20
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Mediterranean diet and inflammaging within the hormesis paradigm

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          A coherent set of epidemiological data shows that the Mediterranean diet has beneficial effects capable of preventing a variety of age-related diseases in which low-grade, chronic inflammation/inflammaging plays a major role, but the underpinning mechanism(s) is/are still unclear. It is suggested here that the Mediterranean diet can be conceptualized as a form of chronic hormetic stress, similar to what has been proposed regarding calorie restriction, the most thoroughly studied nutritional intervention. Data on the presence in key Mediterranean foods of a variety of compounds capable of exerting hormetic effects are summarized, and the mechanistic role of the nuclear factor erythroid 2 pathway is highlighted. Within this conceptual framework, particular attention has been devoted to the neurohormetic and neuroprotective properties of the Mediterranean diet, as well as to its ability to maintain an optimal balance between pro- and anti-inflammaging. Finally, the European Commission–funded project NU-AGE is discussed because it addresses a number of variables not commonly taken into consideration, such as age, sex, and ethnicity/genetics, that can modulate the hormetic effect of the Mediterranean diet.

          Related collections

          Most cited references149

          • Record: found
          • Abstract: found
          • Article: not found

          Inflamm-aging. An evolutionary perspective on immunosenescence.

          In this paper we extend the "network theory of aging," and we argue that a global reduction in the capacity to cope with a variety of stressors and a concomitant progressive increase in proinflammatory status are major characteristics of the aging process. This phenomenon, which we will refer to as "inflamm-aging," is provoked by a continuous antigenic load and stress. On the basis of evolutionary studies, we also argue that the immune and the stress responses are equivalent and that antigens are nothing other than particular types of stressors. We also propose to return macrophage to its rightful place as central actor not only in the inflammatory response and immunity, but also in the stress response. The rate of reaching the threshold of proinflammatory status over which diseases/disabilities ensue and the individual capacity to cope with and adapt to stressors are assumed to be complex traits with a genetic component. Finally, we argue that the persistence of inflammatory stimuli over time represents the biologic background (first hit) favoring the susceptibility to age-related diseases/disabilities. A second hit (absence of robust gene variants and/or presence of frail gene variants) is likely necessary to develop overt organ-specific age-related diseases having an inflammatory pathogenesis, such as atherosclerosis, Alzheimer's disease, osteoporosis, and diabetes. Following this perspective, several paradoxes of healthy centenarians (increase of plasma levels of inflammatory cytokines, acute phase proteins, and coagulation factors) are illustrated and explained. In conclusion, the beneficial effects of inflammation devoted to the neutralization of dangerous/harmful agents early in life and in adulthood become detrimental late in life in a period largely not foreseen by evolution, according to the antagonistic pleiotropy theory of aging.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Sirtuins in mammals: insights into their biological function.

            Sirtuins are a conserved family of proteins found in all domains of life. The first known sirtuin, Sir2 (silent information regulator 2) of Saccharomyces cerevisiae, from which the family derives its name, regulates ribosomal DNA recombination, gene silencing, DNA repair, chromosomal stability and longevity. Sir2 homologues also modulate lifespan in worms and flies, and may underlie the beneficial effects of caloric restriction, the only regimen that slows aging and extends lifespan of most classes of organism, including mammals. Sirtuins have gained considerable attention for their impact on mammalian physiology, since they may provide novel targets for treating diseases associated with aging and perhaps extend human lifespan. In this review we describe our current understanding of the biological function of the seven mammalian sirtuins, SIRT1-7, and we will also discuss their potential as mediators of caloric restriction and as pharmacological targets to delay and treat human age-related diseases.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Sirtuin activators mimic caloric restriction and delay ageing in metazoans.

              Caloric restriction extends lifespan in numerous species. In the budding yeast Saccharomyces cerevisiae this effect requires Sir2 (ref. 1), a member of the sirtuin family of NAD+-dependent deacetylases. Sirtuin activating compounds (STACs) can promote the survival of human cells and extend the replicative lifespan of yeast. Here we show that resveratrol and other STACs activate sirtuins from Caenorhabditis elegans and Drosophila melanogaster, and extend the lifespan of these animals without reducing fecundity. Lifespan extension is dependent on functional Sir2, and is not observed when nutrients are restricted. Together these data indicate that STACs slow metazoan ageing by mechanisms that may be related to caloric restriction.
                Bookmark

                Author and article information

                Journal
                Nutr Rev
                Nutr. Rev
                nutritionreviews
                Nutrition Reviews
                Oxford University Press
                0029-6643
                1753-4887
                June 2017
                08 June 2017
                08 June 2017
                : 75
                : 6
                : 442-455
                Affiliations
                M. Martucci, F. Biondi, E. Bellavista, C. Fabbri, C. Bertarelli, S. Salvioli, M. Capri, and A. Santoro are with the Department of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Bologna, Italy. R. Ostan, S. Salvioli, M. Capri, and A. Santoro are with the Interdepartmental Center “L. Galvani” (CIG), University of Bologna, Bologna, Italy. C. Franceschi is with the Institute of Neurological Sciences (IRCCS), Bologna, Italy.
                Author notes
                [*]

                These authors contributed equally to this work.

                A. Santoro, DIMES, University of Bologna, Via San Giacomo 12, 40126 Bologna, Italy. Email: aurelia.santoro@ 123456unibo.it . Phone: +39-051-2094-758.
                Article
                nux013
                10.1093/nutrit/nux013
                5914347
                28595318
                72ea4f54-1ec7-4f71-9450-dcab154fa1de
                © The Author(s) 2017. Published by Oxford University Press on behalf of the International Life Sciences Institute.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence ( http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                Page count
                Pages: 14
                Funding
                Funded by: European Union’s Seventh Framework
                Award ID: 266486
                Funded by: “The Food Biomarkers Alliance (FOODBALL)”
                Award ID: 749
                Funded by: European Union’s Seventh Framework
                Award ID: 613979
                Funded by: “A.GRIFOOD” N.AZIONALE—“CL.A.N.”
                Award ID: CTN01_00230_413096
                Funded by: (“Promotion of consumer health: nutritional enhancement of traditional Italian agricultural food products [PROS.IT]”
                Categories
                Special Articles

                Nutrition & Dietetics
                hormesis,inflammaging,mediterranean diet,nrf2,stress
                Nutrition & Dietetics
                hormesis, inflammaging, mediterranean diet, nrf2, stress

                Comments

                Comment on this article