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There is a large body of evidence indicating that vascular atherosclerosis exerts a key role in the pathogenesis of cardiovascular diseases and that, among lifestyle patterns, the dietary ones are of fundamental importance in the atherogenic process. In this regard, the ‘Mediterranean diet’ was defined in the late 1950s by Keys and Keys  to identify the food habits of southern European populations. However, to encompass a variety of disparate dietary styles of the Mediterranean region, with marked differences in macro- and micronutrient composition of foods, soil where crops are produced, breeding techniques and cooking procedures, into one single definition remains largely questionable. In spite of this, the definition of the Mediterranean diet has more than just important historical value. Indeed, this term conveys, to both patients and physicians, the immediate message of a healthy isoenergetic diet, with a large variety of foods, mostly of vegetable origin rather than animal, that is clearly able to exert beneficial effects on atherosclerosis and its cardiovascular and cerebrovascular sequelae .The reasons leading to the beneficial actions exerted by the Mediterranean diet cannot be restricted to the sole antiatherogenic effects of its low saturated fat content . Consistent with this, current concepts of atherogenesis include involvement of the immune system and chronic inflammation as crucial steps in the initiation and progression of the atherosclerotic process . Activation of the vascular endothelium with upregulation of adhesion molecules is claimed to play a pivotal role in such vascular inflammation by allowing leucocyte and monocyte adhesion to the vascular endothelium during the earliest phases of atherogenesis . After adhesion, endothelial adhesin upregulation induces leucocyte and monocyte penetration into the subendothelial environment [3,4], where they release tumour necrosis factor-α, interleukin-6 and other cytokines, thus recruiting additional circulating cells and enhancing atherosclerotic processes [3,4]. Of note, the membrane-spanning protein CD40 is also upregulated in activated endothelial cells and leucocytes and, after engagement with its natural ligand CD40L expressed by monocytes and T lymphocytes, subsequently amplifies atherogenesis by promoting cytokine release and circulating cell adhesion to the vascular endothelium . Thus, endothelial cell activation is the initiating event in atherosclerosis, but is also fundamental in maintaining an inflammatory milieu within the vascular wall [3,4].Endothelial adhesion molecules are upregulated by the pleiotropic transcriptional factor nuclear factor-κB (NF-κB) which, in turn, is activated by cytokines in the presence of superoxide anion and other endocellular oxidants . Although other intracellular pathways may play a role, interactions of NF-κB, firstly with oxidants in the cytoplasm and then with inflammatory genes in the nucleus, represent the most important mechanisms underlying endothelial adhesion molecule upregulation . Concordant with this, endothelial activation in vivo and in vitro is promoted by oxidants and prevented by natural antioxidants, such as vitamin E, that are largely represented in the original Mediterranean diets . Interestingly, superoxide anion may transform nitric oxide into the oxidant peroxynitrite and thereby further promote atherogenesis, whereas intact nitric oxide markedly inhibits NF-κB activation and has potent antiatherogenic properties [8,9]. Thus, although allowing a normal endothelium-dependent vasodilatory capability, a normal nitric oxide bioavailability also inhibits endothelial adhesion molecule upregulation. As a consequence, an increased nitric oxide availability, either due to nitric oxide synthase stimulation or to antioxidants avoiding nitric oxide transformation into peroxynitrite, or both, is expected to simultaneously protect the vascular endothelium against abnormal vasoconstriction and accelerated atherogenesis .In this context, the study by Fisher et al.