of lipoproteins changed. Although lipoprotein fractions are formed by lipoprotein subpopulations that differ in size and composition, results can be discussed on the basis of [average] particles. The dietary intervention enriched the lipid contribution of VLDL particles in the whole group and in the hypercholesterolemics. Although triglyceride and cholesterol contributions to the LDL mass changed, there was absence of changes in the total lipids and proteins contributions to the LDL mass. This fact together with the decrease in LDL-mass, LDL-apo B, and the LDL-cholesterol/LDL-apo B ratio suggest that the dietary intervention produces significantly lower number of [average,] similar-sized LDL particles in normocholesterolemics as well as in hypercholesterolemics. This fact should be considered very positive from a CHD point of view. HDL mass decreased mainly due to a reduction in phospholipids and apo AII, suggesting that women presented a higher proportion of HDL-3 particles following the EVOO diet. HDL remodeling may be determined in part by the influence of apo AII on the reactivity toward lipid transfer proteins, enzymes, and the receptors involved in HDL metabolism and, also, by its ability to displace apo AI from the HDL surface [12]. The significant decrease in the contribution of apo AII to the HDL-mass suggests the presence of more antiatherogenic HDL particles in these women after the dietary intervention.

In conclusion, this dietary intervention decreased the CHD estimate risk as a result of a reduction in LDL-cholesterol, LDL-apo B and apo AII levels. The effect on LDL and the 10-years CHD estimate risk was especially notable in normocholesterolemic postmenopausal women but the HDL composition changed more in their hypercholesterolemic counterparts.

	ACKNOWLEDGMENTS

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This study was supported by a grant from the Spanish Comisión Interministerial de Ciencia y Tecnología (CICYT). Proyecto ALI-92-0289-CO2-01 and Danone-Complutense Project PR248/01-10-161. The authors are indebted to the Carmelitas Descalzas nuns (Lerma, Burgos, Spain) for their contribution. We also wish to thank Hoffmann La Roche (Basel, Switzerland), Koipe (Andújar, Jaén, Spain), Laura Barrios, Ana Sánchez, Teresa Ruiz-Pérez and Dr. Melchor Ruiz for their advice and assistance.

Received July 5, 2004. Accepted June 18, 2005.

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